CDC42 and CDH1 |
cell division cycle 42 |
cadherin 1, type 1, E-cadherin (epithelial) |
- Signaling by GPCR
- Costimulation by the CD28 family
- Axon guidance
- DCC mediated attractive signaling
- Signaling by EGFRvIII in Cancer
- VEGFA-VEGFR2 Pathway
- Inactivation of Cdc42 and Rac
- Rho GTPase cycle
- EPHB-mediated forward signaling
- EPH-Ephrin signaling
- G alpha (12/13) signalling events
- Sema4D in semaphorin signaling
- Netrin-1 signaling
- Fcgamma receptor (FCGR) dependent phagocytosis
- Sema4D induced cell migration and growth-cone collapse
- Regulation of actin dynamics for phagocytic cup formation
- Innate Immune System
- EGFR downregulation
- CDO in myogenesis
- Semaphorin interactions
- CD28 co-stimulation
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- Factors involved in megakaryocyte development and platelet production
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- CD28 dependent Vav1 pathway
- Signaling by EGFR
- GPCR downstream signaling
- Myogenesis
- Signaling by VEGF
- Signaling by Rho GTPases
- Signaling by EGFR in Cancer
- GPVI-mediated activation cascade
- Platelet activation, signaling and aggregation
- Signaling by Robo receptor
- Adaptive Immune System
|
- Cell junction organization
- Apoptotic cleavage of cellular proteins
- Adherens junctions interactions
- Apoptotic execution phase
- Degradation of the extracellular matrix
- Apoptotic cleavage of cell adhesion proteins
- Cell-cell junction organization
- Programmed Cell Death
- Integrin cell surface interactions
- Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell
- Adaptive Immune System
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|
|
|
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CDH1 and IRS1 |
cadherin 1, type 1, E-cadherin (epithelial) |
insulin receptor substrate 1 |
- Cell junction organization
- Apoptotic cleavage of cellular proteins
- Adherens junctions interactions
- Apoptotic execution phase
- Degradation of the extracellular matrix
- Apoptotic cleavage of cell adhesion proteins
- Cell-cell junction organization
- Programmed Cell Death
- Integrin cell surface interactions
- Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell
- Adaptive Immune System
|
- Signaling by the B Cell Receptor (BCR)
- Signaling by FGFR in disease
- 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
- SOS-mediated signalling
- PI3K Cascade
- Signaling by PDGF
- DAP12 interactions
- GAB1 signalosome
- Signaling by ERBB4
- Role of LAT2/NTAL/LAB on calcium mobilization
- Constitutive PI3K/AKT Signaling in Cancer
- PI3K events in ERBB4 signaling
- Signaling by ERBB2
- Signaling by EGFR
- Downstream signal transduction
- Fc epsilon receptor (FCERI) signaling
- Signaling by EGFR in Cancer
- PI3K/AKT Signaling in Cancer
- Signaling by Leptin
- Growth hormone receptor signaling
- Adaptive Immune System
- IRS-mediated signalling
- PIP3 activates AKT signaling
- IGF1R signaling cascade
- IRS-related events triggered by IGF1R
- IRS activation
- PI3K events in ERBB2 signaling
- Downstream signaling of activated FGFR
- Signaling by Insulin receptor
- Innate Immune System
- Signalling by NGF
- Insulin receptor signalling cascade
- SOS-mediated signalling
- Cytokine Signaling in Immune system
- IRS-related events
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- NGF signalling via TRKA from the plasma membrane
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Signaling by FGFR
- IRS-mediated signalling
- Signal attenuation
- Signaling by Type 1 Insulin-like Growth Factor 1 Receptor (IGF1R)
- PI3K Cascade
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|
- [4-({5-(AMINOCARBONYL)-4-[(3-METHYLPHENYL)AMINO]PYRIMIDIN-2-YL}AMINO)PHENYL]ACETIC ACID
|
|
|
CDH1 and RRM2 |
cadherin 1, type 1, E-cadherin (epithelial) |
ribonucleotide reductase M2 |
- Cell junction organization
- Apoptotic cleavage of cellular proteins
- Adherens junctions interactions
- Apoptotic execution phase
- Degradation of the extracellular matrix
- Apoptotic cleavage of cell adhesion proteins
- Cell-cell junction organization
- Programmed Cell Death
- Integrin cell surface interactions
- Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell
- Adaptive Immune System
|
- E2F mediated regulation of DNA replication
- G1/S Transition
- G1/S-Specific Transcription
- Metabolism of nucleotides
- Synthesis and interconversion of nucleotide di- and triphosphates
- Mitotic G1-G1/S phases
- Cell Cycle, Mitotic
|
|
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|
CDH1 and TACC3 |
cadherin 1, type 1, E-cadherin (epithelial) |
transforming, acidic coiled-coil containing protein 3 |
- Cell junction organization
- Apoptotic cleavage of cellular proteins
- Adherens junctions interactions
- Apoptotic execution phase
- Degradation of the extracellular matrix
- Apoptotic cleavage of cell adhesion proteins
- Cell-cell junction organization
- Programmed Cell Death
- Integrin cell surface interactions
- Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell
- Adaptive Immune System
|
|
|
|
|
|
CDH1 and GSK3B |
cadherin 1, type 1, E-cadherin (epithelial) |
glycogen synthase kinase 3 beta |
- Cell junction organization
- Apoptotic cleavage of cellular proteins
- Adherens junctions interactions
- Apoptotic execution phase
- Degradation of the extracellular matrix
- Apoptotic cleavage of cell adhesion proteins
- Cell-cell junction organization
- Programmed Cell Death
- Integrin cell surface interactions
- Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell
- Adaptive Immune System
|
- Signaling by the B Cell Receptor (BCR)
- Hedgehog 'off' state
- Signaling by FGFR in disease
