CREBBP and SMAD4 |
CREB binding protein |
SMAD family member 4 |
- Signaling by NOTCH1 HD Domain Mutants in Cancer
- Metabolism of lipids and lipoproteins
- Signaling by Wnt
- Regulation of gene expression by Hypoxia-inducible Factor
- Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant
- Generic Transcription Pathway
- Pre-NOTCH Transcription and Translation
- RNF mutants show enhanced WNT signaling and proliferation
- Signaling by NOTCH1 in Cancer
- Orphan transporters
- Chromatin organization
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- Signaling by NOTCH
- formation of the beta-catenin:TCF transactivating complex
- Factors involved in megakaryocyte development and platelet production
- Chromatin modifying enzymes
- LRR FLII-interacting protein 1 (LRRFIP1) activates type I IFN production
- Signaling by NOTCH1 PEST Domain Mutants in Cancer
- Activation of gene expression by SREBF (SREBP)
- Transcriptional activation of mitochondrial biogenesis
- Constitutive Signaling by NOTCH1 PEST Domain Mutants
- PPARA activates gene expression
- Cellular response to hypoxia
- Organelle biogenesis and maintenance
- Regulation of Hypoxia-inducible Factor (HIF) by oxygen
- Signaling by NOTCH1 HD+PEST Domain Mutants in Cancer
- Attenuation phase
- HATs acetylate histones
- RORA activates circadian gene expression
- Regulation of cholesterol biosynthesis by SREBP (SREBF)
- HSF1-dependent transactivation
- TRAF3-dependent IRF activation pathway
- Signaling by NOTCH1
- Transcriptional regulation of white adipocyte differentiation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Pre-NOTCH Expression and Processing
- Constitutive Signaling by NOTCH1 HD+PEST Domain Mutants
- Innate Immune System
- FBXW7 Mutants and NOTCH1 in Cancer
- Fatty acid, triacylglycerol, and ketone body metabolism
- Cytosolic sensors of pathogen-associated DNA
- Cellular response to heat stress
- REV-ERBA represses gene expression
- Mitochondrial biogenesis
- Notch-HLH transcription pathway
- RIG-I/MDA5 mediated induction of IFN-alpha/beta pathways
- NOTCH1 Intracellular Domain Regulates Transcription
- TCF dependent signaling in response to WNT
- TRAF6 mediated IRF7 activation
- YAP1- and WWTR1 (TAZ)-stimulated gene expression
- Regulation of lipid metabolism by Peroxisome proliferator-activated receptor alpha (PPARalpha)
- Signaling by WNT in cancer
- BMAL1:CLOCK,NPAS2 activates circadian gene expression
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- Loss of Function of TGFBR2 in Cancer
- SMAD2/3 MH2 Domain Mutants in Cancer
- TGF-beta receptor signaling activates SMADs
- TGFBR1 LBD Mutants in Cancer
- Downregulation of SMAD2/3:SMAD4 transcriptional activity
- SMAD2/SMAD3:SMAD4 heterotrimer regulates transcription
- Transcriptional activity of SMAD2/SMAD3:SMAD4 heterotrimer
- Signaling by BMP
- Transcriptional regulation of pluripotent stem cells
- Generic Transcription Pathway
- Signaling by NODAL
- TGFBR2 MSI Frameshift Mutants in Cancer
- SMAD2/3 Phosphorylation Motif Mutants in Cancer
- Loss of Function of SMAD2/3 in Cancer
- Signaling by Activin
- TGFBR2 Kinase Domain Mutants in Cancer
- Loss of Function of SMAD4 in Cancer
- TGFBR1 KD Mutants in Cancer
- Loss of Function of TGFBR1 in Cancer
- Signaling by TGF-beta Receptor Complex in Cancer
- Signaling by TGF-beta Receptor Complex
- SMAD4 MH2 Domain Mutants in Cancer
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CREBBP and CTNNB1 |
CREB binding protein |
catenin (cadherin-associated protein), beta 1, 88kDa |
- Signaling by NOTCH1 HD Domain Mutants in Cancer
- Metabolism of lipids and lipoproteins
- Signaling by Wnt
- Regulation of gene expression by Hypoxia-inducible Factor
- Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant
- Generic Transcription Pathway
- Pre-NOTCH Transcription and Translation
- RNF mutants show enhanced WNT signaling and proliferation
- Signaling by NOTCH1 in Cancer
- Orphan transporters
- Chromatin organization
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- Signaling by NOTCH
- formation of the beta-catenin:TCF transactivating complex
- Factors involved in megakaryocyte development and platelet production
- Chromatin modifying enzymes
- LRR FLII-interacting protein 1 (LRRFIP1) activates type I IFN production
- Signaling by NOTCH1 PEST Domain Mutants in Cancer
- Activation of gene expression by SREBF (SREBP)
- Transcriptional activation of mitochondrial biogenesis
- Constitutive Signaling by NOTCH1 PEST Domain Mutants
- PPARA activates gene expression
- Cellular response to hypoxia
- Organelle biogenesis and maintenance
- Regulation of Hypoxia-inducible Factor (HIF) by oxygen
- Signaling by NOTCH1 HD+PEST Domain Mutants in Cancer
- Attenuation phase
- HATs acetylate histones
- RORA activates circadian gene expression
- Regulation of cholesterol biosynthesis by SREBP (SREBF)
- HSF1-dependent transactivation
- TRAF3-dependent IRF activation pathway
- Signaling by NOTCH1
- Transcriptional regulation of white adipocyte differentiation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Pre-NOTCH Expression and Processing
- Constitutive Signaling by NOTCH1 HD+PEST Domain Mutants
- Innate Immune System
- FBXW7 Mutants and NOTCH1 in Cancer
