GSTM4 and TP53 |
glutathione S-transferase mu 4 |
tumor protein p53 |
- Defective OPLAH causes 5-oxoprolinase deficiency (OPLAHD)
- Defective AHCY causes Hypermethioninemia with S-adenosylhomocysteine hydrolase deficiency (HMAHCHD)
- Defective TPMT causes Thiopurine S-methyltransferase deficiency (TPMT deficiency)
- Defective MAT1A causes Methionine adenosyltransferase deficiency (MATD)
- Defective UGT1A4 causes hyperbilirubinemia
- Glutathione conjugation
- Metabolic disorders of biological oxidation enzymes
- Phase II conjugation
- Defective UGT1A1 causes hyperbilirubinemia
- Defective SLC35D1 causes Schneckenbecken dysplasia (SCHBCKD)
- Biological oxidations
- Defective GCLC causes Hemolytic anemia due to gamma-glutamylcysteine synthetase deficiency (HAGGSD)
- Defective GGT1 causes Glutathionuria (GLUTH)
- Defective GSS causes Glutathione synthetase deficiency (GSS deficiency)
|
- 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
|
- Glutathione
- Glutathione Sulfonic Acid
- S-Octylglutathione
- Gamma-Glutamyl[S-(2-Iodobenzyl)Cysteinyl]Glycine
- 1-Hydroxy-2-S-Glutathionyl-3-Para-Nitrophenoxy-Propane
- S-Hexylglutathione
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GTF2H1 and TP53 |
general transcription factor IIH, polypeptide 1, 62kDa |
tumor protein p53 |
- RNA Polymerase II Promoter Escape
- Formation of HIV-1 elongation complex containing HIV-1 Tat
- Nucleotide Excision Repair
- RNA Polymerase II Transcription Pre-Initiation And Promoter Opening
- RNA Polymerase I Chain Elongation
- RNA Polymerase II Transcription
- RNA Polymerase I, RNA Polymerase III, and Mitochondrial Transcription
- RNA Polymerase I Transcription Initiation
- RNA Polymerase I Promoter Clearance
- HIV Infection
- Formation of the Early Elongation Complex
- Tat-mediated elongation of the HIV-1 transcript
- Formation of transcription-coupled NER (TC-NER) repair complex
- RNA Pol II CTD phosphorylation and interaction with CE
- RNA Polymerase II Pre-transcription Events
- Dual incision reaction in TC-NER
- NoRC negatively regulates rRNA expression
- HIV Transcription Initiation
- HIV Life Cycle
- RNA Pol II CTD phosphorylation and interaction with CE
- RNA Polymerase II HIV Promoter Escape
- HIV Transcription Elongation
- Dual incision reaction in GG-NER
- mRNA Capping
- RNA Polymerase I Transcription
- RNA Polymerase I Promoter Escape
- RNA Polymerase I Transcription Termination
- Epigenetic regulation of gene expression
- Negative epigenetic regulation of rRNA expression
- Late Phase of HIV Life Cycle
- Formation of RNA Pol II elongation complex
- Global Genomic NER (GG-NER)
- RNA Polymerase II Transcription Initiation And Promoter Clearance
- Transcription-coupled NER (TC-NER)
- Formation of HIV elongation complex in the absence of HIV Tat
- Formation of the HIV-1 Early Elongation Complex
- Formation of incision complex in GG-NER
- RNA Polymerase II Transcription Initiation
- Transcription of the HIV genome
- RNA Polymerase II Transcription Elongation
|
- 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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GTF2H4 and TP53 |
general transcription factor IIH, polypeptide 4, 52kDa |
tumor protein p53 |
- RNA Polymerase II Promoter Escape
- Formation of HIV-1 elongation complex containing HIV-1 Tat
- Nucleotide Excision Repair
- RNA Polymerase II Transcription Pre-Initiation And Promoter Opening
- RNA Polymerase I Chain Elongation
- RNA Polymerase II Transcription
- RNA Polymerase I, RNA Polymerase III, and Mitochondrial Transcription
- RNA Polymerase I Transcription Initiation
- RNA Polymerase I Promoter Clearance
- HIV Infection
- Formation of the Early Elongation Complex
- Tat-mediated elongation of the HIV-1 transcript