- 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
- AKT phosphorylates targets in the cytosol
- Signaling by EGFRvIII in Cancer
- Signaling by SCF-KIT
- DAP12 signaling
- Downstream signaling events of B Cell Receptor (BCR)
- Degradation of beta-catenin by the destruction complex
- PI3K/AKT activation
- PI-3K cascade
- 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
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- Signaling by PDGF
- DAP12 interactions
- GAB1 signalosome
- 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
- Signaling by ERBB4
- Constitutive PI3K/AKT Signaling in Cancer
- Role of LAT2/NTAL/LAB on calcium mobilization
- PI3K events in ERBB4 signaling
- Signaling by ERBB2
- Signaling by EGFR
- deletions in the AMER1 gene destabilize the destruction complex
- AMER1 mutants destabilize the destruction complex
- Downstream signal transduction
- Fc epsilon receptor (FCERI) signaling
- Signaling by EGFR in Cancer
- PI3K/AKT Signaling in Cancer
- CRMPs in Sema3A signaling
- Adaptive Immune System
- Axon guidance
- PIP3 activates AKT signaling
- APC truncation mutants have impaired AXIN binding
- 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
- PI3K events in ERBB2 signaling
- Downstream signaling of activated FGFR
- XAV939 inhibits tankyrase, stabilizing AXIN
- Innate Immune System
- Signalling by NGF
- Semaphorin interactions
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- Regulation of HSF1-mediated heat shock response
- Cellular response to heat stress
- NGF signalling via TRKA from the plasma membrane
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Signaling by FGFR
- TCF dependent signaling in response to WNT
- Signaling by Hedgehog
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
|
|
- Lithium
- 3-[3-(2,3-Dihydroxy-Propylamino)-Phenyl]-4-(5-Fluoro-1-Methyl-1h-Indol-3-Yl)-Pyrrole-2,5-Dione
- I-5
- N-(4-Methoxybenzyl)-N\'-(5-Nitro-1,3-Thiazol-2-Yl)Urea
- Staurosporine
- Indirubin-3\'-Monoxime
- Adenosine-5\'-Diphosphate
- (3e)-6\'-Bromo-2,3\'-Biindole-2\',3(1h,1\'h)-Dione 3-Oxime
- Alsterpaullone
- Phosphoaminophosphonic Acid-Adenylate Ester
- 2-(1,3-benzodioxol-5-yl)-5-[(3-fluoro-4-methoxybenzyl)sulfanyl]-1,3,4-oxadiazole
- 5-[1-(4-methoxyphenyl)-1H-benzimidazol-6-yl]-1,3,4-oxadiazole-2(3H)-thione
- (7S)-2-(2-aminopyrimidin-4-yl)-7-(2-fluoroethyl)-1,5,6,7-tetrahydro-4H-pyrrolo[3,2-c]pyridin-4-one
- N-[2-(5-methyl-4H-1,2,4-triazol-3-yl)phenyl]-7H-pyrrolo[2,3-d]pyrimidin-4-amine
- 5-(5-chloro-7H-pyrrolo[2,3-d]pyrimidin-4-yl)-4,5,6,7-tetrahydro-1H-imidazo[4,5-c]pyridine
- 3-({[(3S)-3,4-dihydroxybutyl]oxy}amino)-1H,2\'H-2,3\'-biindol-2\'-one
- N-[(1S)-2-amino-1-phenylethyl]-5-(1H-pyrrolo[2,3-b]pyridin-4-yl)thiophene-2-carboxamide
- 4-(4-CHLOROPHENYL)-4-[4-(1H-PYRAZOL-4-YL)PHENYL]PIPERIDINE
- ISOQUINOLINE-5-SULFONIC ACID (2-(2-(4-CHLOROBENZYLOXY)ETHYLAMINO)ETHYL)AMIDE
- (2S)-1-(1H-INDOL-3-YL)-3-{[5-(3-METHYL-1H-INDAZOL-5-YL)PYRIDIN-3-YL]OXY}PROPAN-2-AMINE
|
|
|
CDH1 and PPP1CA |
cadherin 1, type 1, E-cadherin (epithelial) |
protein phosphatase 1, catalytic subunit, alpha isozyme |
- Cell junction organization
- Apoptotic cleavage of cellular proteins
- Adherens junctions interactions
- Apoptotic execution phase
- Degradation of the extracellular matrix
- Apoptotic cleavage of cell adhesion proteins
- Cell-cell junction organization
- Programmed Cell Death
- Integrin cell surface interactions
- Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell
- Adaptive Immune System
|
- Loss of Function of TGFBR2 in Cancer
- Signaling by GPCR
- TGFBR2 MSI Frameshift Mutants in Cancer
- Metabolism of lipids and lipoproteins
- SMAD2/3 Phosphorylation Motif Mutants in Cancer
- Loss of Function of SMAD2/3 in Cancer
- Opioid Signalling
- TGFBR2 Kinase Domain Mutants in Cancer
- Loss of Function of SMAD4 in Cancer
- Downregulation of TGF-beta receptor signaling
- SMAD2/3 MH2 Domain Mutants in Cancer
- TGFBR1 KD Mutants in Cancer
- Lipid digestion, mobilization, and transport
- TGF-beta receptor signaling activates SMADs
- TGFBR1 LBD Mutants in Cancer
- Loss of Function of TGFBR1 in Cancer
- Signaling by TGF-beta Receptor Complex
- Signaling by TGF-beta Receptor Complex in Cancer
- Hormone-sensitive lipase (HSL)-mediated triacylglycerol hydrolysis
- DARPP-32 events
- SMAD4 MH2 Domain Mutants in Cancer
|
|
|
|
|
CDH1 and CSNK2A1 |
cadherin 1, type 1, E-cadherin (epithelial) |
casein kinase 2, alpha 1 polypeptide |
- Cell junction organization
- Apoptotic cleavage of cellular proteins
- Adherens junctions interactions
- Apoptotic execution phase
- Degradation of the extracellular matrix
- Apoptotic cleavage of cell adhesion proteins
- Cell-cell junction organization
- Programmed Cell Death
- Integrin cell surface interactions
- Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell
- Adaptive Immune System
|
- 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
|
|
- (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
|
|
|
CDH1 and FYN |
cadherin 1, type 1, E-cadherin (epithelial) |
FYN proto-oncogene, Src family tyrosine kinase |
- Cell junction organization
- Apoptotic cleavage of cellular proteins
- Adherens junctions interactions
- Apoptotic execution phase
- Degradation of the extracellular matrix
- Apoptotic cleavage of cell adhesion proteins
- Cell-cell junction organization
- Programmed Cell Death
- Integrin cell surface interactions
- Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell
- Adaptive Immune System
|
- Signaling by the B Cell Receptor (BCR)
- Signaling by FGFR in disease
- DCC mediated attractive signaling
- Netrin mediated repulsion signals
- Signaling by EGFRvIII in Cancer