- Fatty acid, triacylglycerol, and ketone body metabolism
- Cytosolic sensors of pathogen-associated DNA
- Cellular response to heat stress
- REV-ERBA represses gene expression
- Mitochondrial biogenesis
- Notch-HLH transcription pathway
- RIG-I/MDA5 mediated induction of IFN-alpha/beta pathways
- NOTCH1 Intracellular Domain Regulates Transcription
- TCF dependent signaling in response to WNT
- TRAF6 mediated IRF7 activation
- YAP1- and WWTR1 (TAZ)-stimulated gene expression
- Regulation of lipid metabolism by Peroxisome proliferator-activated receptor alpha (PPARalpha)
- Signaling by WNT in cancer
- BMAL1:CLOCK,NPAS2 activates circadian gene expression
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- APC truncation mutants have impaired AXIN binding
- misspliced GSK3beta mutants stabilize beta-catenin
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- binding of TCF/LEF:CTNNB1 to target gene promoters
- deactivation of the beta-catenin transactivating complex
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- RNF mutants show enhanced WNT signaling and proliferation
- S33 mutants of beta-catenin aren't phosphorylated
- XAV939 inhibits tankyrase, stabilizing AXIN
- Innate Immune System
- truncations of AMER1 destabilize the destruction complex
- CDO in myogenesis
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- Cytosolic sensors of pathogen-associated DNA
- formation of the beta-catenin:TCF transactivating complex
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- repression of WNT target genes
- beta-catenin independent WNT signaling
- deletions in the AMER1 gene destabilize the destruction complex
- Ca2+ pathway
- Myogenesis
- AMER1 mutants destabilize the destruction complex
- TCF dependent signaling in response to WNT
- LRR FLII-interacting protein 1 (LRRFIP1) activates type I IFN production
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by WNT in cancer
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CREBBP and SMAD2 |
CREB binding protein |
SMAD family member 2 |
- Signaling by NOTCH1 HD Domain Mutants in Cancer
- Metabolism of lipids and lipoproteins
- Signaling by Wnt
- Regulation of gene expression by Hypoxia-inducible Factor
- Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant
- Generic Transcription Pathway
- Pre-NOTCH Transcription and Translation
- RNF mutants show enhanced WNT signaling and proliferation
- Signaling by NOTCH1 in Cancer
- Orphan transporters
- Chromatin organization
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- Signaling by NOTCH
- formation of the beta-catenin:TCF transactivating complex
- Factors involved in megakaryocyte development and platelet production
- Chromatin modifying enzymes
- LRR FLII-interacting protein 1 (LRRFIP1) activates type I IFN production
- Signaling by NOTCH1 PEST Domain Mutants in Cancer
- Activation of gene expression by SREBF (SREBP)
- Transcriptional activation of mitochondrial biogenesis
- Constitutive Signaling by NOTCH1 PEST Domain Mutants
- PPARA activates gene expression
- Cellular response to hypoxia
- Organelle biogenesis and maintenance
- Regulation of Hypoxia-inducible Factor (HIF) by oxygen
- Signaling by NOTCH1 HD+PEST Domain Mutants in Cancer
- Attenuation phase
- HATs acetylate histones
- RORA activates circadian gene expression
- Regulation of cholesterol biosynthesis by SREBP (SREBF)
- HSF1-dependent transactivation
- TRAF3-dependent IRF activation pathway
- Signaling by NOTCH1
- Transcriptional regulation of white adipocyte differentiation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Pre-NOTCH Expression and Processing
- Constitutive Signaling by NOTCH1 HD+PEST Domain Mutants
- Innate Immune System
- FBXW7 Mutants and NOTCH1 in Cancer
- Fatty acid, triacylglycerol, and ketone body metabolism
- Cytosolic sensors of pathogen-associated DNA
- Cellular response to heat stress
- REV-ERBA represses gene expression
- Mitochondrial biogenesis
- Notch-HLH transcription pathway
- RIG-I/MDA5 mediated induction of IFN-alpha/beta pathways
- NOTCH1 Intracellular Domain Regulates Transcription
- TCF dependent signaling in response to WNT
- TRAF6 mediated IRF7 activation
- YAP1- and WWTR1 (TAZ)-stimulated gene expression
- Regulation of lipid metabolism by Peroxisome proliferator-activated receptor alpha (PPARalpha)
- Signaling by WNT in cancer
- BMAL1:CLOCK,NPAS2 activates circadian gene expression
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- Loss of Function of TGFBR2 in Cancer
- SMAD2/3 MH2 Domain Mutants in Cancer
- Downregulation of TGF-beta receptor signaling
- TGF-beta receptor signaling activates SMADs
- TGFBR1 LBD Mutants in Cancer
- Downregulation of SMAD2/3:SMAD4 transcriptional activity
- SMAD2/SMAD3:SMAD4 heterotrimer regulates transcription
- Transcriptional activity of SMAD2/SMAD3:SMAD4 heterotrimer
- Generic Transcription Pathway
- Signaling by NODAL
- TGFBR2 MSI Frameshift Mutants in Cancer
- SMAD2/3 Phosphorylation Motif Mutants in Cancer
- Loss of Function of SMAD2/3 in Cancer
- Signaling by Activin
- TGFBR2 Kinase Domain Mutants in Cancer
- Loss of Function of SMAD4 in Cancer
- TGFBR1 KD Mutants in Cancer
- Loss of Function of TGFBR1 in Cancer