- Formation of transcription-coupled NER (TC-NER) repair complex
- RNA Pol II CTD phosphorylation and interaction with CE
- RNA Polymerase II Pre-transcription Events
- Dual incision reaction in TC-NER
- NoRC negatively regulates rRNA expression
- HIV Transcription Initiation
- HIV Life Cycle
- RNA Pol II CTD phosphorylation and interaction with CE
- RNA Polymerase II HIV Promoter Escape
- HIV Transcription Elongation
- Dual incision reaction in GG-NER
- mRNA Capping
- RNA Polymerase I Transcription
- RNA Polymerase I Promoter Escape
- RNA Polymerase I Transcription Termination
- Epigenetic regulation of gene expression
- Negative epigenetic regulation of rRNA expression
- Late Phase of HIV Life Cycle
- Formation of RNA Pol II elongation complex
- Global Genomic NER (GG-NER)
- RNA Polymerase II Transcription Initiation And Promoter Clearance
- Transcription-coupled NER (TC-NER)
- Formation of HIV elongation complex in the absence of HIV Tat
- Formation of the HIV-1 Early Elongation Complex
- Formation of incision complex in GG-NER
- RNA Polymerase II Transcription Initiation
- Transcription of the HIV genome
- RNA Polymerase II Transcription Elongation
|
- 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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BRF1 and TP53 |
BRF1, RNA polymerase III transcription initiation factor 90 kDa subunit |
tumor protein p53 |
- RNA Polymerase III Transcription
- RNA Polymerase III Transcription Initiation
- RNA Polymerase III Transcription Initiation From Type 1 Promoter
- RNA Polymerase I, RNA Polymerase III, and Mitochondrial Transcription
- RNA Polymerase III Abortive And Retractive Initiation
- RNA Polymerase III Transcription Initiation From Type 2 Promoter
|
- 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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HDAC1 and TP53 |
histone deacetylase 1 |
tumor protein p53 |
- 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
|
- 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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HDAC2 and TP53 |
histone deacetylase 2 |
tumor protein p53 |
- 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
|
- 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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HIF1A and TP53 |
hypoxia inducible factor 1, alpha subunit (basic helix-loop-helix transcription factor) |
tumor protein p53 |
- Signaling by NOTCH1 HD Domain Mutants in Cancer
- Cellular response to hypoxia
- Regulation of Hypoxia-inducible Factor (HIF) by oxygen
- Signaling by NOTCH1 HD+PEST Domain Mutants in Cancer
- Oxygen-dependent proline hydroxylation of Hypoxia-inducible Factor Alpha
- Signaling by NOTCH
- Regulation of gene expression by Hypoxia-inducible Factor
- Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant
- NOTCH1 Intracellular Domain Regulates Transcription
- Oxygen-dependent asparagine hydroxylation of Hypoxia-inducible Factor Alpha
- Signaling by NOTCH1
- Signaling by NOTCH1 PEST Domain Mutants in Cancer
- Signaling by NOTCH1 in Cancer
- FBXW7 Mutants and NOTCH1 in Cancer
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- 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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UBE2K and TP53 |
ubiquitin-conjugating enzyme E2K |
tumor protein p53 |
- RIG-I/MDA5 mediated induction of IFN-alpha/beta pathways
- Antigen processing: Ubiquitination & Proteasome degradation
- Negative regulators of RIG-I/MDA5 signaling
- Class I MHC mediated antigen processing & presentation
- Innate Immune System
- Adaptive Immune System
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- 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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HMGB1 and TP53 |