- Nef and signal transduction
- Signaling by SCF-KIT
- DAP12 signaling
- Downstream signaling events of B Cell Receptor (BCR)
- Regulation of KIT signaling
- PI3K/AKT activation
- PI-3K cascade
- EPH-Ephrin signaling
- Fcgamma receptor (FCGR) dependent phagocytosis
- FCGR activation
- Signaling by PDGF
- DAP12 interactions
- GAB1 signalosome
- Host Interactions of HIV factors
- CD28 co-stimulation
- CD28 dependent PI3K/Akt signaling
- The role of Nef in HIV-1 replication and disease pathogenesis
- Signaling by ERBB4
- Constitutive PI3K/AKT Signaling in Cancer
- Role of LAT2/NTAL/LAB on calcium mobilization
- PI3K events in ERBB4 signaling
- Signaling by ERBB2
- Signaling by EGFR
- Signaling by Interleukins
- Signaling by VEGF
- Downstream signal transduction
- Sema3A PAK dependent Axon repulsion
- Fc epsilon receptor (FCERI) signaling
- Signaling by EGFR in Cancer
- Nephrin interactions
- SEMA3A-Plexin repulsion signaling by inhibiting Integrin adhesion
- CRMPs in Sema3A signaling
- PI3K/AKT Signaling in Cancer
- Platelet activation, signaling and aggregation
- Interleukin-3, 5 and GM-CSF signaling
- Adaptive Immune System
- Platelet Adhesion to exposed collagen
- Axon guidance
- Costimulation by the CD28 family
- PIP3 activates AKT signaling
- HIV Infection
- VEGFA-VEGFR2 Pathway
- EPHB-mediated forward signaling
- EPHA-mediated growth cone collapse
- Ephrin signaling
- EPH-ephrin mediated repulsion of cells
- PI3K events in ERBB2 signaling
- Regulation of signaling by CBL
- Downstream signaling of activated FGFR
- NCAM signaling for neurite out-growth
- Netrin-1 signaling
- Antigen activates B Cell Receptor (BCR) leading to generation of second messengers
- Innate Immune System
- Signalling by NGF
- Semaphorin interactions
- CTLA4 inhibitory signaling
- Cytokine Signaling in Immune system
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- NGF signalling via TRKA from the plasma membrane
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- PECAM1 interactions
- CD28 dependent Vav1 pathway
- Signaling by FGFR
- Cell surface interactions at the vascular wall
- GPVI-mediated activation cascade
|
|
- Dasatinib
- 1-Methoxy-2-[2-(2-Methoxy-Ethoxy]-Ethane
|
|
|
CDH1 and HDAC1 |
cadherin 1, type 1, E-cadherin (epithelial) |
histone deacetylase 1 |
- Cell junction organization
- Apoptotic cleavage of cellular proteins
- Adherens junctions interactions
- Apoptotic execution phase
- Degradation of the extracellular matrix
- Apoptotic cleavage of cell adhesion proteins
- Cell-cell junction organization
- Programmed Cell Death
- Integrin cell surface interactions
- Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell
- Adaptive Immune System
|
- Loss of Function of TGFBR2 in Cancer
- Signaling by NOTCH1 HD Domain Mutants in Cancer
- RNA Polymerase I, RNA Polymerase III, and Mitochondrial Transcription
- misspliced GSK3beta mutants stabilize beta-catenin
- T41 mutants of beta-catenin aren't phosphorylated
- SMAD2/3 MH2 Domain Mutants in Cancer
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- Downregulation of SMAD2/3:SMAD4 transcriptional activity
- SMAD2/SMAD3:SMAD4 heterotrimer regulates transcription
- Transcriptional activity of SMAD2/SMAD3:SMAD4 heterotrimer
- Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant
- Degradation of beta-catenin by the destruction complex
- NoRC negatively regulates rRNA expression
- Generic Transcription Pathway
- 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
- Signaling by NOTCH1 in Cancer
- Mitotic G1-G1/S phases
- truncations of AMER1 destabilize the destruction complex
- TGFBR2 MSI Frameshift Mutants in Cancer
- SMAD2/3 Phosphorylation Motif Mutants in Cancer
- Chromatin organization
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- Signaling by NOTCH
- formation of the beta-catenin:TCF transactivating complex
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- Loss of Function of SMAD4 in Cancer
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- TGFBR1 KD Mutants in Cancer
- Factors involved in megakaryocyte development and platelet production
- Chromatin modifying enzymes
- deletions in the AMER1 gene destabilize the destruction complex
- AMER1 mutants destabilize the destruction complex
- Signaling by NOTCH1 PEST Domain Mutants in Cancer
- Constitutive Signaling by NOTCH1 PEST Domain Mutants
- Signaling by NOTCH1 HD+PEST Domain Mutants in Cancer
- RNA Polymerase I Transcription Initiation
- APC truncation mutants have impaired AXIN binding
- RNA Polymerase I Promoter Clearance
- TGFBR1 LBD Mutants in Cancer
- deactivation of the beta-catenin transactivating complex
- APC truncation mutants are not K63 polyubiquitinated
- S37 mutants of beta-catenin aren't phosphorylated
- Signaling by NOTCH1
- XAV939 inhibits tankyrase, stabilizing AXIN
- Constitutive Signaling by NOTCH1 HD+PEST Domain Mutants
- FBXW7 Mutants and NOTCH1 in Cancer
- Signalling by NGF
- HDACs deacetylate histones
- p75NTR negatively regulates cell cycle via SC1
- Loss of Function of SMAD2/3 in Cancer
- RNA Polymerase I Transcription
- TGFBR2 Kinase Domain Mutants in Cancer
- Epigenetic regulation of gene expression
- p75 NTR receptor-mediated signalling
- G0 and Early G1
- Negative epigenetic regulation of rRNA expression
- repression of WNT target genes
- Loss of Function of TGFBR1 in Cancer
- Cell Cycle, Mitotic
- NOTCH1 Intracellular Domain Regulates Transcription
- Signaling by TGF-beta Receptor Complex in Cancer
- Signaling by TGF-beta Receptor 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
- SMAD4 MH2 Domain Mutants in Cancer
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|
|
|
|
CDH1 and HDAC2 |