- Signaling by TGF-beta Receptor Complex in Cancer
- Signaling by TGF-beta Receptor Complex
- SMAD4 MH2 Domain Mutants in Cancer
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CSK and SHC1 |
c-src tyrosine kinase |
SHC (Src homology 2 domain containing) transforming protein 1 |
- Costimulation by the CD28 family
- GAB1 signalosome
- Integrin alphaIIb beta3 signaling
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- Signaling by EGFRvIII in Cancer
- Platelet Aggregation (Plug Formation)
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Signaling by EGFR
- TCR signaling
- Signaling by EGFR in Cancer
- PD-1 signaling
- Platelet activation, signaling and aggregation
- Phosphorylation of CD3 and TCR zeta chains
- Adaptive Immune System
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- Signaling by GPCR
- Signaling by EGFRvIII in Cancer
- Platelet Aggregation (Plug Formation)
- SHC1 events in ERBB2 signaling
- IRE1alpha activates chaperones
- Constitutive Signaling by Ligand-Responsive EGFR Cancer Variants
- Interleukin receptor SHC signaling
- SHC-mediated signalling
- G-protein beta:gamma signalling
- SHC-related events triggered by IGF1R
- Signaling by ERBB4
- Signaling by ERBB2
- Signaling by EGFR
- Signaling by Interleukins
- GPCR downstream signaling
- SHC1 events in ERBB4 signaling
- Signalling to RAS
- Signaling by EGFR in Cancer
- Interleukin-2 signaling
- Platelet activation, signaling and aggregation
- Interleukin-3, 5 and GM-CSF signaling
- Signalling to ERKs
- IGF1R signaling cascade
- XBP1(S) activates chaperone genes
- G beta:gamma signalling through PI3Kgamma
- Unfolded Protein Response (UPR)
- Signaling by Insulin receptor
- Signalling by NGF
- Insulin receptor signalling cascade
- SHC-mediated signalling
- Integrin alphaIIb beta3 signaling
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- Cytokine Signaling in Immune system
- NGF signalling via TRKA from the plasma membrane
- SHC-related events
- Tie2 Signaling
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Cell surface interactions at the vascular wall
- SHC1 events in EGFR signaling
- Signal attenuation
- Signaling by Type 1 Insulin-like Growth Factor 1 Receptor (IGF1R)
- Interleukin receptor SHC signaling
- GPVI-mediated activation cascade
- Constitutive Signaling by EGFRvIII
- SHC activation
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CSNK1A1 and TGFBR1 |
casein kinase 1, alpha 1 |
transforming growth factor, beta receptor 1 |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
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- Loss of Function of TGFBR2 in Cancer
- TGF-beta receptor signaling in EMT (epithelial to mesenchymal transition)
- TGFBR2 MSI Frameshift Mutants in Cancer
- SMAD2/3 Phosphorylation Motif Mutants in Cancer
- Loss of Function of SMAD2/3 in Cancer
- TGFBR2 Kinase Domain Mutants in Cancer
- Downregulation of TGF-beta receptor signaling
- SMAD2/3 MH2 Domain Mutants in Cancer
- Loss of Function of SMAD4 in Cancer
- TGFBR1 KD Mutants in Cancer
- TGF-beta receptor signaling activates SMADs
- TGFBR1 LBD Mutants in Cancer
- Loss of Function of TGFBR1 in Cancer
- Signaling by TGF-beta Receptor Complex in Cancer
- Signaling by TGF-beta Receptor Complex
- SMAD4 MH2 Domain Mutants in Cancer
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CSNK1A1 and PPP2R5A |
casein kinase 1, alpha 1 |
protein phosphatase 2, regulatory subunit B, alpha |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
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- Mitotic Prometaphase
- Costimulation by the CD28 family
- Separation of Sister Chromatids
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- truncated APC mutants destabilize the destruction complex
- TCF7L2 mutants don't bind CTBP
- Mitotic Anaphase
- Signaling by Wnt
- M Phase
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- Degradation of beta-catenin by the destruction complex
- S37 mutants of beta-catenin aren't phosphorylated
- RNF mutants show enhanced WNT signaling and proliferation
- S33 mutants of beta-catenin aren't phosphorylated
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- CTLA4 inhibitory signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- Cell Cycle, Mitotic
- Platelet homeostasis
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- Platelet sensitization by LDL
- AMER1 mutants destabilize the destruction complex
- Resolution of Sister Chromatid Cohesion
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by WNT in cancer
- Mitotic Metaphase and Anaphase
- Adaptive Immune System
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CSNK1A1 and PDE4D |
casein kinase 1, alpha 1 |
phosphodiesterase 4D, cAMP-specific |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
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- Signaling by GPCR
- GPCR downstream signaling
- G alpha (s) signalling events
- Opioid Signalling
- DARPP-32 events
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- Adenosine monophosphate
- Dyphylline
- Ketotifen
- Iloprost
- Roflumilast
- Piclamilast
- 4-[3-(Cyclopentyloxy)-4-Methoxyphenyl]-2-Pyrrolidinone
- 3,5-Dimethyl-1-(3-Nitrophenyl)-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester
- 2-[3-(2-Hydroxy-1,1-Dihydroxymethyl-Ethylamino)-Propylamino]-2-Hydroxymethyl-Propane-1,3-Diol
- 6-(4-Difluoromethoxy-3-Methoxy-Phenyl)-2h-Pyridazin-3-One
- 1-(4-Aminophenyl)-3,5-Dimethyl-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester
- (S)-Rolipram
- Cis-4-Cyano-4-[3-(Cyclopentyloxy)-4-Methoxyphenyl]Cyclohexanecarboxylic Acid
- (R)-Rolipram
- 3,5-Dimethyl-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester
- 1-(4-Methoxyphenyl)-3,5-Dimethyl-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester
- Ibudilast
- (4R)-4-(3-butoxy-4-methoxybenzyl)imidazolidin-2-one
- 3,5-DIMETHYL-1-PHENYL-1H-PYRAZOLE-4-CARBOXYLIC ACID ETHYL ESTER
- 3-ISOBUTYL-1-METHYLXANTHINE
- 4-[8-(3-nitrophenyl)-1,7-naphthyridin-6-yl]benzoic acid
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CSNK1A1 and PSEN2 |
casein kinase 1, alpha 1 |
presenilin 2 |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
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- Signaling by NOTCH1 HD Domain Mutants in Cancer
- Axon guidance
- Signaling by NOTCH1 HD+PEST Domain Mutants in Cancer
- Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant
- Signaling by NOTCH2
- EPH-ephrin mediated repulsion of cells
- Signaling by NOTCH1
- EPH-Ephrin signaling
- Signaling by NOTCH1 in Cancer
- Constitutive Signaling by NOTCH1 HD+PEST Domain Mutants
- FBXW7 Mutants and NOTCH1 in Cancer
- Signaling by NOTCH4
- Regulated proteolysis of p75NTR
- Signalling by NGF
- Cell death signalling via NRAGE, NRIF and NADE
- Signaling by NOTCH
- p75 NTR receptor-mediated signalling
- Signaling by ERBB4
- NOTCH2 Activation and Transmission of Signal to the Nucleus
- Activated NOTCH1 Transmits Signal to the Nucleus
- Nuclear signaling by ERBB4
- NRIF signals cell death from the nucleus
- Signaling by NOTCH1 PEST Domain Mutants in Cancer
- Signaling by NOTCH3
- Constitutive Signaling by NOTCH1 PEST Domain Mutants
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CSNK1A1 and PHLPP1 |
casein kinase 1, alpha 1 |
PH domain and leucine rich repeat protein phosphatase 1 |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
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- Signaling by the B Cell Receptor (BCR)
- Signaling by FGFR in disease
- PIP3 activates AKT signaling
- Signaling by EGFRvIII in Cancer
- Signaling by SCF-KIT
- DAP12 signaling
- Downstream signaling events of B Cell Receptor (BCR)
- PI3K/AKT activation
- PI-3K cascade
- PI3K events in ERBB2 signaling
- Downstream signaling of activated FGFR
- Innate Immune System
- Signaling by PDGF
- DAP12 interactions
- Signalling by NGF
- GAB1 signalosome
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- NGF signalling via TRKA from the plasma membrane
- Signaling by ERBB4
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Negative regulation of the PI3K/AKT network
- Role of LAT2/NTAL/LAB on calcium mobilization
- PI3K events in ERBB4 signaling
- Signaling by FGFR
- Signaling by ERBB2
- Signaling by EGFR
- Downstream signal transduction
- Fc epsilon receptor (FCERI) signaling
- Signaling by EGFR in Cancer
- PI3K/AKT Signaling in Cancer
- Adaptive Immune System
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CSNK1A1 and PARK2 |
casein kinase 1, alpha 1 |
parkin RBR E3 ubiquitin protein ligase |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
|
- Antigen processing: Ubiquitination & Proteasome degradation
- Class I MHC mediated antigen processing & presentation
- Adaptive Immune System
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CSNK1A1 and MDM4 |
casein kinase 1, alpha 1 |
MDM4, p53 regulator |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
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|
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CSNK1A1 and YWHAZ |
casein kinase 1, alpha 1 |
tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
|
- Translocation of GLUT4 to the plasma membrane
- Activation of BH3-only proteins
- Signaling by Wnt
- deactivation of the beta-catenin transactivating complex
- Rap1 signalling
- RNF mutants show enhanced WNT signaling and proliferation
- Programmed Cell Death
- XAV939 inhibits tankyrase, stabilizing AXIN
- Intrinsic Pathway for Apoptosis
- Regulation of mRNA stability by proteins that bind AU-rich elements
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- Cytokine Signaling in Immune system
- Activation of BAD and translocation to mitochondria
- Signaling by Interleukins
- TCF dependent signaling in response to WNT
- KSRP destabilizes mRNA
- GP1b-IX-V activation signalling
- Signaling by WNT in cancer
- Platelet activation, signaling and aggregation
- Interleukin-3, 5 and GM-CSF signaling
- Adaptive Immune System
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CSNK1A1 and TP53 |
casein kinase 1, alpha 1 |
tumor protein p53 |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
|
- Cellular Senescence
- Activation of BH3-only proteins
- p53-Dependent G1/S DNA damage checkpoint
- Oncogene Induced Senescence
- p53-Dependent G1 DNA Damage Response
- Formation of Senescence-Associated Heterochromatin Foci (SAHF)
- Pre-NOTCH Transcription and Translation
- Stabilization of p53
- Transcriptional activation of p53 responsive genes
