DAXX and TP53 |
death-domain associated protein |
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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GADD45A and TP53 |
growth arrest and DNA-damage-inducible, alpha |
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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DHFR and TP53 |
dihydrofolate reductase |
tumor protein p53 |
- Metabolism of vitamins and cofactors
- Defective CD320 causes methylmalonic aciduria
- Defective LMBRD1 causes methylmalonic aciduria and homocystinuria type cblF
- 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
- Defective AMN causes hereditary megaloblastic anemia 1
- Metabolism of nitric oxide
- G1/S Transition
- G1/S-Specific Transcription
- Metabolism of folate and pterines
- eNOS activation and regulation
- Tetrahydrobiopterin (BH4) synthesis, recycling, salvage and regulation
- Mitotic G1-G1/S phases
- Defects in cobalamin (B12) metabolism
- Defective GIF causes intrinsic factor deficiency
- E2F mediated regulation of DNA replication
- Defective HLCS causes multiple carboxylase deficiency
- Defective MMAB causes methylmalonic aciduria type cblB
- Defective MMADHC causes methylmalonic aciduria and homocystinuria type cblD
- Cell Cycle, Mitotic
- Defective MMAA causes methylmalonic aciduria type cblA
- Defective CUBN causes hereditary megaloblastic anemia 1
- Defective MUT causes methylmalonic aciduria mut type
- Metabolism of water-soluble vitamins and cofactors
- Defects in biotin (Btn) metabolism
- Defective TCN2 causes hereditary megaloblastic anemia
- Defects in vitamin and cofactor metabolism
|
- 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
|
- NADH
- Pyrimethamine
- Trimethoprim
- Methotrexate
- Pemetrexed
- Proguanil
- Trimetrexate
- 2,4-Diamino-5-Methyl-6-[(3,4,5-Trimethoxy-N-Methylanilino)Methyl]Pyrido[2,3-D]Pyrimidine
- 2,4-Diamino-6-[N-(2\',5\'-Dimethoxybenzyl)-N-Methylamino]Quinazoline
- 6-(Octahydro-1h-Indol-1-Ylmethyl)Decahydroquinazoline-2,4-Diamine
- N6-(2,5-Dimethoxy-Benzyl)-N6-Methyl-Pyrido[2,3-D]Pyrimidine-2,4,6-Triamine
- 2,4-Diamino-6-[N-(3\',4\',5\'-Trimethoxybenzyl)-N-Methylamino]Pyrido[2,3-D]Pyrimidine
- Sri-9662
- 2,4-Diamino-5-(3,4,5-Trimethoxy-Benzyl)-Pyrimidin-1-Ium
- Sri-9439
- 2\'-Monophosphoadenosine 5\'-Diphosphoribose
- 6-(2,5-Dimethoxy-Benzyl)-5-Methyl-Pyrido[2,3-D]Pyrimidine-2,4-Diamine
- Biopterin
- 2,4-Diamino-6-[N-(3\',5\'-Dimethoxybenzyl)-N-Methylamino]Pyrido[2,3-D]Pyrimidine
- Pralatrexate
- 5-[(3R)-3-(5-methoxybiphenyl-3-yl)but-1-yn-1-yl]-6-methylpyrimidine-2,4-diamine
- 5-[(3R)-3-(5-methoxy-4\'-methylbiphenyl-3-yl)but-1-yn-1-yl]-6-methylpyrimidine-2,4-diamine
- 5-[(3R)-3-(5-methoxy-3\',5\'-dimethylbiphenyl-3-yl)but-1-yn-1-yl]-6-methylpyrimidine-2,4-diamine
- 5-[(3R)-3-(5-methoxy-2\',6\'-dimethylbiphenyl-3-yl)but-1-yn-1-yl]-6-methylpyrimidine-2,4-diamine
- 5-[3-(2,5-dimethoxyphenyl)prop-1-yn-1-yl]-6-ethylpyrimidine-2,4-diamine
- [N-(2,4-DIAMINOPTERIDIN-6-YL)-METHYL]-DIBENZ[B,F]AZEPINE
- (4aS)-5-[(2,4-diaminopteridin-6-yl)methyl]-4a,5-dihydro-2H-dibenzo[b,f]azepin-8-ol
- (2R,6S)-6-{[methyl(3,4,5-trimethoxyphenyl)amino]methyl}-1,2,5,6,7,8-hexahydroquinazoline-2,4-diamine