cadherin 1, type 1, E-cadherin (epithelial) |
histone deacetylase 2 |
- Cell junction organization
- Apoptotic cleavage of cellular proteins
- Adherens junctions interactions
- Apoptotic execution phase
- Degradation of the extracellular matrix
- Apoptotic cleavage of cell adhesion proteins
- Cell-cell junction organization
- Programmed Cell Death
- Integrin cell surface interactions
- Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell
- Adaptive Immune System
|
- Signaling by NOTCH1 HD Domain Mutants in Cancer
- RNA Polymerase I, RNA Polymerase III, and Mitochondrial Transcription
- Signaling by NOTCH1 HD+PEST Domain Mutants in Cancer
- RNA Polymerase I Transcription Initiation
- RNA Polymerase I Promoter Clearance
- Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant
- NoRC negatively regulates rRNA expression
- Signaling by NOTCH1
- Signaling by NOTCH1 in Cancer
- Constitutive Signaling by NOTCH1 HD+PEST Domain Mutants
- FBXW7 Mutants and NOTCH1 in Cancer
- Signalling by NGF
- Chromatin organization
- HDACs deacetylate histones
- p75NTR negatively regulates cell cycle via SC1
- RNA Polymerase I Transcription
- Signaling by NOTCH
- Epigenetic regulation of gene expression
- Negative epigenetic regulation of rRNA expression
- p75 NTR receptor-mediated signalling
- Factors involved in megakaryocyte development and platelet production
- NOTCH1 Intracellular Domain Regulates Transcription
- Chromatin modifying enzymes
- Signaling by NOTCH1 PEST Domain Mutants in Cancer
- Constitutive Signaling by NOTCH1 PEST Domain Mutants
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|
|
|
|
CDH8 and CTNNB1 |
cadherin 8, type 2 |
catenin (cadherin-associated protein), beta 1, 88kDa |
- Cell junction organization
- Cell-cell junction organization
- Adherens junctions interactions
|
- 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
|
|
|
|
|
CDH9 and CTNNB1 |
cadherin 9, type 2 (T1-cadherin) |
catenin (cadherin-associated protein), beta 1, 88kDa |
- Cell junction organization
- Cell-cell junction organization
- Adherens junctions interactions
|
- 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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|
|
CDK2 and CDKN1A |
cyclin-dependent kinase 2 |
cyclin-dependent kinase inhibitor 1A (p21, Cip1) |
- CDK-mediated phosphorylation and removal of Cdc6
- G2/M Checkpoints
- Activation of the pre-replicative complex
- Cellular Senescence
- Phosphorylation of proteins involved in G1/S transition by active Cyclin E:Cdk2 complexes
- G2/M Transition
- p53-Dependent G1/S DNA damage checkpoint
- Activation of the pre-replicative complex
- Orc1 removal from chromatin
- Cyclin E associated events during G1/S transition
- CDK-mediated phosphorylation and removal of Cdc6
- p53-Dependent G1 DNA Damage Response
- Cyclin A/B1 associated events during G2/M transition
- G2 Phase
- Activation of ATR in response to replication stress
- G1/S Transition
- Removal of licensing factors from origins
- Mitotic G1-G1/S phases
- Switching of origins to a post-replicative state
- G1/S DNA Damage Checkpoints
- Meiotic recombination
- DNA Damage/Telomere Stress Induced Senescence
- Synthesis of DNA
- DNA Replication Pre-Initiation
- M/G1 Transition
- Regulation of DNA replication
- Senescence-Associated Secretory Phenotype (SASP)
- G0 and Early G1
- S Phase
- Regulation of APC/C activators between G1/S and early anaphase
- Factors involved in megakaryocyte development and platelet production
- Cell Cycle, Mitotic
- APC/C-mediated degradation of cell cycle proteins
- SCF(Skp2)-mediated degradation of p27/p21
- Orc1 removal from chromatin
- Regulation of mitotic cell cycle
- Cell Cycle Checkpoints
- SCF(Skp2)-mediated degradation of p27/p21
- Cyclin A:Cdk2-associated events at S phase entry
- Mitotic G2-G2/M phases
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- Signaling by the B Cell Receptor (BCR)
- Signaling by FGFR in disease
- Cellular Senescence
- p53-Dependent G1/S DNA damage checkpoint
- Cyclin E associated events during G1/S transition
- AKT phosphorylates targets in the cytosol
- Signaling by EGFRvIII in Cancer
- Signaling by SCF-KIT
- Downstream signaling events of B Cell Receptor (BCR)
- DAP12 signaling
- PI3K/AKT activation
- PI-3K cascade
- G1/S Transition
- Removal of licensing factors from origins
- Switching of origins to a post-replicative state
- Mitotic G1-G1/S phases
- Signaling by PDGF
- DAP12 interactions
- DNA Damage/Telomere Stress Induced Senescence
- GAB1 signalosome
- Senescence-Associated Secretory Phenotype (SASP)
- S Phase
- Signaling by ERBB4
- Constitutive PI3K/AKT Signaling in Cancer
- Role of LAT2/NTAL/LAB on calcium mobilization
- PI3K events in ERBB4 signaling
- Signaling by ERBB2
- Signaling by EGFR
- SCF(Skp2)-mediated degradation of p27/p21
- Downstream signal transduction
- Signaling by EGFR in Cancer
- Fc epsilon receptor (FCERI) signaling
- PI3K/AKT Signaling in Cancer
- Cyclin A:Cdk2-associated events at S phase entry
- SCF(Skp2)-mediated degradation of p27/p21
- Adaptive Immune System
- PIP3 activates AKT signaling
- Orc1 removal from chromatin
- p53-Dependent G1 DNA Damage Response
- PI3K events in ERBB2 signaling
- Transcriptional activation of p53 responsive genes
- Downstream signaling of activated FGFR
- G1/S DNA Damage Checkpoints
- Innate Immune System
- Transcriptional activation of cell cycle inhibitor p21
- Signalling by NGF
- Synthesis of DNA
- G1 Phase
- Regulation of DNA replication
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- NGF signalling via TRKA from the plasma membrane
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Cell Cycle, Mitotic