- Programmed Cell Death
- Pre-NOTCH Expression and Processing
- G1/S DNA Damage Checkpoints
- Intrinsic Pathway for Apoptosis
- Transcriptional activation of cell cycle inhibitor p21
- DNA Damage/Telomere Stress Induced Senescence
- Signaling by NOTCH
- Factors involved in megakaryocyte development and platelet production
- Activation of NOXA and translocation to mitochondria
- Oxidative Stress Induced Senescence
- Autodegradation of the E3 ubiquitin ligase COP1
- Activation of PUMA and translocation to mitochondria
- Cell Cycle Checkpoints
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CSNK1A1 and AXIN1 |
casein kinase 1, alpha 1 |
axin 1 |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
|
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- RNF mutants show enhanced WNT signaling and proliferation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- AMER1 mutants destabilize the destruction complex
- TCF dependent signaling in response to WNT
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- degradation of AXIN
- Signaling by WNT in cancer
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|
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CSNK1A1 and PPP1CC |
casein kinase 1, alpha 1 |
protein phosphatase 1, catalytic subunit, gamma isozyme |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
|
- Loss of Function of TGFBR2 in Cancer
- Mitotic Prometaphase
- Metabolism of lipids and lipoproteins
- Separation of Sister Chromatids
- Downregulation of TGF-beta receptor signaling
- SMAD2/3 MH2 Domain Mutants in Cancer
- TGF-beta receptor signaling activates SMADs
- Mitotic Anaphase
- TGFBR1 LBD Mutants in Cancer
- M Phase
- Hormone-sensitive lipase (HSL)-mediated triacylglycerol hydrolysis
- TGFBR2 MSI Frameshift Mutants in Cancer
- SMAD2/3 Phosphorylation Motif Mutants in Cancer
- Loss of Function of SMAD2/3 in Cancer
- TGFBR2 Kinase Domain Mutants in Cancer
- Loss of Function of SMAD4 in Cancer
- TGFBR1 KD Mutants in Cancer
- Lipid digestion, mobilization, and transport
- Cell Cycle, Mitotic
- Loss of Function of TGFBR1 in Cancer
- Signaling by TGF-beta Receptor Complex in Cancer
- Signaling by TGF-beta Receptor Complex
- Resolution of Sister Chromatid Cohesion
- Mitotic Metaphase and Anaphase
- SMAD4 MH2 Domain Mutants in Cancer
|
|
- 9,10-Deepithio-9,10-Didehydroacanthifolicin
- Calyculin A
- (2S,5R,8S,11R,12S,15S,18S,19S,E)-8-ISOBUTYL-18-((5S,6S)-6-METHOXY-3,5-DIMETHYL-7-PHENYLHEPTYL)-1,2,5,12,15,19-HEXAMETHYL-3,6,9,13,16,20,25-HEPTAOXO-1,4,7,10,14,17,21-HEPTAAZACYCLOPENTACOS-21-ENE-11,22-DICARBOXYLIC ACID
- Motuporin
|
|
|
CSNK1E and AXIN2 |
casein kinase 1, epsilon |
axin 2 |
- Organelle biogenesis and maintenance
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- G2/M Transition
- Assembly of the primary cilium
- Signaling by Wnt
- Regulation of PLK1 Activity at G2/M Transition
- Anchoring of the basal body to the plasma membrane
- Cell Cycle, Mitotic
- WNT mediated activation of DVL
- Loss of proteins required for interphase microtubule organization from the centrosome
- TCF dependent signaling in response to WNT
- RNF mutants show enhanced WNT signaling and proliferation
- Loss of Nlp from mitotic centrosomes
- XAV939 inhibits tankyrase, stabilizing AXIN
- Centrosome maturation
- Signaling by WNT in cancer
- Mitotic G2-G2/M phases
- Recruitment of mitotic centrosome proteins and complexes
|
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- TCF dependent signaling in response to WNT
- RNF mutants show enhanced WNT signaling and proliferation
- formation of the beta-catenin:TCF transactivating complex
- XAV939 inhibits tankyrase, stabilizing AXIN
- degradation of AXIN
- Signaling by Wnt
- binding of TCF/LEF:CTNNB1 to target gene promoters
- Signaling by WNT in cancer
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|
|
|
|
CSNK2A1 and TCF7L2 |
casein kinase 2, alpha 1 polypeptide |
transcription factor 7-like 2 (T-cell specific, HMG-box) |
- Mitotic Prometaphase
- Signal transduction by L1
- Axon guidance
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- L1CAM interactions
- Signaling by Wnt
- Cell Cycle, Mitotic
- M Phase
- WNT mediated activation of DVL
- TCF dependent signaling in response to WNT
- RNF mutants show enhanced WNT signaling and proliferation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Signaling by WNT in cancer
- Condensation of Prometaphase Chromosomes
|
- APC truncation mutants have impaired AXIN binding
- misspliced GSK3beta mutants stabilize beta-catenin
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- binding of TCF/LEF:CTNNB1 to target gene promoters
- deactivation of the beta-catenin transactivating complex
- APC truncation mutants are not K63 polyubiquitinated
- S37 mutants of beta-catenin aren't phosphorylated
- Peptide hormone metabolism
- Degradation of beta-catenin by the destruction complex
- S33 mutants of beta-catenin aren't phosphorylated
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- RNF mutants show enhanced WNT signaling and proliferation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Incretin synthesis, secretion, and inactivation