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NQO1 and TP53 |
NAD(P)H dehydrogenase, quinone 1 |
tumor protein p53 |
- Regulation of ornithine decarboxylase (ODC)
- Metabolism of amino acids and derivatives
|
- 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
|
- Menadione
- Dicumarol
- Duroquinone
- 3-Hydroxymethyl-5-Aziridinyl-1methyl-2-[1h-Indole-4,7-Dione]-Propanol
- 5-Methoxy-1,2-Dimethyl-3-(4-Nitrophenoxymethyl)Indole-4,7-Dione
- Cibacron Blue
- Flavin-Adenine Dinucleotide
- 5-Methoxy-1,2-Dimethyl-3-(Phenoxymethyl)Indole-4,7-Dione
- 2,5-Diaziridin-1-Yl-3-(Hydroxymethyl)-6-Methylcyclohexa-2,5-Diene-1,4-Dione
- Bishydroxy[2h-1-Benzopyran-2-One,1,2-Benzopyrone]
- 3-(HYDROXYMETHYL)-1-METHYL-5-(2-METHYLAZIRIDIN-1-YL)-2-PHENYL-1H-INDOLE-4,7-DIONE
|
|
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ARID3A and TP53 |
AT rich interactive domain 3A (BRIGHT-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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|
TSC22D3 and TP53 |
TSC22 domain family, member 3 |
tumor protein p53 |
- Ion channel transport
- Stimuli-sensing channels
|
- 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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DVL2 and TP53 |
dishevelled segment polarity protein 2 |
tumor protein p53 |
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- Signaling by Wnt
- negative regulation of TCF-dependent signaling by DVL-interacting proteins
- beta-catenin independent WNT signaling
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- WNT mediated activation of DVL
- Signaling by Hippo
- TCF dependent signaling in response to WNT
- RNF mutants show enhanced WNT signaling and proliferation
- Asymmetric localization of PCP proteins
- WNT5A-dependent internalization of FZD4
- XAV939 inhibits tankyrase, stabilizing AXIN
- degradation of DVL
- Signaling by WNT in cancer
- PCP/CE pathway
|
- 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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E2F1 and TP53 |
E2F transcription factor 1 |
tumor protein p53 |
- Cellular Senescence
- Activation of BH3-only proteins
- Oncogene Induced Senescence
- Assembly of the pre-replicative complex
- Pre-NOTCH Transcription and Translation
- G2 Phase
- G1/S Transition
- G1/S-Specific Transcription
- Programmed Cell Death
- Pre-NOTCH Expression and Processing
- Mitotic G1-G1/S phases
- Intrinsic Pathway for Apoptosis
- E2F mediated regulation of DNA replication
- Signaling by NOTCH
- DNA Replication Pre-Initiation
- G1 Phase
- M/G1 Transition
- Regulation of DNA replication
- G0 and Early G1
- CDC6 association with the ORC:origin complex
- Cell Cycle, Mitotic
- Activation of NOXA and translocation to mitochondria
- Cyclin D associated events in G1
- Oxidative Stress Induced Senescence
- Activation of PUMA and translocation to mitochondria
- Association of licensing factors with the pre-replicative complex
- Mitotic G2-G2/M phases
- Inhibition of replication initiation of damaged DNA by RB1/E2F1
|
- 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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E4F1 and TP53 |
E4F transcription factor 1 |