- Signaling by FGFR
- Orc1 removal from chromatin
- Cyclin D associated events in G1
- Cell Cycle Checkpoints
|
- Double Oxidized Cysteine
- 4-[5-(Trans-4-Aminocyclohexylamino)-3-Isopropylpyrazolo[1,5-a]Pyrimidin-7-Ylamino]-N,N-Dimethylbenzenesulfonamide
- Staurosporine
- Indirubin-3\'-Monoxime
- 4-(2,4-Dimethyl-Thiazol-5-Yl)-Pyrimidin-2-Ylamine
- Olomoucine
- 4-[(4-Imidazo[1,2-a]Pyridin-3-Ylpyrimidin-2-Yl)Amino]Benzenesulfonamide
- 2-Amino-6-Chloropyrazine
- 6-O-Cyclohexylmethyl Guanine
- N-[4-(2-Methylimidazo[1,2-a]Pyridin-3-Yl)-2-Pyrimidinyl]Acetamide
- 1-Amino-6-Cyclohex-3-Enylmethyloxypurine
- N-(5-Cyclopropyl-1h-Pyrazol-3-Yl)Benzamide
- Purvalanol
- [4-(2-Amino-4-Methyl-Thiazol-5-Yl)-Pyrimidin-2-Yl]-(3-Nitro-Phenyl)-Amine
- 5-{[(2-Amino-9h-Purin-6-Yl)Oxy]Methyl}-2-Pyrrolidinone
- 4-(2,4-Dimethyl-Thiazol-5-Yl)-Pyrimidin-2-Yl]-(4-Trifluoromethyl-Phenyl)-Amine
- Hymenialdisine
- (5-Chloropyrazolo[1,5-a]Pyrimidin-7-Yl)-(4-Methanesulfonylphenyl)Amine
- 4-(5-Bromo-2-Oxo-2h-Indol-3-Ylazo)-Benzenesulfonamide
- 4-(2,5-Dichloro-Thiophen-3-Yl)-Pyrimidin-2-Ylamine
- 4-[(6-Amino-4-Pyrimidinyl)Amino]Benzenesulfonamide
- 4-[3-Hydroxyanilino]-6,7-Dimethoxyquinazoline
- SU9516
- 3-Pyridin-4-Yl-2,4-Dihydro-Indeno[1,2-.C.]Pyrazole
- Flavopiridol
- (2e,3s)-3-Hydroxy-5\'-[(4-Hydroxypiperidin-1-Yl)Sulfonyl]-3-Methyl-1,3-Dihydro-2,3\'-Biindol-2\'(1\'h)-One
- 1-[(2-Amino-6,9-Dihydro-1h-Purin-6-Yl)Oxy]-3-Methyl-2-Butanol
- 4-((3r,4s,5r)-4-Amino-3,5-Dihydroxy-Hex-1-Ynyl)-5-Fluoro-3-[1-(3-Methoxy-1h-Pyrrol-2-Yl)-Meth-(Z)-Ylidene]-1,3-Dihydro-Indol-2-One
- Lysine Nz-Carboxylic Acid
- [2-Amino-6-(2,6-Difluoro-Benzoyl)-Imidazo[1,2-a]Pyridin-3-Yl]-Phenyl-Methanone
- Alsterpaullone
- N-[4-(2,4-Dimethyl-1,3-Thiazol-5-Yl)Pyrimidin-2-Yl]-N\'-Hydroxyimidoformamide
- N\'-(Pyrrolidino[2,1-B]Isoindolin-4-On-8-Yl)-N-(Pyridin-2-Yl)Urea
- 2-[Trans-(4-Aminocyclohexyl)Amino]-6-(Benzyl-Amino)-9-Cyclopentylpurine
- 4-[4-(4-Methyl-2-Methylamino-Thiazol-5-Yl)-Pyrimidin-2-Ylamino]-Phenol
- 3-[4-(2,4-Dimethyl-Thiazol-5-Yl)-Pyrimidin-2-Ylamino]-Phenol
- PHENYLAMINOIMIDAZO(1,2-ALPHA)PYRIDINE
- OLOMOUCINE II
- TRIAZOLOPYRIMIDINE
- Bosutinib
- 4-[(7-OXO-7H-THIAZOLO[5,4-E]INDOL-8-YLMETHYL)-AMINO]-N-PYRIDIN-2-YL-BENZENESULFONAMIDE
- (13R,15S)-13-METHYL-16-OXA-8,9,12,22,24-PENTAAZAHEXACYCLO[15.6.2.16,9.1,12,15.0,2,7.0,21,25]HEPTACOSA-1(24),2,4,6,17(25),18,20-HEPTAENE-23,26-DIONE
- N-(3-CYCLOPROPYL-1H-PYRAZOL-5-YL)-2-(2-NAPHTHYL)ACETAMIDE
- 2-ANILINO-6-CYCLOHEXYLMETHOXYPURINE
- 1-(5-OXO-2,3,5,9B-TETRAHYDRO-1H-PYRROLO[2,1-A]ISOINDOL-9-YL)-3-(5-PYRROLIDIN-2-YL-1H-PYRAZOL-3-YL)-UREA
- (5-phenyl-7-(pyridin-3-ylmethylamino)pyrazolo[1,5-a]pyrimidin-3-yl)methanol
- 2-(3,4-DIHYDROXYPHENYL)-8-(1,1-DIOXIDOISOTHIAZOLIDIN-2-YL)-3-HYDROXY-6-METHYL-4H-CHROMEN-4-ONE
- (2R)-1-(DIMETHYLAMINO)-3-{4-[(6-{[2-FLUORO-5-(TRIFLUOROMETHYL)PHENYL]AMINO}PYRIMIDIN-4-YL)AMINO]PHENOXY}PROPAN-2-OL
- 5-(2,3-dichlorophenyl)-N-(pyridin-4-ylmethyl)-3-thiocyanatopyrazolo[1,5-a]pyrimidin-7-amine
- O6-CYCLOHEXYLMETHOXY-2-(4\'-SULPHAMOYLANILINO) PURINE
- (2S)-N-[(3Z)-5-CYCLOPROPYL-3H-PYRAZOL-3-YLIDENE]-2-[4-(2-OXOIMIDAZOLIDIN-1-YL)PHENYL]PROPANAMIDE
- 5-[(2-AMINOETHYL)AMINO]-6-FLUORO-3-(1H-PYRROL-2-YL)BENZO[CD]INDOL-2(1H)-ONE
- N-cyclopropyl-4-pyrazolo[1,5-b]pyridazin-3-ylpyrimidin-2-amine
- 3-((3-bromo-5-o-tolylpyrazolo[1,5-a]pyrimidin-7-ylamino)methyl)pyridine 1-oxide
- 6-CYCLOHEXYLMETHOXY-2-(3\'-CHLOROANILINO) PURINE
- 3-bromo-5-phenyl-N-(pyridin-4-ylmethyl)pyrazolo[1,5-a]pyrimidin-7-amine
- N-[5-(1,1-DIOXIDOISOTHIAZOLIDIN-2-YL)-1H-INDAZOL-3-YL]-2-(4-PIPERIDIN-1-YLPHENYL)ACETAMIDE
- (3R)-3-(aminomethyl)-9-methoxy-1,2,3,4-tetrahydro-5H-[1]benzothieno[3,2-e][1,4]diazepin-5-one
- 5-[5,6-BIS(METHYLOXY)-1H-BENZIMIDAZOL-1-YL]-3-{[1-(2-CHLOROPHENYL)ETHYL]OXY}-2-THIOPHENECARBOXAMIDE
- (2Z)-5\'-BROMO-2,3\'-BIINDOLE-2\',3(1H,1\'H)-DIONE AMMONIATE
- (2S)-1-{4-[(4-ANILINO-5-BROMOPYRIMIDIN-2-YL)AMINO]PHENOXY}-3-(DIMETHYLAMINO)PROPAN-2-OL
- (2R)-1-{4-[(4-ANILINO-5-BROMOPYRIMIDIN-2-YL)AMINO]PHENOXY}-3-(DIMETHYLAMINO)PROPAN-2-OL
- 2-IMINO-5-(1-PYRIDIN-2-YL-METH-(E)-YLIDENE)-1,3-THIAZOLIDIN-4-ONE
- 4-{5-[(Z)-(2,4-DIOXO-1,3-THIAZOLIDIN-5-YLIDENE)METHYL]FURAN-2-YL}BENZENESULFONAMIDE
- 4-{5-[(Z)-(2-IMINO-4-OXO-1,3-THIAZOLIDIN-5-YLIDENE)METHYL]-2-FURYL}-N-METHYLBENZENESULFONAMIDE
- 4-{5-[(Z)-(2-IMINO-4-OXO-1,3-THIAZOLIDIN-5-YLIDENE)METHYL]FURAN-2-YL}BENZENESULFONAMIDE
- 4-{5-[(Z)-(2-IMINO-4-OXO-1,3-THIAZOLIDIN-5-YLIDENE)METHYL]FURAN-2-YL}-2-(TRIFLUOROMETHYL)BENZENESULFONAMIDE
- 4-{5-[(Z)-(2-IMINO-4-OXO-1,3-THIAZOLIDIN-5-YLIDENE)METHYL]FURAN-2-YL}BENZOIC ACID
- 4-{5-[(1Z)-1-(2-IMINO-4-OXO-1,3-THIAZOLIDIN-5-YLIDENE)ETHYL]-2-FURYL}BENZENESULFONAMIDE
- N-[4-(2,4-DIMETHYL-THIAZOL-5-YL)-PYRIMIDIN-2-YL]-N\',N\'-DIMETHYL-BENZENE-1,4-DIAMINE
- (5Z)-5-(3-BROMOCYCLOHEXA-2,5-DIEN-1-YLIDENE)-N-(PYRIDIN-4-YLMETHYL)-1,5-DIHYDROPYRAZOLO[1,5-A]PYRIMIDIN-7-AMINE
- 6-(3,4-DIHYDROXYBENZYL)-3-ETHYL-1-(2,4,6-TRICHLOROPHENYL)-1H-PYRAZOLO[3,4-D]PYRIMIDIN-4(5H)-ONE
- 6-(3-AMINOPHENYL)-N-(TERT-BUTYL)-2-(TRIFLUOROMETHYL)QUINAZOLIN-4-AMINE
- 2-(4-(AMINOMETHYL)PIPERIDIN-1-YL)-N-(3_CYCLOHEXYL-4-OXO-2,4-DIHYDROINDENO[1,2-C]PYRAZOL-5-YL)ACETAMIDE
- 1-(3-(2,4-DIMETHYLTHIAZOL-5-YL)-4-OXO-2,4-DIHYDROINDENO[1,2-C]PYRAZOL-5-YL)-3-(4-METHYLPIPERAZIN-1-YL)UREA
- 4-{[5-(CYCLOHEXYLMETHOXY)[1,2,4]TRIAZOLO[1,5-A]PYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE
- 4-{[5-(CYCLOHEXYLAMINO)[1,2,4]TRIAZOLO[1,5-A]PYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE
- 4-({5-[(4-AMINOCYCLOHEXYL)AMINO][1,2,4]TRIAZOLO[1,5-A]PYRIMIDIN-7-YL}AMINO)BENZENESULFONAMIDE
- 4-{[5-(CYCLOHEXYLOXY)[1,2,4]TRIAZOLO[1,5-A]PYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE
- 4-[(E)-(3,5-DIAMINO-1H-PYRAZOL-4-YL)DIAZENYL]PHENOL
- (2R)-1-[4-({4-[(2,5-DICHLOROPHENYL)AMINO]PYRIMIDIN-2-YL}AMINO)PHENOXY]-3-(DIMETHYLAMINO)PROPAN-2-OL
- (2S)-1-[4-({6-[(2,6-DIFLUOROPHENYL)AMINO]PYRIMIDIN-4-YL}AMINO)PHENOXY]-3-(DIMETHYLAMINO)PROPAN-2-OL
- (2S)-1-[4-({4-[(2,5-DICHLOROPHENYL)AMINO]PYRIMIDIN-2-YL}AMINO)PHENOXY]-3-(DIMETHYLAMINO)PROPAN-2-OL
- (2R)-1-[4-({6-[(2,6-DIFLUOROPHENYL)AMINO]PYRIMIDIN-4-YL}AMINO)PHENOXY]-3-(DIMETHYLAMINO)PROPAN-2-OL
- N-(2-METHOXYETHYL)-4-({4-[2-METHYL-1-(1-METHYLETHYL)-1H-IMIDAZOL-5-YL]PYRIMIDIN-2-YL}AMINO)BENZENESULFONAMIDE
- 4-{[4-(1-CYCLOPROPYL-2-METHYL-1H-IMIDAZOL-5-YL)PYRIMIDIN-2-YL]AMINO}-N-METHYLBENZENESULFONAMIDE
- 1-(3,5-DICHLOROPHENYL)-5-METHYL-1H-1,2,4-TRIAZOLE-3-CARBOXYLIC ACID
- 1-(DIMETHYLAMINO)-3-(4-{{4-(2-METHYLIMIDAZO[1,2-A]PYRIDIN-3-YL)PYRIMIDIN-2-YL]AMINO}PHENOXY)PROPAN-2-OL
- N-(4-{[(3S)-3-(dimethylamino)pyrrolidin-1-yl]carbonyl}phenyl)-5-fluoro-4-[2-methyl-1-(1-methylethyl)-1H-imidazol-5-yl]pyrimidin-2-amine
- 2-{4-[4-({4-[2-methyl-1-(1-methylethyl)-1H-imidazol-5-yl]pyrimidin-2-yl}amino)phenyl]piperazin-1-yl}-2-oxoethanol
- N-[3-(1H-BENZIMIDAZOL-2-YL)-1H-PYRAZOL-4-YL]BENZAMIDE
- (4-AMINO-2-{[1-(METHYLSULFONYL)PIPERIDIN-4-YL]AMINO}PYRIMIDIN-5-YL)(2,3-DIFLUORO-6-METHOXYPHENYL)METHANONE
- N-METHYL-4-{[(2-OXO-1,2-DIHYDRO-3H-INDOL-3-YLIDENE)METHYL]AMINO}BENZENESULFONAMIDE
- N-METHYL-{4-[2-(7-OXO-6,7-DIHYDRO-8H-[1,3]THIAZOLO[5,4-E]INDOL-8-YLIDENE)HYDRAZINO]PHENYL}METHANESULFONAMIDE
- 3-{[(2,2-DIOXIDO-1,3-DIHYDRO-2-BENZOTHIEN-5-YL)AMINO]METHYLENE}-5-(1,3-OXAZOL-5-YL)-1,3-DIHYDRO-2H-INDOL-2-ONE
- 4-{[(2-OXO-1,2-DIHYDRO-3H-INDOL-3-YLIDENE)METHYL]AMINO}-N-(1,3-THIAZOL-2-YL)BENZENESULFONAMIDE
- 3-{[4-([AMINO(IMINO)METHYL]AMINOSULFONYL)ANILINO]METHYLENE}-2-OXO-2,3-DIHYDRO-1H-INDOLE
- 5-hydroxynaphthalene-1-sulfonamide
- N-(4-sulfamoylphenyl)-1H-indazole-3-carboxamide
- 4-[(6-chloropyrazin-2-yl)amino]benzenesulfonamide
- N-phenyl-1H-pyrazole-3-carboxamide
- 4-(acetylamino)-N-(4-fluorophenyl)-1H-pyrazole-3-carboxamide
- (4E)-N-(4-fluorophenyl)-4-[(phenylcarbonyl)imino]-4H-pyrazole-3-carboxamide
- {[(2,6-difluorophenyl)carbonyl]amino}-N-(4-fluorophenyl)-1H-pyrazole-3-carboxamide
- 5-chloro-7-[(1-methylethyl)amino]pyrazolo[1,5-a]pyrimidine-3-carbonitrile
- 5-[(4-AMINOCYCLOHEXYL)AMINO]-7-(PROPAN-2-YLAMINO)PYRAZOLO[1,5-A]PYRIMIDINE-3-CARBONITRILE
- 4-{[(2,6-difluorophenyl)carbonyl]amino}-N-[(3S)-piperidin-3-yl]-1H-pyrazole-3-carboxamide
- 4-{[(2,6-dichlorophenyl)carbonyl]amino}-N-piperidin-4-yl-1H-pyrazole-3-carboxamide
- 4-(4-methoxy-1H-pyrrolo[2,3-b]pyridin-3-yl)pyrimidin-2-amine
- 4-(4-propoxy-1H-pyrrolo[2,3-b]pyridin-3-yl)pyrimidin-2-amine
- HYDROXY(OXO)(3-{[(2Z)-4-[3-(1H-1,2,4-TRIAZOL-1-YLMETHYL)PHENYL]PYRIMIDIN-2(5H)-YLIDENE]AMINO}PHENYL)AMMONIUM
- 4-METHYL-5-{(2E)-2-[(4-MORPHOLIN-4-YLPHENYL)IMINO]-2,5-DIHYDROPYRIMIDIN-4-YL}-1,3-THIAZOL-2-AMINE
- 6-CYCLOHEXYLMETHYLOXY-2-(4\'-HYDROXYANILINO)PURINE
- 4-(6-CYCLOHEXYLMETHOXY-9H-PURIN-2-YLAMINO)--BENZAMIDE
- 6-(CYCLOHEXYLMETHOXY)-8-ISOPROPYL-9H-PURIN-2-AMINE
- 3-(6-CYCLOHEXYLMETHOXY-9H-PURIN-2-YLAMINO)-BENZENESULFONAMIDE
- (2R)-2-{[4-(benzylamino)-8-(1-methylethyl)pyrazolo[1,5-a][1,3,5]triazin-2-yl]amino}butan-1-ol
- 3-({2-[(4-{[6-(CYCLOHEXYLMETHOXY)-9H-PURIN-2-YL]AMINO}PHENYL)SULFONYL]ETHYL}AMINO)PROPAN-1-OL
- 6-CYCLOHEXYLMETHYLOXY-5-NITROSO-PYRIMIDINE-2,4-DIAMINE
- 1-methyl-8-(phenylamino)-4,5-dihydro-1H-pyrazolo[4,3-h]quinazoline-3-carboxylic acid
- 6-BROMO-13-THIA-2,4,8,12,19-PENTAAZATRICYCLO[12.3.1.1~3,7~]NONADECA-1(18),3(19),4,6,14,16-HEXAENE 13,13-DIOXIDE
- (2R)-2-({9-(1-methylethyl)-6-[(4-pyridin-2-ylbenzyl)amino]-9H-purin-2-yl}amino)butan-1-ol
- 1-[4-(AMINOSULFONYL)PHENYL]-1,6-DIHYDROPYRAZOLO[3,4-E]INDAZOLE-3-CARBOXAMIDE
- 5-(2,3-dichlorophenyl)-N-(pyridin-4-ylmethyl)pyrazolo[1,5-a]pyrimidin-7-amine
- 6-(2-fluorophenyl)-N-(pyridin-3-ylmethyl)imidazo[1,2-a]pyrazin-8-amine
- 3-methyl-N-(pyridin-4-ylmethyl)imidazo[1,2-a]pyrazin-8-amine
- 5-(2-fluorophenyl)-N-(pyridin-4-ylmethyl)pyrazolo[1,5-a]pyrimidin-7-amine
- 3-bromo-5-phenyl-N-(pyridin-3-ylmethyl)pyrazolo[1,5-a]pyrimidin-7-amine
- 3-bromo-5-phenyl-N-(pyrimidin-5-ylmethyl)pyrazolo[1,5-a]pyridin-7-amine
- 3-bromo-6-phenyl-N-(pyrimidin-5-ylmethyl)imidazo[1,2-a]pyridin-8-amine
- N-((2-aminopyrimidin-5-yl)methyl)-5-(2,6-difluorophenyl)-3-ethylpyrazolo[1,5-a]pyrimidin-7-amine
- 3-cyclopropyl-5-phenyl-N-(pyridin-3-ylmethyl)pyrazolo[1,5-a]pyrimidin-7-amine
- 4-{[4-AMINO-6-(CYCLOHEXYLMETHOXY)-5-NITROSOPYRIMIDIN-2-YL]AMINO}BENZAMIDE
- 4-[(5-ISOPROPYL-1,3-THIAZOL-2-YL)AMINO]BENZENESULFONAMIDE
- N-(5-ISOPROPYL-THIAZOL-2-YL)-2-PYRIDIN-3-YL-ACETAMIDE
- 9-amino-5-(2-aminopyrimidin-4-yl)pyrido[3\',2\':4,5]pyrrolo[1,2-c]pyrimidin-4-ol
- N-(3-METHYLBUT-2-EN-1-YL)-9H-PURIN-6-AMINE
|
|
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CDK3 and CDKN1A |
cyclin-dependent kinase 3 |
cyclin-dependent kinase inhibitor 1A (p21, Cip1) |
|
- Signaling by the B Cell Receptor (BCR)
- Signaling by FGFR in disease
- Cellular Senescence
- p53-Dependent G1/S DNA damage checkpoint
- Cyclin E associated events during G1/S transition
- AKT phosphorylates targets in the cytosol
- Signaling by EGFRvIII in Cancer
- Signaling by SCF-KIT
- Downstream signaling events of B Cell Receptor (BCR)
- DAP12 signaling
- PI3K/AKT activation
- PI-3K cascade
- G1/S Transition
- Removal of licensing factors from origins
- Switching of origins to a post-replicative state
- Mitotic G1-G1/S phases
- Signaling by PDGF
- DAP12 interactions
- DNA Damage/Telomere Stress Induced Senescence
- GAB1 signalosome
- Senescence-Associated Secretory Phenotype (SASP)
- S Phase
- Signaling by ERBB4
- Constitutive PI3K/AKT Signaling in Cancer
- Role of LAT2/NTAL/LAB on calcium mobilization