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- formation of the beta-catenin:TCF transactivating complex
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- repression of WNT target genes
- beta-catenin independent WNT signaling
- deletions in the AMER1 gene destabilize the destruction complex
- Ca2+ pathway
- AMER1 mutants destabilize the destruction complex
- TCF dependent signaling in response to WNT
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by WNT in cancer
- Synthesis, secretion, and inactivation of Glucagon-like Peptide-1 (GLP-1)
|
- (5-Oxo-5,6-Dihydro-Indolo[1,2-a]Quinazolin-7-Yl)-Acetic Acid
- 1,8-Di-Hydroxy-4-Nitro-Xanthen-9-One
- Resveratrol
- 1,8-Di-Hydroxy-4-Nitro-Anthraquinone
- Benzamidine
- 5,8-Di-Amino-1,4-Dihydroxy-Anthraquinone
- Phosphoaminophosphonic Acid-Adenylate Ester
- Tetrabromo-2-Benzotriazole
- DIMETHYL-(4,5,6,7-TETRABROMO-1H-BENZOIMIDAZOL-2-YL)-AMINE
- S-METHYL-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- N1,N2-ETHYLENE-2-METHYLAMINO-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- 3-METHYL-1,6,8-TRIHYDROXYANTHRAQUINONE
- 3,8-DIBROMO-7-HYDROXY-4-METHYL-2H-CHROMEN-2-ONE
- 19-(cyclopropylamino)-4,6,7,15-tetrahydro-5H-16,1-(azenometheno)-10,14-(metheno)pyrazolo[4,3-o][1,3,9]triazacyclohexadecin-8(9H)-one
- N,N\'-DIPHENYLPYRAZOLO[1,5-A][1,3,5]TRIAZINE-2,4-DIAMINE
- 4-(2-(1H-IMIDAZOL-4-YL)ETHYLAMINO)-2-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(CYCLOHEXYLMETHYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-CHLOROBENZYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-ETHYLPIPERAZIN-1-YL)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- N-(3-(8-CYANO-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZIN-2-YLAMINO)PHENYL)ACETAMIDE
- 2,3,7,8-tetrahydroxychromeno[5,4,3-cde]chromene-5,10-dione
- 5,6-dichloro-1-beta-D-ribofuranosyl-1H-benzimidazole
- 1,2,5,8-tetrahydroxyanthracene-9,10-dione
- Ellagic Acid
|
|
|
|
CSNK2A1 and PRKACB |
casein kinase 2, alpha 1 polypeptide |
protein kinase, cAMP-dependent, catalytic, beta |
- Mitotic Prometaphase
- Signal transduction by L1
- Axon guidance
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- L1CAM interactions
- Signaling by Wnt
- Cell Cycle, Mitotic
- M Phase
- WNT mediated activation of DVL
- TCF dependent signaling in response to WNT
- RNF mutants show enhanced WNT signaling and proliferation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Signaling by WNT in cancer
- Condensation of Prometaphase Chromosomes
|
- Signaling by GPCR
- Ca-dependent events
- CaM pathway
- Glucagon-like Peptide-1 (GLP1) regulates insulin secretion
- Metabolism of lipids and lipoproteins
- Integration of energy metabolism
- Hedgehog 'off' state
- Phospholipase C-mediated cascade
- Signaling by FGFR in disease
- Signaling by EGFRvIII in Cancer
- PLCG1 events in ERBB2 signaling
- Gluconeogenesis
- Glucose metabolism
- DAP12 signaling
- Rap1 signalling
- Myoclonic epilepsy of Lafora
- Hormone-sensitive lipase (HSL)-mediated triacylglycerol hydrolysis
- Glycogen storage diseases
- PKA-mediated phosphorylation of key metabolic factors
- Neurotransmitter Receptor Binding And Downstream Transmission In The Postsynaptic Cell
- Glucagon signaling in metabolic regulation
- Signaling by PDGF
- Calmodulin induced events
- DAP12 interactions
- PKA-mediated phosphorylation of CREB
- Opioid Signalling
- PKA activation
- Aquaporin-mediated transport
- Factors involved in megakaryocyte development and platelet production
- CREB phosphorylation through the activation of Adenylate Cyclase
- EGFR interacts with phospholipase C-gamma
- Signaling by ERBB2
- Signaling by EGFR
- PKA-mediated phosphorylation of CREB
- Signaling by VEGF
- Downstream signal transduction
- Calmodulin induced events
- Signaling by EGFR in Cancer
- PKA activation
- Metabolism of carbohydrates
- Transmission across Chemical Synapses
- Adaptive Immune System
- VEGFA-VEGFR2 Pathway
- DAG and IP3 signaling
- CaM pathway
- Activation of NMDA receptor upon glutamate binding and postsynaptic events
- Downstream signaling of activated FGFR
- DARPP-32 events
- Post NMDA receptor activation events
- Innate Immune System
- PKA activation in glucagon signalling
- Signalling by NGF
- PLC beta mediated events
- Vasopressin regulates renal water homeostasis via Aquaporins
- Regulation of insulin secretion
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- Lipid digestion, mobilization, and transport
- NGF signalling via TRKA from the plasma membrane
- G-protein mediated events
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Signaling by FGFR
- PLC-gamma1 signalling
- Signaling by Hedgehog
- Degradation of GLI1 by the proteasome
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
|
- (5-Oxo-5,6-Dihydro-Indolo[1,2-a]Quinazolin-7-Yl)-Acetic Acid
- 1,8-Di-Hydroxy-4-Nitro-Xanthen-9-One
- Resveratrol
- 1,8-Di-Hydroxy-4-Nitro-Anthraquinone
- Benzamidine
- 5,8-Di-Amino-1,4-Dihydroxy-Anthraquinone
- Phosphoaminophosphonic Acid-Adenylate Ester
- Tetrabromo-2-Benzotriazole
- DIMETHYL-(4,5,6,7-TETRABROMO-1H-BENZOIMIDAZOL-2-YL)-AMINE
- S-METHYL-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- N1,N2-ETHYLENE-2-METHYLAMINO-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- 3-METHYL-1,6,8-TRIHYDROXYANTHRAQUINONE
