PTEN and TP53 |
phosphatase and tensin homolog |
tumor protein p53 |
- Signaling by the B Cell Receptor (BCR)
- Downstream TCR signaling
- Metabolism of lipids and lipoproteins
- Signaling by FGFR in disease
- PIP3 activates AKT signaling
- Signaling by EGFRvIII in Cancer
- Synthesis of PIPs at the plasma membrane
- Signaling by SCF-KIT
- DAP12 signaling
- Downstream signaling events of B Cell Receptor (BCR)
- PI3K/AKT activation
- Synthesis of IP3 and IP4 in the cytosol
- PI-3K cascade
- PI3K events in ERBB2 signaling
- Downstream signaling of activated FGFR
- Phospholipid metabolism
- PI Metabolism
- Innate Immune System
- Signaling by PDGF
- DAP12 interactions
- Signalling by NGF
- GAB1 signalosome
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- NGF signalling via TRKA from the plasma membrane
- Signaling by ERBB4
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Negative regulation of the PI3K/AKT network
- Constitutive PI3K/AKT Signaling in Cancer
- Role of LAT2/NTAL/LAB on calcium mobilization
- Inositol phosphate metabolism
- PI3K events in ERBB4 signaling
- Signaling by FGFR
- Signaling by ERBB2
- Signaling by EGFR
- TCR signaling
- Downstream signal transduction
- Fc epsilon receptor (FCERI) signaling
- Signaling by EGFR in Cancer
- PI3K/AKT Signaling in Cancer
- Adaptive Immune System
|
- 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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BCL2 and TP53 |
B-cell CLL/lymphoma 2 |
tumor protein p53 |
- Activation of BAD and translocation to mitochondria
- Inflammasomes
- The NLRP1 inflammasome
- Nucleotide-binding domain, leucine rich repeat containing receptor (NLR) signaling pathways
- Programmed Cell Death
- Activation of BH3-only proteins
- BH3-only proteins associate with and inactivate anti-apoptotic BCL-2 members
- Innate Immune System
- Intrinsic Pathway for Apoptosis
|
- 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
|
- Ibuprofen
- Paclitaxel
- Docetaxel
- Rasagiline
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TP53 and TP63 |
tumor protein p53 |
tumor protein p63 |
- 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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MDM2 and TP53 |
MDM2 proto-oncogene, E3 ubiquitin protein ligase |
tumor protein p53 |
- Signaling by the B Cell Receptor (BCR)
- Signaling by FGFR in disease
- Cellular Senescence
- p53-Dependent G1/S DNA damage checkpoint
- 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
- Stabilization of p53
- Neurotransmitter Receptor Binding And Downstream Transmission In The Postsynaptic Cell
- Signaling by PDGF
- DAP12 interactions
- GAB1 signalosome
- 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
- Downstream signal transduction
- Signaling by EGFR in Cancer
- Fc epsilon receptor (FCERI) signaling
- PI3K/AKT Signaling in Cancer
- Adaptive Immune System
- Transmission across Chemical Synapses
- PIP3 activates AKT signaling
- Oncogene Induced Senescence
- 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
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- NGF signalling via TRKA from the plasma membrane
- Trafficking of AMPA receptors
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- Signaling by FGFR
- Oxidative Stress Induced Senescence
- Cell Cycle Checkpoints
- Glutamate Binding, Activation of AMPA Receptors and Synaptic Plasticity
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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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- Cis-[4,5-Bis-(4-Bromophenyl)-2-(2-Ethoxy-4-Methoxyphenyl)-4,5-Dihydroimidazol-1-Yl]-[4-(2-Hydroxyethyl)Piperazin-1-Yl]Methanone
- Cis-[4,5-Bis-(4-Chlorophenyl)-2-(2-Isopropoxy-4-Methoxyphenyl)-4,5-Dihyd Roimidazol-1-Yl]-Piperazin-1-Yl-Methanone
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ATM and TP53 |
ATM serine/threonine kinase |
tumor protein p53 |
- Ubiquitin Mediated Degradation of Phosphorylated Cdc25A
- Fanconi Anemia pathway
- G2/M Checkpoints
- Cellular Senescence