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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EEF2 and TP53 |
eukaryotic translation elongation factor 2 |
tumor protein p53 |
- Synthesis of diphthamide-EEF2
- Uptake and actions of bacterial toxins
- Translation
- Post-translational protein modification
- Peptide chain elongation
- Eukaryotic Translation Elongation
- Gamma carboxylation, hypusine formation and arylsulfatase activation
- Uptake and function of diphtheria toxin
|
- 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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EGR1 and TP53 |
early growth response 1 |
tumor protein p53 |
- Interferon Signaling
- Cytokine Signaling in Immune system
- Interferon alpha/beta signaling
|
- 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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EPHA3 and TP53 |
EPH receptor A3 |
tumor protein p53 |
- EPHA-mediated growth cone collapse
- EPH-ephrin mediated repulsion of cells
- Axon guidance
- EPH-Ephrin signaling
|
- 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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ERH and TP53 |
enhancer of rudimentary homolog (Drosophila) |
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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ESR1 and TP53 |
estrogen receptor 1 |
tumor protein p53 |
- Nuclear signaling by ERBB4
- Generic Transcription Pathway
- Nuclear Receptor transcription pathway
- Signaling by ERBB4
|
- 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
|
- Diethylstilbestrol
- Chlorotrianisene
- Conjugated Estrogens
- Etonogestrel
- Desogestrel
- Levonorgestrel
- Progesterone
- Raloxifene
- Toremifene
- Medroxyprogesterone
- Estrone
- Tamoxifen
- Estradiol
- Ethynodiol Diacetate
- Clomifene
- Dienestrol
- Fulvestrant
- Norgestimate
- Ethinyl Estradiol
- Melatonin
- Trilostane
- Naloxone
- Fluoxymesterone
- Estramustine
- Mestranol
- Danazol
- Allylestrenol
- Genistein
- Compound 19
- Compound 18
- Compound 4-D
- 1-[4-(Octahydro-Pyrido[1,2-a]Pyrazin-2-Yl)-Phenyl]-2-Phenyl-1,2,3,4-Tetrahydro-Isoquinolin-6-Ol
- 2-Phenyl-1-[4-(2-Piperidin-1-Yl-Ethoxy)-Phenyl]-1,2,3,4-Tetrahydro-Isoquinolin-6-Ol
- Estriol
- Estropipate
- Quinestrol
- Ospemifene
- 17-METHYL-17-ALPHA-DIHYDROEQUILENIN
- 4-(2-amino-1-methyl-1H-imidazo[4,5-b]pyridin-6-yl)phenol
- [5-HYDROXY-2-(4-HYDROXYPHENYL)-1-BENZOFURAN-7-YL]ACETONITRILE
- 4-[(1S,2S,5S)-5-(HYDROXYMETHYL)-8-METHYL-3-OXABICYCLO[3.3.1]NON-7-EN-2-YL]PHENOL
- 4-[(1S,2S,5S,9R)-5-(HYDROXYMETHYL)-8,9-DIMETHYL-3-OXABICYCLO[3.3.1]NON-7-EN-2-YL]PHENOL
- 4-[(1S,2S,5S)-5-(HYDROXYMETHYL)-6,8,9-TRIMETHYL-3-OXABICYCLO[3.3.1]NON-7-EN-2-YL]PHENOL
- (2R,3R,4S)-3-(4-HYDROXYPHENYL)-4-METHYL-2-[4-(2-PYRROLIDIN-1-YLETHOXY)PHENYL]CHROMAN-6-OL
- (3AS,4R,9BR)-2,2-DIFLUORO-4-(4-HYDROXYPHENYL)-1,2,3,3A,4,9B-HEXAHYDROCYCLOPENTA[C]CHROMEN-8-OL
- (9ALPHA,13BETA,17BETA)-2-[(1Z)-BUT-1-EN-1-YL]ESTRA-1,3,5(10)-TRIENE-3,17-DIOL
- (9BETA,11ALPHA,13ALPHA,14BETA,17ALPHA)-11-(METHOXYMETHYL)ESTRA-1(10),2,4-TRIENE-3,17-DIOL
- 3-CHLORO-2-(4-HYDROXYPHENYL)-2H-INDAZOL-5-OL
- 3-ETHYL-2-(4-HYDROXYPHENYL)-2H-INDAZOL-5-OL