high mobility group box 1 |
tumor protein p53 |
- Toll Like Receptor 7/8 (TLR7/8) Cascade
- RIP-mediated NFkB activation via ZBP1
- Toll Like Receptor TLR6:TLR2 Cascade
- DEx/H-box helicases activate type I IFN and inflammatory cytokines production
- Toll Like Receptor TLR1:TLR2 Cascade
- Activated TLR4 signalling
- MyD88 cascade initiated on plasma membrane
- Activation of DNA fragmentation factor
- Toll Like Receptor 5 (TLR5) Cascade
- ZBP1(DAI) mediated induction of type I IFNs
- Programmed Cell Death
- MyD88 dependent cascade initiated on endosome
- MyD88:Mal cascade initiated on plasma membrane
- TRAF6 mediated induction of NFkB and MAP kinases upon TLR7/8 or 9 activation
- Toll Like Receptor 9 (TLR9) Cascade
- Advanced glycosylation endproduct receptor signaling
- Innate Immune System
- TRIF-mediated TLR3/TLR4 signaling
- Cytosolic sensors of pathogen-associated DNA
- Apoptotic execution phase
- MyD88-independent cascade
- Toll Like Receptor 2 (TLR2) Cascade
- RIG-I/MDA5 mediated induction of IFN-alpha/beta pathways
- Toll-Like Receptors Cascades
- Toll Like Receptor 10 (TLR10) Cascade
- Apoptosis induced DNA fragmentation
- Toll Like Receptor 4 (TLR4) Cascade
- Toll Like Receptor 3 (TLR3) Cascade
- TRAF6 mediated NF-kB activation
- TAK1 activates NFkB by phosphorylation and activation of IKKs complex
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- 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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HMGB2 and TP53 |
high mobility group box 2 |
tumor protein p53 |
- Activation of DNA fragmentation factor
- Apoptosis induced DNA fragmentation
- Programmed Cell Death
- Apoptotic execution phase
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- 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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NR4A1 and TP53 |
nuclear receptor subfamily 4, group A, member 1 |
tumor protein p53 |
- Signaling by the B Cell Receptor (BCR)
- Signaling by FGFR in disease
- PIP3 activates AKT signaling
- Nuclear Receptor transcription pathway
- Signaling by EGFRvIII in Cancer
- Signaling by SCF-KIT
- DAP12 signaling
- Downstream signaling events of B Cell Receptor (BCR)
- PI3K/AKT activation
- Generic Transcription Pathway
- 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 Overexpressed Wild-Type EGFR in Cancer
- Signaling by ERBB4
- Constitutive PI3K/AKT Signaling in Cancer
- Role of LAT2/NTAL/LAB on calcium mobilization
- PI3K events in ERBB4 signaling
- Signaling by FGFR
- Signaling by ERBB2
- Signaling by EGFR
- AKT phosphorylates targets in the nucleus
- 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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- 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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PRMT1 and TP53 |
protein arginine methyltransferase 1 |
tumor protein p53 |
- Chromatin modifying enzymes
- Chromatin organization
- RMTs methylate histone arginines
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- 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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HSPA1A and TP53 |
heat shock 70kDa protein 1A |
tumor protein p53 |
- Regulation of mRNA stability by proteins that bind AU-rich elements
- Viral RNP Complexes in the Host Cell Nucleus
- Attenuation phase
- Regulation of HSF1-mediated heat shock response
- Cellular response to heat stress
- AUF1 (hnRNP D0) destabilizes mRNA
- Influenza Infection
- Influenza Life Cycle
- HSF1-dependent transactivation
- Export of Viral Ribonucleoproteins from Nucleus
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- 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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HSPA9 and TP53 |