- p53-Dependent G1/S DNA damage checkpoint
- p53-Dependent G1 DNA Damage Response
- Regulation of the Fanconi anemia pathway
- Stabilization of p53
- p53-Independent DNA Damage Response
- Homologous recombination repair of replication-independent double-strand breaks
- p53-Independent G1/S DNA damage checkpoint
- Double-Strand Break Repair
- G1/S DNA Damage Checkpoints
- ATM mediated phosphorylation of repair proteins
- DNA Damage/Telomere Stress Induced Senescence
- Meiotic recombination
- ATM mediated response to DNA double-strand break
- G2/M DNA damage checkpoint
- Regulation of HSF1-mediated heat shock response
- Cellular response to heat stress
- Autodegradation of the E3 ubiquitin ligase COP1
- Homologous Recombination Repair
- Recruitment of repair and signaling proteins to double-strand breaks
- Cell Cycle Checkpoints
|
- 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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BRCA2 and TP53 |
breast cancer 2, early onset |
tumor protein p53 |
- Homologous DNA pairing and strand exchange
- Meiotic recombination
- Fanconi Anemia pathway
- Homologous Recombination Repair
- Homologous recombination repair of replication-independent double-strand breaks
- Double-Strand Break Repair
- Presynaptic phase of homologous DNA pairing and strand exchange
|
- 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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MEN1 and TP53 |
multiple endocrine neoplasia I |
tumor protein p53 |
- Loss of Function of TGFBR2 in Cancer
- SMAD2/3 MH2 Domain Mutants in Cancer
- Signaling by Wnt
- TGFBR1 LBD Mutants in Cancer
- deactivation of the beta-catenin transactivating complex
- SMAD2/SMAD3:SMAD4 heterotrimer regulates transcription
- Transcriptional activity of SMAD2/SMAD3:SMAD4 heterotrimer
- Generic Transcription Pathway
- RNF mutants show enhanced WNT signaling and proliferation
- XAV939 inhibits tankyrase, stabilizing AXIN
- 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
- TGFBR2 Kinase Domain Mutants in Cancer
- formation of the beta-catenin:TCF transactivating complex
- 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
- Signaling by TGF-beta Receptor Complex in Cancer
- TCF dependent signaling in response to WNT
- Signaling by WNT in cancer
- SMAD4 MH2 Domain Mutants 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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ACTA1 and TP53 |
actin, alpha 1, skeletal muscle |
tumor protein p53 |
- Striated Muscle Contraction
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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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ERCC6 and TP53 |
excision repair cross-complementation group 6 |
tumor protein p53 |
- Nucleotide Excision Repair
- RNA Polymerase I, RNA Polymerase III, and Mitochondrial Transcription
- Transcription-coupled NER (TC-NER)
- RNA Polymerase I Transcription
- RNA Polymerase I Transcription Initiation
- RNA Polymerase I Promoter Clearance
- Formation of transcription-coupled NER (TC-NER) repair complex
- Dual incision reaction in TC-NER
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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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MSX1 and TP53 |
msh homeobox 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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PTGS2 and TP53 |
prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) |
tumor protein p53 |
- Metabolism of vitamins and cofactors
- Defective CD320 causes methylmalonic aciduria
- Defective LMBRD1 causes methylmalonic aciduria and homocystinuria type cblF
- Metabolism of lipids and lipoproteins
- Defective BTD causes biotidinase deficiency
- Defective MMACHC causes methylmalonic aciduria and homocystinuria type cblC
- Defective MTR causes methylmalonic aciduria and homocystinuria type cblG
- Defective MTRR causes methylmalonic aciduria and homocystinuria type cblE
- Arachidonic acid metabolism