- 3,8-DIBROMO-7-HYDROXY-4-METHYL-2H-CHROMEN-2-ONE
- 19-(cyclopropylamino)-4,6,7,15-tetrahydro-5H-16,1-(azenometheno)-10,14-(metheno)pyrazolo[4,3-o][1,3,9]triazacyclohexadecin-8(9H)-one
- N,N\'-DIPHENYLPYRAZOLO[1,5-A][1,3,5]TRIAZINE-2,4-DIAMINE
- 4-(2-(1H-IMIDAZOL-4-YL)ETHYLAMINO)-2-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(CYCLOHEXYLMETHYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-CHLOROBENZYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-ETHYLPIPERAZIN-1-YL)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- N-(3-(8-CYANO-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZIN-2-YLAMINO)PHENYL)ACETAMIDE
- 2,3,7,8-tetrahydroxychromeno[5,4,3-cde]chromene-5,10-dione
- 5,6-dichloro-1-beta-D-ribofuranosyl-1H-benzimidazole
- 1,2,5,8-tetrahydroxyanthracene-9,10-dione
- Ellagic Acid
|
|
|
|
CSNK2A1 and CTNNB1 |
casein kinase 2, alpha 1 polypeptide |
catenin (cadherin-associated protein), beta 1, 88kDa |
- Mitotic Prometaphase
- Signal transduction by L1
- Axon guidance
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- L1CAM interactions
- Signaling by Wnt
- Cell Cycle, Mitotic
- M Phase
- WNT mediated activation of DVL
- TCF dependent signaling in response to WNT
- RNF mutants show enhanced WNT signaling and proliferation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Signaling by WNT in cancer
- Condensation of Prometaphase Chromosomes
|
- APC truncation mutants have impaired AXIN binding
- misspliced GSK3beta mutants stabilize beta-catenin
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- binding of TCF/LEF:CTNNB1 to target gene promoters
- deactivation of the beta-catenin transactivating complex
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- RNF mutants show enhanced WNT signaling and proliferation
- S33 mutants of beta-catenin aren't phosphorylated
- XAV939 inhibits tankyrase, stabilizing AXIN
- Innate Immune System
- truncations of AMER1 destabilize the destruction complex
- CDO in myogenesis
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- Cytosolic sensors of pathogen-associated DNA
- formation of the beta-catenin:TCF transactivating complex
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- repression of WNT target genes
- beta-catenin independent WNT signaling
- deletions in the AMER1 gene destabilize the destruction complex
- Ca2+ pathway
- Myogenesis
- AMER1 mutants destabilize the destruction complex
- TCF dependent signaling in response to WNT
- LRR FLII-interacting protein 1 (LRRFIP1) activates type I IFN production
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by WNT in cancer
|
- (5-Oxo-5,6-Dihydro-Indolo[1,2-a]Quinazolin-7-Yl)-Acetic Acid
- 1,8-Di-Hydroxy-4-Nitro-Xanthen-9-One
- Resveratrol
- 1,8-Di-Hydroxy-4-Nitro-Anthraquinone
- Benzamidine
- 5,8-Di-Amino-1,4-Dihydroxy-Anthraquinone
- Phosphoaminophosphonic Acid-Adenylate Ester
- Tetrabromo-2-Benzotriazole
- DIMETHYL-(4,5,6,7-TETRABROMO-1H-BENZOIMIDAZOL-2-YL)-AMINE
- S-METHYL-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- N1,N2-ETHYLENE-2-METHYLAMINO-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- 3-METHYL-1,6,8-TRIHYDROXYANTHRAQUINONE
- 3,8-DIBROMO-7-HYDROXY-4-METHYL-2H-CHROMEN-2-ONE
- 19-(cyclopropylamino)-4,6,7,15-tetrahydro-5H-16,1-(azenometheno)-10,14-(metheno)pyrazolo[4,3-o][1,3,9]triazacyclohexadecin-8(9H)-one
- N,N\'-DIPHENYLPYRAZOLO[1,5-A][1,3,5]TRIAZINE-2,4-DIAMINE
- 4-(2-(1H-IMIDAZOL-4-YL)ETHYLAMINO)-2-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(CYCLOHEXYLMETHYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-CHLOROBENZYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-ETHYLPIPERAZIN-1-YL)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- N-(3-(8-CYANO-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZIN-2-YLAMINO)PHENYL)ACETAMIDE
- 2,3,7,8-tetrahydroxychromeno[5,4,3-cde]chromene-5,10-dione
- 5,6-dichloro-1-beta-D-ribofuranosyl-1H-benzimidazole
- 1,2,5,8-tetrahydroxyanthracene-9,10-dione
- Ellagic Acid
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CSNK2A1 and PSMA4 |
casein kinase 2, alpha 1 polypeptide |
proteasome (prosome, macropain) subunit, alpha type, 4 |
- Mitotic Prometaphase
- Signal transduction by L1
- Axon guidance
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- L1CAM interactions
- Signaling by Wnt
- Cell Cycle, Mitotic
- M Phase
- WNT mediated activation of DVL
- TCF dependent signaling in response to WNT
- RNF mutants show enhanced WNT signaling and proliferation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Signaling by WNT in cancer
- Condensation of Prometaphase Chromosomes
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- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- Hh ligand biogenesis disease
- T41 mutants of beta-catenin aren't phosphorylated
- Downstream signaling events of B Cell Receptor (BCR)
- Degradation of beta-catenin by the destruction complex
- Stabilization of p53
- S33 mutants of beta-catenin aren't phosphorylated
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- Removal of licensing factors from origins
- Switching of origins to a post-replicative state
- Mitotic G1-G1/S phases
- Regulation of mRNA stability by proteins that bind AU-rich elements