- PI3K events in ERBB4 signaling
- Signaling by ERBB2
- Signaling by EGFR
- SCF(Skp2)-mediated degradation of p27/p21
- Downstream signal transduction
- Signaling by EGFR in Cancer
- Fc epsilon receptor (FCERI) signaling
- PI3K/AKT Signaling in Cancer
- Cyclin A:Cdk2-associated events at S phase entry
- SCF(Skp2)-mediated degradation of p27/p21
- Adaptive Immune System
- PIP3 activates AKT signaling
- Orc1 removal from chromatin
- p53-Dependent G1 DNA Damage Response
- PI3K events in ERBB2 signaling
- Transcriptional activation of p53 responsive genes
- Downstream signaling of activated FGFR
- G1/S DNA Damage Checkpoints
- Innate Immune System
- Transcriptional activation of cell cycle inhibitor p21
- Signalling by NGF
- Synthesis of DNA
- G1 Phase
- Regulation of DNA replication
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- NGF signalling via TRKA from the plasma membrane
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Cell Cycle, Mitotic
- Signaling by FGFR
- Orc1 removal from chromatin
- Cyclin D associated events in G1
- Cell Cycle Checkpoints
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CDK4 and CDKN1B |
cyclin-dependent kinase 4 |
cyclin-dependent kinase inhibitor 1B (p27, Kip1) |
- Meiotic recombination
- Chromatin organization
- Ubiquitin-dependent degradation of Cyclin D
- Cellular Senescence
- G1 Phase
- Senescence-Associated Secretory Phenotype (SASP)
- S Phase
- Oncogene Induced Senescence
- Cell Cycle, Mitotic
- Ubiquitin-dependent degradation of Cyclin D1
- RMTs methylate histone arginines
- Cyclin D associated events in G1
- Chromatin modifying enzymes
- Oxidative Stress Induced Senescence
- Transcriptional regulation of white adipocyte differentiation
- Mitotic G1-G1/S phases
|
- Signaling by the B Cell Receptor (BCR)
- Signaling by FGFR in disease
- Cellular Senescence
- p53-Dependent G1/S DNA damage checkpoint
- Cyclin E associated events during G1/S transition
- AKT phosphorylates targets in the cytosol
- Signaling by EGFRvIII in Cancer
- Signaling by SCF-KIT
- Downstream signaling events of B Cell Receptor (BCR)
- DAP12 signaling
- PI3K/AKT activation
- PI-3K cascade
- G1/S Transition
- Removal of licensing factors from origins
- Switching of origins to a post-replicative state
- Mitotic G1-G1/S phases
- Signaling by PDGF
- DAP12 interactions
- DNA Damage/Telomere Stress Induced Senescence
- GAB1 signalosome
- Senescence-Associated Secretory Phenotype (SASP)
- S Phase
- Signaling by ERBB4
- Constitutive PI3K/AKT Signaling in Cancer
- Role of LAT2/NTAL/LAB on calcium mobilization
- PI3K events in ERBB4 signaling
- Signaling by ERBB2
- Signaling by EGFR
- SCF(Skp2)-mediated degradation of p27/p21
- Downstream signal transduction
- Signaling by EGFR in Cancer
- Fc epsilon receptor (FCERI) signaling
- Cyclin A:Cdk2-associated events at S phase entry
- SCF(Skp2)-mediated degradation of p27/p21
- PI3K/AKT Signaling in Cancer
- Adaptive Immune System
- PIP3 activates AKT signaling
- Orc1 removal from chromatin
- p53-Dependent G1 DNA Damage Response
- PI3K events in ERBB2 signaling
- Downstream signaling of activated FGFR
- G1/S DNA Damage Checkpoints
- Innate Immune System
- Signalling by NGF
- Synthesis of DNA
- G1 Phase
- Regulation of DNA replication
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- NGF signalling via TRKA from the plasma membrane
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Cell Cycle, Mitotic
- Signaling by FGFR
- Orc1 removal from chromatin
- Cyclin D associated events in G1
- Cell Cycle Checkpoints
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CDK4 and CDKN2A |
cyclin-dependent kinase 4 |
cyclin-dependent kinase inhibitor 2A |
- Meiotic recombination
- Chromatin organization
- Ubiquitin-dependent degradation of Cyclin D
- Cellular Senescence
- G1 Phase
- Senescence-Associated Secretory Phenotype (SASP)
- S Phase
- Oncogene Induced Senescence
- Cell Cycle, Mitotic
- Ubiquitin-dependent degradation of Cyclin D1
- RMTs methylate histone arginines
- Cyclin D associated events in G1
- Chromatin modifying enzymes
- Oxidative Stress Induced Senescence
- Transcriptional regulation of white adipocyte differentiation
- Mitotic G1-G1/S phases
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- Cyclin D associated events in G1
- Oxidative Stress Induced Senescence
- G1 Phase
- Cellular Senescence
- Senescence-Associated Secretory Phenotype (SASP)
- Oncogene Induced Senescence
- Mitotic G1-G1/S phases
- Cell Cycle, Mitotic
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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CDK4 and CDKN2B |
cyclin-dependent kinase 4 |
cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) |
- Meiotic recombination
- Chromatin organization
- Ubiquitin-dependent degradation of Cyclin D
- Cellular Senescence
- G1 Phase
- Senescence-Associated Secretory Phenotype (SASP)
- S Phase
- Oncogene Induced Senescence
- Cell Cycle, Mitotic
- Ubiquitin-dependent degradation of Cyclin D1
- RMTs methylate histone arginines
- Cyclin D associated events in G1
- Chromatin modifying enzymes
- Oxidative Stress Induced Senescence
- Transcriptional regulation of white adipocyte differentiation
- Mitotic G1-G1/S phases
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- Loss of Function of TGFBR2 in Cancer
- SMAD2/3 MH2 Domain Mutants in Cancer
- Cellular Senescence
- Oncogene Induced Senescence
- TGFBR1 LBD Mutants in Cancer
- SMAD2/SMAD3:SMAD4 heterotrimer regulates transcription
- Transcriptional activity of SMAD2/SMAD3:SMAD4 heterotrimer
- Generic Transcription Pathway
- Mitotic G1-G1/S phases
- 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