- Defective AMN causes hereditary megaloblastic anemia 1
- Nicotinamide salvaging
- Defects in cobalamin (B12) metabolism
- Defective GIF causes intrinsic factor deficiency
- Defective HLCS causes multiple carboxylase deficiency
- Defective MMAB causes methylmalonic aciduria type cblB
- Synthesis of 15-eicosatetraenoic acid derivatives
- Defective MMADHC causes methylmalonic aciduria and homocystinuria type cblD
- Defective MMAA causes methylmalonic aciduria type cblA
- Defective CUBN causes hereditary megaloblastic anemia 1
- Metabolism of water-soluble vitamins and cofactors
- Defective MUT causes methylmalonic aciduria mut type
- Defects in biotin (Btn) metabolism
- Synthesis of Prostaglandins (PG) and Thromboxanes (TX)
- Defective TCN2 causes hereditary megaloblastic anemia
- Nicotinate metabolism
- Defects in vitamin and cofactor metabolism
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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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- gamma-Homolinolenic acid
- Icosapent
- Aminosalicylic Acid
- Mesalazine
- Acetaminophen
- Indomethacin
- Nabumetone
- Ketorolac
- Tenoxicam
- Lenalidomide
- Celecoxib
- Tolmetin
- Rofecoxib
- Piroxicam
- Fenoprofen
- Valdecoxib
- Diclofenac
- Sulindac
- Flurbiprofen
- Etodolac
- Mefenamic acid
- Naproxen
- Sulfasalazine
- Phenylbutazone
- Meloxicam
- Carprofen
- Diflunisal
- Suprofen
- Salicyclic acid
- Meclofenamic acid
- Acetylsalicylic acid
- Bromfenac
- Oxaprozin
- Ketoprofen
- Balsalazide
- Thalidomide
- Ibuprofen
- Lumiracoxib
- Magnesium salicylate
- Salicylate-sodium
- Salsalate
- Trisalicylate-choline
- Ginseng
- Antrafenine
- Antipyrine
- Tiaprofenic acid
- Etoricoxib
- Flufenamic Acid
- Resveratrol
- Heme
- 1-Phenylsulfonamide-3-Trifluoromethyl-5-Parabromophenylpyrazole
- Prostaglandin G2
- Niflumic Acid
- Nimesulide
- Lornoxicam
- Nepafenac
- Pomalidomide
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ABL1 and TP53 |
ABL proto-oncogene 1, non-receptor tyrosine kinase |
tumor protein p53 |
- Role of Abl in Robo-Slit signaling
- CDO in myogenesis
- Axon guidance
- Myogenesis
- Fcgamma receptor (FCGR) dependent phagocytosis
- Factors involved in megakaryocyte development and platelet production
- Signaling by Robo receptor
- Regulation of actin dynamics for phagocytic cup formation
- 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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- Adenosine triphosphate
- Imatinib
- Dasatinib
- N-[4-Methyl-3-[[4-(3-Pyridinyl)-2-Pyrimidinyl]Amino]Phenyl]-3-Pyridinecarboxamide
- Nilotinib
- Bosutinib
- 2-{[(6-OXO-1,6-DIHYDROPYRIDIN-3-YL)METHYL]AMINO}-N-[4-PROPYL-3-(TRIFLUOROMETHYL)PHENYL]BENZAMIDE
- 1-[4-(PYRIDIN-4-YLOXY)PHENYL]-3-[3-(TRIFLUOROMETHYL)PHENYL]UREA
- MYRISTIC ACID
- 6-(2,6-DICHLOROPHENYL)-2-{[3-(HYDROXYMETHYL)PHENYL]AMINO}-8-METHYLPYRIDO[2,3-D]PYRIMIDIN-7(8H)-ONE
- 5-[3-(2-METHOXYPHENYL)-1H-PYRROLO[2,3-B]PYRIDIN-5-YL]-N,N-DIMETHYLPYRIDINE-3-CARBOXAMIDE
- 2-amino-5-[3-(1-ethyl-1H-pyrazol-5-yl)-1H-pyrrolo[2,3-b]pyridin-5-yl]-N,N-dimethylbenzamide
- Regorafenib
- Ponatinib
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ATR and TP53 |
ATR serine/threonine kinase |
tumor protein p53 |
- Fanconi Anemia pathway
- G2/M DNA damage checkpoint
- G2/M Checkpoints
- Meiotic synapsis
- Regulation of HSF1-mediated heat shock response
- Cellular response to heat stress
- Regulation of the Fanconi anemia pathway
- Activation of ATR in response to replication stress
- Cell Cycle Checkpoints
|
- 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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BCR and TP53 |
breakpoint cluster region |
tumor protein p53 |
- Rho GTPase cycle
- Signaling by FGFR in disease
- Signaling by Rho GTPases
- Signaling by FGFR1 mutants
- Signaling by FGFR mutants
- Signaling by FGFR1 fusion mutants
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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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BLM and TP53 |