heat shock 70kDa protein 9 (mortalin) |
tumor protein p53 |
- Mitochondrial protein import
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- 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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HSP90AA1 and TP53 |
heat shock protein 90kDa alpha (cytosolic), class A member 1 |
tumor protein p53 |
- HSF1 activation
- Regulatory RNA pathways
- Signaling by EGFRvIII in Cancer
- Regulation of PLK1 Activity at G2/M Transition
- Influenza Life Cycle
- Influenza Viral RNA Transcription and Replication
- Constitutive Signaling by Ligand-Responsive EGFR Cancer Variants
- Uptake and actions of bacterial toxins
- EPH-Ephrin signaling
- Tetrahydrobiopterin (BH4) synthesis, recycling, salvage and regulation
- Fcgamma receptor (FCGR) dependent phagocytosis
- Recruitment of mitotic centrosome proteins and complexes
- Regulation of actin dynamics for phagocytic cup formation
- vRNP Assembly
- Influenza Infection
- Signaling by ERBB2
- Signaling by VEGF
- Signaling by EGFR in Cancer
- Sema3A PAK dependent Axon repulsion
- Mitotic G2-G2/M phases
- Uptake and function of diphtheria toxin
- PIWI-interacting RNA (piRNA) biogenesis
- Organelle biogenesis and maintenance
- Axon guidance
- Attenuation phase
- G2/M Transition
- VEGFA-VEGFR2 Pathway
- HSF1-dependent transactivation
- EPHA-mediated growth cone collapse
- Metabolism of nitric oxide
- VEGFR2 mediated vascular permeability
- Loss of Nlp from mitotic centrosomes
- Scavenging by Class F Receptors
- eNOS activation and regulation
- Innate Immune System
- Semaphorin interactions
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- Assembly of the primary cilium
- Cellular response to heat stress
- Anchoring of the basal body to the plasma membrane
- Cell Cycle, Mitotic
- eNOS activation
- Loss of proteins required for interphase microtubule organization from the centrosome
- Centrosome maturation
- Constitutive Signaling by EGFRvIII
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- 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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- Rifabutin
- Nedocromil
- 9-Butyl-8-(2,5-Dimethoxy-Benzyl)-9h-Purin-6-Ylamine
- Geldanamycin
- 8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-2-Fluoro-9-Pent-4-Ylnyl-9h-Purin-6-Ylamine
- 9-Butyl-8-(3,4,5-Trimethoxybenzyl)-9h-Purin-6-Amine
- 4-(1,3-Benzodioxol-5-Yl)-5-(5-Ethyl-2,4-Dihydroxyphenyl)-2h-Pyrazole-3-Carboxylic Acid
- 17-Dmag
- 8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9h-Purin-6-Ylamine
- 8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9-Pent-9h-Purin-6-Ylamine
- Adenosine-5\'-Diphosphate
- 9-Butyl-8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-9h-Purin-6-Ylamine
- 4-(1h-Imidazol-4-Yl)-3-(5-Ethyl-2,4-Dihydroxy-Phenyl)-1h-Pyrazole
- 9-Butyl-8-(3-Methoxybenzyl)-9h-Purin-6-Amine
- 9-Butyl-8-(4-Methoxybenzyl)-9h-Purin-6-Amine
- 9-Butyl-8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9h-Purin-6-Ylamine
- 8-Benzo[1,3]Dioxol-,5-Ylmethyl-9-Butyl-2-Fluoro-9h-Purin-6-Ylamine
- 8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-9-Pent-4-Ylnyl-9h-Purin-6-Ylamine
- N-[4-(AMINOSULFONYL)BENZYL]-5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-1H-PYRAZOLE-4-CARBOXAMIDE
- N-(4-ACETYLPHENYL)-5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-1H-PYRAZOLE-4-CARBOXAMIDE
- 4-CHLORO-6-(4-{4-[4-(METHYLSULFONYL)BENZYL]PIPERAZIN-1-YL}-1H-PYRAZOL-5-YL)BENZENE-1,3-DIOL
- 5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-PIPERAZIN-1-YL-1H-PYRAZOLE-3-CARBOXAMIDE
- 5-(5-chloro-2,4-dihydroxyphenyl)-N-ethyl-4-[4-(morpholin-4-ylmethyl)phenyl]isoxazole-3-carboxamide
- 5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-(4-METHOXYPHENYL)ISOXAZOLE-3-CARBOXAMIDE