- G1 Phase
- Senescence-Associated Secretory Phenotype (SASP)
- TGFBR1 KD Mutants in Cancer
- Cell Cycle, Mitotic
- Loss of Function of TGFBR1 in Cancer
- Cyclin D associated events in G1
- Signaling by TGF-beta Receptor Complex in Cancer
- Signaling by TGF-beta Receptor Complex
- Oxidative Stress Induced Senescence
- SMAD4 MH2 Domain Mutants in Cancer
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CDK4 and SMAD2 |
cyclin-dependent kinase 4 |
SMAD family member 2 |
- Meiotic recombination
- Chromatin organization
- Ubiquitin-dependent degradation of Cyclin D
- Cellular Senescence
- G1 Phase
- Senescence-Associated Secretory Phenotype (SASP)
- S Phase
- Oncogene Induced Senescence
- Cell Cycle, Mitotic
- Ubiquitin-dependent degradation of Cyclin D1
- RMTs methylate histone arginines
- Cyclin D associated events in G1
- Chromatin modifying enzymes
- Oxidative Stress Induced Senescence
- Transcriptional regulation of white adipocyte differentiation
- Mitotic G1-G1/S phases
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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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CDK6 and MYC |
cyclin-dependent kinase 6 |
v-myc avian myelocytomatosis viral oncogene homolog |
- Cyclin D associated events in G1
- Oxidative Stress Induced Senescence
- G1 Phase
- Cellular Senescence
- Senescence-Associated Secretory Phenotype (SASP)
- Oncogene Induced Senescence
- Mitotic G1-G1/S phases
- Cell Cycle, Mitotic
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- Loss of Function of TGFBR2 in Cancer
- Signaling by NOTCH1 HD Domain Mutants in Cancer
- Signaling by NOTCH1 HD+PEST Domain Mutants in Cancer
- SMAD2/3 MH2 Domain Mutants in Cancer
- Signaling by Wnt
- Cyclin E associated events during G1/S transition
- binding of TCF/LEF:CTNNB1 to target gene promoters
- TGFBR1 LBD Mutants in Cancer
- SMAD2/SMAD3:SMAD4 heterotrimer regulates transcription
- Transcriptional activity of SMAD2/SMAD3:SMAD4 heterotrimer
- Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant
- Generic Transcription Pathway
- RNF mutants show enhanced WNT signaling and proliferation
- G1/S Transition
- Signaling by NOTCH1
- XAV939 inhibits tankyrase, stabilizing AXIN
- Signaling by NOTCH1 in Cancer
- Constitutive Signaling by NOTCH1 HD+PEST Domain Mutants
- Mitotic G1-G1/S phases
- FBXW7 Mutants and NOTCH1 in Cancer
- TGFBR2 MSI Frameshift Mutants in Cancer
- SMAD2/3 Phosphorylation Motif Mutants in Cancer
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- Loss of Function of SMAD2/3 in Cancer
- Signaling by NOTCH
- formation of the beta-catenin:TCF transactivating complex
- TGFBR2 Kinase Domain Mutants in Cancer
- Loss of Function of SMAD4 in Cancer
- TGFBR1 KD Mutants in Cancer
- S Phase
- Cell Cycle, Mitotic
- Loss of Function of TGFBR1 in Cancer
- NOTCH1 Intracellular Domain Regulates Transcription
- Signaling by TGF-beta Receptor Complex in Cancer
- Signaling by TGF-beta Receptor Complex
- TCF dependent signaling in response to WNT
- Signaling by NOTCH1 PEST Domain Mutants in Cancer
- Cyclin A:Cdk2-associated events at S phase entry
- Signaling by WNT in cancer
- Constitutive Signaling by NOTCH1 PEST Domain Mutants
- SMAD4 MH2 Domain Mutants in Cancer
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CDK6 and CDKN1A |
cyclin-dependent kinase 6 |
cyclin-dependent kinase inhibitor 1A (p21, Cip1) |
- Cyclin D associated events in G1
- Oxidative Stress Induced Senescence
- G1 Phase
- Cellular Senescence
- Senescence-Associated Secretory Phenotype (SASP)
- Oncogene Induced Senescence
- Mitotic G1-G1/S phases
- Cell Cycle, Mitotic
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- Signaling by the B Cell Receptor (BCR)
- Signaling by FGFR in disease
- Cellular Senescence
- p53-Dependent G1/S DNA damage checkpoint
- Cyclin E associated events during G1/S transition
- AKT phosphorylates targets in the cytosol
- Signaling by EGFRvIII in Cancer
- Signaling by SCF-KIT
- Downstream signaling events of B Cell Receptor (BCR)
- DAP12 signaling
- PI3K/AKT activation
- PI-3K cascade
- G1/S Transition
- Removal of licensing factors from origins
- Switching of origins to a post-replicative state
- Mitotic G1-G1/S phases
- Signaling by PDGF
- DAP12 interactions
- DNA Damage/Telomere Stress Induced Senescence
- GAB1 signalosome
- Senescence-Associated Secretory Phenotype (SASP)
- S Phase
- Signaling by ERBB4
- Constitutive PI3K/AKT Signaling in Cancer
- Role of LAT2/NTAL/LAB on calcium mobilization
- PI3K events in ERBB4 signaling
- Signaling by ERBB2
- Signaling by EGFR
- SCF(Skp2)-mediated degradation of p27/p21
- Downstream signal transduction
- Signaling by EGFR in Cancer
- Fc epsilon receptor (FCERI) signaling
- PI3K/AKT Signaling in Cancer
- Cyclin A:Cdk2-associated events at S phase entry
- SCF(Skp2)-mediated degradation of p27/p21
- Adaptive Immune System
- PIP3 activates AKT signaling
- Orc1 removal from chromatin
- p53-Dependent G1 DNA Damage Response
- PI3K events in ERBB2 signaling
- Transcriptional activation of p53 responsive genes
- Downstream signaling of activated FGFR
- G1/S DNA Damage Checkpoints
- Innate Immune System
- Transcriptional activation of cell cycle inhibitor p21
- Signalling by NGF
- Synthesis of DNA
- G1 Phase
- Regulation of DNA replication
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- NGF signalling via TRKA from the plasma membrane
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Cell Cycle, Mitotic
- Signaling by FGFR
- Orc1 removal from chromatin
- Cyclin D associated events in G1
- Cell Cycle Checkpoints
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