- dimethyl (1R,4S)-5,6-bis(4-hydroxyphenyl)-7-oxabicyclo[2.2.1]hepta-2,5-diene-2,3-dicarboxylate
- (3AS,4R,9BR)-4-(4-HYDROXYPHENYL)-1,2,3,3A,4,9B-HEXAHYDROCYCLOPENTA[C]CHROMEN-8-OL
- N-[(1R)-3-(4-HYDROXYPHENYL)-1-METHYLPROPYL]-2-(2-PHENYL-1H-INDOL-3-YL)ACETAMIDE
- (3AS,4R,9BR)-4-(4-HYDROXYPHENYL)-6-(METHOXYMETHYL)-1,2,3,3A,4,9B-HEXAHYDROCYCLOPENTA[C]CHROMEN-8-OL
- 4-[1-allyl-7-(trifluoromethyl)-1H-indazol-3-yl]benzene-1,3-diol
- 4-(6-HYDROXY-1H-INDAZOL-3-YL)BENZENE-1,3-DIOL
- DIETHYL (1R,2S,3R,4S)-5,6-BIS(4-HYDROXYPHENYL)-7-OXABICYCLO[2.2.1]HEPT-5-ENE-2,3-DICARBOXYLATE
- 2-AMINO-1-METHYL-6-PHENYLIMIDAZO[4,5-B]PYRIDINE
- 4-[(1S,2R,5S)-4,4,8-TRIMETHYL-3-OXABICYCLO[3.3.1]NON-7-EN-2-YL]PHENOL
- (3AS,4R,9BR)-4-(4-HYDROXYPHENYL)-1,2,3,3A,4,9B-HEXAHYDROCYCLOPENTA[C]CHROMEN-9-OL
- RALOXIFENE CORE
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XRCC6 and TP53 |
X-ray repair complementing defective repair in Chinese hamster cells 6 |
tumor protein p53 |
- Cytosolic sensors of pathogen-associated DNA
- HIV Infection
- Processing of DNA ends prior to end rejoining
- Integration of provirus
- Early Phase of HIV Life Cycle
- HIV Life Cycle
- Nonhomologous End-joining (NHEJ)
- STING mediated induction of host immune responses
- Double-Strand Break Repair
- IRF3-mediated induction of type I IFN
- 2-LTR circle formation
- Innate 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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SFN and TP53 |
stratifin |
tumor protein p53 |
- Activation of BAD and translocation to mitochondria
- Programmed Cell Death
- Translocation of GLUT4 to the plasma membrane
- Activation of BH3-only proteins
- Intrinsic Pathway for Apoptosis
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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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GPS1 and TP53 |
G protein pathway suppressor 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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GPS2 and TP53 |
G protein pathway suppressor 2 |
tumor protein p53 |
- Chromatin modifying enzymes
- Chromatin organization
- HDACs deacetylate histones
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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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GPX2 and TP53 |
glutathione peroxidase 2 (gastrointestinal) |
tumor protein p53 |
- Arachidonic acid metabolism
- Synthesis of 5-eicosatetraenoic acids
- Metabolism of lipids and lipoproteins
- Synthesis of 12-eicosatetraenoic acid derivatives
- Synthesis of 15-eicosatetraenoic acid derivatives
- Detoxification of Reactive Oxygen Species
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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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GSK3B and TP53 |
glycogen synthase kinase 3 beta |
tumor protein p53 |
- 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
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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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- 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
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