- 2-amino-4-[2,4-dichloro-5-(2-pyrrolidin-1-ylethoxy)phenyl]-N-ethylthieno[2,3-d]pyrimidine-6-carboxamide
- 4-CHLORO-6-(4-PIPERAZIN-1-YL-1H-PYRAZOL-5-YL)BENZENE-1,3-DIOL
- (3E)-3-[(phenylamino)methylidene]dihydrofuran-2(3H)-one
- 6-(3-BROMO-2-NAPHTHYL)-1,3,5-TRIAZINE-2,4-DIAMINE
- 3-({2-[(2-AMINO-6-METHYLPYRIMIDIN-4-YL)ETHYNYL]BENZYL}AMINO)-1,3-OXAZOL-2(3H)-ONE
- N-[(2-AMINO-6-METHYLPYRIMIDIN-4-YL)METHYL]-3-{[(E)-(2-OXODIHYDROFURAN-3(2H)-YLIDENE)METHYL]AMINO}BENZENESULFONAMIDE
- 5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-(4-METHOXYPHENYL)-1H-PYRAZOLE-3-CARBOXAMIDE
- 4-bromo-6-(6-hydroxy-1,2-benzisoxazol-3-yl)benzene-1,3-diol
- 4-[4-(2,3-DIHYDRO-1,4-BENZODIOXIN-6-YL)-3-METHYL-1H-PYRAZOL-5-YL]-6-ETHYLBENZENE-1,3-DIOL
- 4-chloro-6-{5-[(2-morpholin-4-ylethyl)amino]-1,2-benzisoxazol-3-yl}benzene-1,3-diol
- 8-(6-BROMO-BENZO[1,3]DIOXOL-5-YLSULFANYL)-9-(3-ISOPROPYLAMINO-PROPYL)-ADENINE
- 4-methyl-7,8-dihydro-5H-thiopyrano[4,3-d]pyrimidin-2-amine
- (5E,7S)-2-amino-7-(4-fluoro-2-pyridin-3-ylphenyl)-4-methyl-7,8-dihydroquinazolin-5(6H)-one oxime
- 8-BENZO[1,3]DIOXOL-,5-YLMETHYL-9-BUTYL-9H-
- 4-{[(2R)-2-(2-methylphenyl)pyrrolidin-1-yl]carbonyl}benzene-1,3-diol
- 2-(1H-pyrrol-1-ylcarbonyl)benzene-1,3,5-triol
- 2-[(2-methoxyethyl)amino]-4-(4-oxo-1,2,3,4-tetrahydro-9H-carbazol-9-yl)benzamide
- 4-(2-methoxyethoxy)-6-methylpyrimidin-2-amine
- 4-(2,4-dichlorophenyl)-5-phenyldiazenyl-pyrimidin-2-amine
- 3,6-DIAMINO-5-CYANO-4-(4-ETHOXYPHENYL)THIENO[2,3-B]PYRIDINE-2-CARBOXAMIDE
- 2-AMINO-4-(2,4-DICHLOROPHENYL)-N-ETHYLTHIENO[2,3-D]PYRIMIDINE-6-CARBOXAMIDE
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HSP90AB1 and TP53 |
heat shock protein 90kDa alpha (cytosolic), class B member 1 |
tumor protein p53 |
- HSF1 activation
- Axon guidance
- Semaphorin interactions
- Inflammasomes
- Attenuation phase
- Cellular response to heat stress
- HSF1-dependent transactivation
- Uptake and actions of bacterial toxins
- The NLRP3 inflammasome
- Nucleotide-binding domain, leucine rich repeat containing receptor (NLR) signaling pathways
- Sema3A PAK dependent Axon repulsion
- Fcgamma receptor (FCGR) dependent phagocytosis
- Regulation of actin dynamics for phagocytic cup formation
- Uptake and function of diphtheria toxin
- Innate Immune System
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- 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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- Geldanamycin
- 9-Butyl-8-(3,4,5-Trimethoxybenzyl)-9h-Purin-6-Amine
- Adenosine-5\'-Diphosphate
- Radicicol
- 4-[4-(2,3-DIHYDRO-1,4-BENZODIOXIN-6-YL)-3-METHYL-1H-PYRAZOL-5-YL]-6-ETHYLBENZENE-1,3-DIOL
- 8-(6-BROMO-BENZO[1,3]DIOXOL-5-YLSULFANYL)-9-(3-ISOPROPYLAMINO-PROPYL)-ADENINE
- 4-{4-[4-(3-AMINOPROPOXY)PHENYL]-1H-PYRAZOL-5-YL}-6-CHLOROBENZENE-1,3-DIOL
- (5E)-14-CHLORO-15,17-DIHYDROXY-4,7,8,9,10,11-HEXAHYDRO-2-BENZOXACYCLOPENTADECINE-1,12(3H,13H)-DIONE
- (5Z)-12-CHLORO-13,15-DIHYDROXY-4,7,8,9-TETRAHYDRO-2-BENZOXACYCLOTRIDECINE-1,10(3H,11H)-DIONE
- (5E)-12-CHLORO-13,15-DIHYDROXY-4,7,8,9-TETRAHYDRO-2-BENZOXACYCLOTRIDECINE-1,10(3H,11H)-DIONE
- (5Z)-13-CHLORO-14,16-DIHYDROXY-3,4,7,8,9,10-HEXAHYDRO-1H-2-BENZOXACYCLOTETRADECINE-1,11(12H)-DIONE
- METHYL 3-CHLORO-2-{3-[(2,5-DIHYDROXY-4-METHOXYPHENYL)AMINO]-3-OXOPROPYL}-4,6-DIHYDROXYBENZOATE
- 2-(3-AMINO-2,5,6-TRIMETHOXYPHENYL)ETHYL 5-CHLORO-2,4-DIHYDROXYBENZOATE
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IFI16 and TP53 |
interferon, gamma-inducible protein 16 |
tumor protein p53 |
- Cytosolic sensors of pathogen-associated DNA
- STING mediated induction of host immune responses
- IRF3-mediated induction of type I IFN
- Innate Immune System