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- DNA Replication Pre-Initiation
- S45 mutants of beta-catenin aren't phosphorylated
- APC/C:Cdc20 mediated degradation of mitotic proteins
- Regulation of APC/C activators between G1/S and early anaphase
- SCF(Skp2)-mediated degradation of p27/p21
- deletions in the AMER1 gene destabilize the destruction complex
- Autodegradation of the E3 ubiquitin ligase COP1
- AMER1 mutants destabilize the destruction complex
- Activation of APC/C and APC/C:Cdc20 mediated degradation of mitotic proteins
- APC:Cdc20 mediated degradation of cell cycle proteins prior to satisfation of the cell cycle checkpoint
- PCP/CE pathway
- Adaptive Immune System
- CDK-mediated phosphorylation and removal of Cdc6
- Hedgehog ligand biogenesis
- APC/C:Cdh1 mediated degradation of Cdc20 and other APC/C:Cdh1 targeted proteins in late mitosis/early G1
- Separation of Sister Chromatids
- HIV Infection
- Ubiquitin-dependent degradation of Cyclin D
- APC truncation mutants have impaired AXIN binding
- Assembly of the pre-replicative complex
- Autodegradation of Cdh1 by Cdh1:APC/C
- p53-Dependent G1 DNA Damage Response
- S37 mutants of beta-catenin aren't phosphorylated
- XAV939 inhibits tankyrase, stabilizing AXIN
- p53-Independent DNA Damage Response
- p53-Independent G1/S DNA damage checkpoint
- G1/S DNA Damage Checkpoints
- Vpu mediated degradation of CD4
- Synthesis of DNA
- M/G1 Transition
- Ubiquitin-dependent degradation of Cyclin D1
- TCF dependent signaling in response to WNT
- SCF-beta-TrCP mediated degradation of Emi1
- degradation of AXIN
- Signaling by Hedgehog
- Regulation of mitotic cell cycle
- Degradation of GLI1 by the proteasome
- degradation of DVL
- Cell Cycle Checkpoints
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Regulation of Apoptosis
- Degradation of GLI2 by the proteasome
- Signaling by the B Cell Receptor (BCR)
- Vif-mediated degradation of APOBEC3G
- Ubiquitin Mediated Degradation of Phosphorylated Cdc25A
- p53-Dependent G1/S DNA damage checkpoint
- truncated APC mutants destabilize the destruction complex
- TCF7L2 mutants don't bind CTBP
- Signaling by Wnt
- Cyclin E associated events during G1/S transition
- APC/C:Cdc20 mediated degradation of Securin
- AUF1 (hnRNP D0) destabilizes mRNA
- CDK-mediated phosphorylation and removal of Cdc6
- RNF mutants show enhanced WNT signaling and proliferation
- G1/S Transition
- truncations of AMER1 destabilize the destruction complex
- Processing-defective Hh variants abrogate ligand secretion
- Host Interactions of HIV factors
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- Regulation of activated PAK-2p34 by proteasome mediated degradation
- AXIN missense mutants destabilize the destruction complex
- S Phase
- APC/C-mediated degradation of cell cycle proteins
- Cyclin A:Cdk2-associated events at S phase entry
- SCF(Skp2)-mediated degradation of p27/p21
- Mitotic Metaphase and Anaphase
- Regulation of ornithine decarboxylase (ODC)
- Antigen processing: Ubiquitination & Proteasome degradation
- Orc1 removal from chromatin
- Mitotic Anaphase
- M Phase
- APC truncation mutants are not K63 polyubiquitinated
- Metabolism of amino acids and derivatives
- Hedgehog 'on' state
- Programmed Cell Death
- Class I MHC mediated antigen processing & presentation
- Regulation of DNA replication
- Cell Cycle, Mitotic
- beta-catenin independent WNT signaling
- Orc1 removal from chromatin
- Activation of NF-kappaB in B cells
- Asymmetric localization of PCP proteins
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Cross-presentation of soluble exogenous antigens (endosomes)
- Antigen processing-Cross presentation
- CDT1 association with the CDC6:ORC:origin complex
- ER-Phagosome pathway
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- (5-Oxo-5,6-Dihydro-Indolo[1,2-a]Quinazolin-7-Yl)-Acetic Acid
- 1,8-Di-Hydroxy-4-Nitro-Xanthen-9-One
- Resveratrol
- 1,8-Di-Hydroxy-4-Nitro-Anthraquinone
- Benzamidine
- 5,8-Di-Amino-1,4-Dihydroxy-Anthraquinone
- Phosphoaminophosphonic Acid-Adenylate Ester
- Tetrabromo-2-Benzotriazole
- DIMETHYL-(4,5,6,7-TETRABROMO-1H-BENZOIMIDAZOL-2-YL)-AMINE
- S-METHYL-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- N1,N2-ETHYLENE-2-METHYLAMINO-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- 3-METHYL-1,6,8-TRIHYDROXYANTHRAQUINONE
- 3,8-DIBROMO-7-HYDROXY-4-METHYL-2H-CHROMEN-2-ONE
- 19-(cyclopropylamino)-4,6,7,15-tetrahydro-5H-16,1-(azenometheno)-10,14-(metheno)pyrazolo[4,3-o][1,3,9]triazacyclohexadecin-8(9H)-one
- N,N\'-DIPHENYLPYRAZOLO[1,5-A][1,3,5]TRIAZINE-2,4-DIAMINE
- 4-(2-(1H-IMIDAZOL-4-YL)ETHYLAMINO)-2-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(CYCLOHEXYLMETHYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-CHLOROBENZYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-ETHYLPIPERAZIN-1-YL)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- N-(3-(8-CYANO-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZIN-2-YLAMINO)PHENYL)ACETAMIDE
- 2,3,7,8-tetrahydroxychromeno[5,4,3-cde]chromene-5,10-dione
- 5,6-dichloro-1-beta-D-ribofuranosyl-1H-benzimidazole
- 1,2,5,8-tetrahydroxyanthracene-9,10-dione
- Ellagic Acid
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