Bloom syndrome, RecQ helicase-like |
tumor protein p53 |
|
- 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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BRCA1 and TP53 |
breast cancer 1, early onset |
tumor protein p53 |
- ATM mediated phosphorylation of repair proteins
- Meiotic recombination
- Fanconi Anemia pathway
- ATM mediated response to DNA double-strand break
- Homologous Recombination Repair
- Meiotic synapsis
- Homologous recombination repair of replication-independent double-strand breaks
- Recruitment of repair and signaling proteins to double-strand breaks
- Double-Strand Break Repair
|
- 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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BTK and TP53 |
Bruton agammaglobulinemia tyrosine kinase |
tumor protein p53 |
- Signaling by the B Cell Receptor (BCR)
- DAP12 interactions
- Toll Like Receptor TLR6:TLR2 Cascade
- Toll Like Receptor 2 (TLR2) Cascade
- Toll Like Receptor TLR1:TLR2 Cascade
- DAP12 signaling
- Activated TLR4 signalling
- Toll-Like Receptors Cascades
- Toll Like Receptor 4 (TLR4) Cascade
- Fc epsilon receptor (FCERI) signaling
- MyD88:Mal cascade initiated on plasma membrane
- FCERI mediated Ca+2 mobilization
- Fcgamma receptor (FCGR) dependent phagocytosis
- Antigen activates B Cell Receptor (BCR) leading to generation of second messengers
- Regulation of actin dynamics for phagocytic cup formation
- Adaptive Immune System
- 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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- Inositol 1,3,4,5-Tetrakisphosphate
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NFKBIA and TP53 |
nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha |
tumor protein p53 |
- Signaling by the B Cell Receptor (BCR)
- NF-kB is activated and signals survival
- Downstream TCR signaling
- Toll Like Receptor 7/8 (TLR7/8) Cascade
- RIP-mediated NFkB activation via ZBP1
- Toll Like Receptor TLR6:TLR2 Cascade
- Downstream signaling events of B Cell Receptor (BCR)
- Toll Like Receptor TLR1:TLR2 Cascade
- Activated TLR4 signalling
- FCERI mediated NF-kB activation
- MyD88 cascade initiated on plasma membrane
- Toll Like Receptor 5 (TLR5) Cascade
- ZBP1(DAI) mediated induction of type I IFNs
- p75NTR signals via NF-kB
- 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
- Innate Immune System
- Signalling by NGF
- TRIF-mediated TLR3/TLR4 signaling
- Cytosolic sensors of pathogen-associated DNA
- p75 NTR receptor-mediated signalling
- MyD88-independent cascade
- Toll Like Receptor 2 (TLR2) Cascade
- RIG-I/MDA5 mediated induction of IFN-alpha/beta pathways
- TCR signaling
- Toll-Like Receptors Cascades
- Toll Like Receptor 10 (TLR10) Cascade
- Activation of NF-kappaB in B cells
- Toll Like Receptor 4 (TLR4) Cascade
- Toll Like Receptor 3 (TLR3) Cascade
- Fc epsilon receptor (FCERI) signaling
- TRAF6 mediated NF-kB activation
- Adaptive Immune System
- 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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STK11 and TP53 |
serine/threonine kinase 11 |
tumor protein p53 |
- Insulin receptor signalling cascade
- Integration of energy metabolism
- IRS-mediated signalling
- Regulation of AMPK activity via LKB1
- mTOR signalling
- IRS-related events
- mTOR signalling
- IGF1R signaling cascade
- IRS-related events triggered by IGF1R
- IRS-mediated signalling
- Signaling by Type 1 Insulin-like Growth Factor 1 Receptor (IGF1R)
- Energy dependent regulation of mTOR by LKB1-AMPK
- AMPK inhibits chREBP transcriptional activation activity
- PKB-mediated events
- PI3K Cascade
- PKB-mediated events
- PI3K Cascade
- Signaling by Insulin receptor
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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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TP53 and WT1 |
tumor protein p53 |
Wilms tumor 1 |
- 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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