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- 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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IKBKB and TP53 |
inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase beta |
tumor protein p53 |
- Signaling by the B Cell Receptor (BCR)
- NF-kB is activated and signals survival
- RIP-mediated NFkB activation via ZBP1
- IRAK1 recruits IKK complex
- Downstream signaling events of B Cell Receptor (BCR)
- Toll Like Receptor TLR1:TLR2 Cascade
- FCERI mediated NF-kB activation
- Toll Like Receptor 5 (TLR5) Cascade
- NOD1/2 Signaling Pathway
- MyD88 dependent cascade initiated on endosome
- Toll Like Receptor 9 (TLR9) Cascade
- IRAK1 recruits IKK complex
- TRIF-mediated TLR3/TLR4 signaling
- Toll Like Receptor 2 (TLR2) Cascade
- TCR signaling
- Signaling by Interleukins
- Toll Like Receptor 4 (TLR4) Cascade
- Toll Like Receptor 3 (TLR3) Cascade
- Fc epsilon receptor (FCERI) signaling
- Interleukin-1 signaling
- Adaptive Immune System
- TAK1 activates NFkB by phosphorylation and activation of IKKs complex
- Downstream TCR signaling
- p75NTR recruits signalling complexes
- Toll Like Receptor 7/8 (TLR7/8) Cascade
- Toll Like Receptor TLR6:TLR2 Cascade
- Activated TLR4 signalling
- MyD88 cascade initiated on plasma membrane
- ZBP1(DAI) mediated induction of type I IFNs
- p75NTR signals via NF-kB
- MyD88:Mal cascade initiated on plasma membrane
- TRAF6 mediated induction of NFkB and MAP kinases upon TLR7/8 or 9 activation
- Innate Immune System
- Signalling by NGF
- IKK complex recruitment mediated by RIP1
- Cytosolic sensors of pathogen-associated DNA
- p75 NTR receptor-mediated signalling
- Cytokine Signaling in Immune system
- MyD88-independent cascade
- Toll-Like Receptors Cascades
- RIG-I/MDA5 mediated induction of IFN-alpha/beta pathways
- Toll Like Receptor 10 (TLR10) Cascade
- Nucleotide-binding domain, leucine rich repeat containing receptor (NLR) signaling pathways
- Activation of NF-kappaB in B cells
- TRAF6 mediated NF-kB activation
- NF-kB activation through FADD/RIP-1 pathway mediated by caspase-8 and -10
- IRAK1 recruits IKK complex upon TLR7/8 or 9 stimulation
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- 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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- Mesalazine
- Sulfasalazine
- Auranofin
- Arsenic trioxide
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ING1 and TP53 |
inhibitor of growth family, member 1 |
tumor protein p53 |
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- 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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IRF7 and TP53 |
interferon regulatory factor 7 |
tumor protein p53 |
- TRIF-mediated TLR3/TLR4 signaling
- Cytosolic sensors of pathogen-associated DNA
- Toll Like Receptor 7/8 (TLR7/8) Cascade
- Interferon Signaling
- Cytokine Signaling in Immune system
- Factors involved in megakaryocyte development and platelet production
- MyD88-independent cascade
- Activation of IRF3/IRF7 mediated by TBK1/IKK epsilon
- DEx/H-box helicases activate type I IFN and inflammatory cytokines production
- Interferon gamma signaling
- Activated TLR4 signalling
- TRAF3-dependent IRF activation pathway
- RIG-I/MDA5 mediated induction of IFN-alpha/beta pathways
- Toll-Like Receptors Cascades
- Toll Like Receptor 4 (TLR4) Cascade
- Toll Like Receptor 3 (TLR3) Cascade
- MyD88 dependent cascade initiated on endosome
- TRAF6 mediated IRF7 activation
- Interferon alpha/beta signaling
- TRAF6 mediated IRF7 activation in TLR7/8 or 9 signaling
- Toll Like Receptor 9 (TLR9) Cascade
- Innate Immune System
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- 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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