| CDC25C and TP53 |
cell division cycle 25C |
tumor protein p53 |
- Cyclin A/B1 associated events during G2/M transition
- G2/M DNA damage checkpoint
- G2/M Checkpoints
- Activation of ATR in response to replication stress
- Chk1/Chk2(Cds1) mediated inactivation of Cyclin B:Cdk1 complex
- G2/M Transition
- Cell Cycle Checkpoints
- Mitotic G2-G2/M phases
- Cyclin B2 mediated events
- Polo-like kinase mediated events
- Cell Cycle, Mitotic
|
- 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
|
|
|
|
|
| CDC42 and TP53 |
cell division cycle 42 |
tumor protein p53 |
- Signaling by GPCR
- Costimulation by the CD28 family
- Axon guidance
- DCC mediated attractive signaling
- Signaling by EGFRvIII in Cancer
- VEGFA-VEGFR2 Pathway
- Inactivation of Cdc42 and Rac
- Rho GTPase cycle
- EPHB-mediated forward signaling
- EPH-Ephrin signaling
- G alpha (12/13) signalling events
- Sema4D in semaphorin signaling
- Netrin-1 signaling
- Fcgamma receptor (FCGR) dependent phagocytosis
- Sema4D induced cell migration and growth-cone collapse
- Regulation of actin dynamics for phagocytic cup formation
- Innate Immune System
- EGFR downregulation
- CDO in myogenesis
- Semaphorin interactions
- CD28 co-stimulation
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- Factors involved in megakaryocyte development and platelet production
- Signaling by Overexpressed Wild-Type EGFR in Cancer
- CD28 dependent Vav1 pathway
- Signaling by EGFR
- GPCR downstream signaling
- Myogenesis
- Signaling by VEGF
- Signaling by Rho GTPases
- Signaling by EGFR in Cancer
- GPVI-mediated activation cascade
- Platelet activation, signaling and aggregation
- Signaling by Robo receptor
- Adaptive Immune System
|
- 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
|
|
|
|
|
| CDK2 and TP53 |
cyclin-dependent kinase 2 |
tumor protein p53 |
- CDK-mediated phosphorylation and removal of Cdc6
- G2/M Checkpoints
- Activation of the pre-replicative complex
- Cellular Senescence
- Phosphorylation of proteins involved in G1/S transition by active Cyclin E:Cdk2 complexes
- G2/M Transition
- p53-Dependent G1/S DNA damage checkpoint
- Activation of the pre-replicative complex
- Orc1 removal from chromatin
- Cyclin E associated events during G1/S transition
- CDK-mediated phosphorylation and removal of Cdc6
- p53-Dependent G1 DNA Damage Response
- Cyclin A/B1 associated events during G2/M transition
- G2 Phase
- Activation of ATR in response to replication stress
- G1/S Transition
- Removal of licensing factors from origins
- Mitotic G1-G1/S phases
- Switching of origins to a post-replicative state
- G1/S DNA Damage Checkpoints
- Meiotic recombination
- DNA Damage/Telomere Stress Induced Senescence
- Synthesis of DNA
- DNA Replication Pre-Initiation
- M/G1 Transition
- Regulation of DNA replication
- Senescence-Associated Secretory Phenotype (SASP)
- G0 and Early G1
- S Phase
- Regulation of APC/C activators between G1/S and early anaphase
- Factors involved in megakaryocyte development and platelet production
- Cell Cycle, Mitotic
- APC/C-mediated degradation of cell cycle proteins
- SCF(Skp2)-mediated degradation of p27/p21
- Orc1 removal from chromatin
- Regulation of mitotic cell cycle
- Cell Cycle Checkpoints
- SCF(Skp2)-mediated degradation of p27/p21
- Cyclin A:Cdk2-associated events at S phase entry
- Mitotic G2-G2/M phases
|
- 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
|
- Double Oxidized Cysteine
- 4-[5-(Trans-4-Aminocyclohexylamino)-3-Isopropylpyrazolo[1,5-a]Pyrimidin-7-Ylamino]-N,N-Dimethylbenzenesulfonamide
- Staurosporine
- Indirubin-3\'-Monoxime
- 4-(2,4-Dimethyl-Thiazol-5-Yl)-Pyrimidin-2-Ylamine
- Olomoucine
- 4-[(4-Imidazo[1,2-a]Pyridin-3-Ylpyrimidin-2-Yl)Amino]Benzenesulfonamide
- 2-Amino-6-Chloropyrazine
- 6-O-Cyclohexylmethyl Guanine
- N-[4-(2-Methylimidazo[1,2-a]Pyridin-3-Yl)-2-Pyrimidinyl]Acetamide
- 1-Amino-6-Cyclohex-3-Enylmethyloxypurine
- N-(5-Cyclopropyl-1h-Pyrazol-3-Yl)Benzamide
- Purvalanol
- [4-(2-Amino-4-Methyl-Thiazol-5-Yl)-Pyrimidin-2-Yl]-(3-Nitro-Phenyl)-Amine
- 5-{[(2-Amino-9h-Purin-6-Yl)Oxy]Methyl}-2-Pyrrolidinone
- 4-(2,4-Dimethyl-Thiazol-5-Yl)-Pyrimidin-2-Yl]-(4-Trifluoromethyl-Phenyl)-Amine
- Hymenialdisine
- (5-Chloropyrazolo[1,5-a]Pyrimidin-7-Yl)-(4-Methanesulfonylphenyl)Amine
- 4-(5-Bromo-2-Oxo-2h-Indol-3-Ylazo)-Benzenesulfonamide
- 4-(2,5-Dichloro-Thiophen-3-Yl)-Pyrimidin-2-Ylamine
- 4-[(6-Amino-4-Pyrimidinyl)Amino]Benzenesulfonamide
- 4-[3-Hydroxyanilino]-6,7-Dimethoxyquinazoline
- SU9516
- 3-Pyridin-4-Yl-2,4-Dihydro-Indeno[1,2-.C.]Pyrazole
- Flavopiridol
- (2e,3s)-3-Hydroxy-5\'-[(4-Hydroxypiperidin-1-Yl)Sulfonyl]-3-Methyl-1,3-Dihydro-2,3\'-Biindol-2\'(1\'h)-One
- 1-[(2-Amino-6,9-Dihydro-1h-Purin-6-Yl)Oxy]-3-Methyl-2-Butanol
- 4-((3r,4s,5r)-4-Amino-3,5-Dihydroxy-Hex-1-Ynyl)-5-Fluoro-3-[1-(3-Methoxy-1h-Pyrrol-2-Yl)-Meth-(Z)-Ylidene]-1,3-Dihydro-Indol-2-One
- Lysine Nz-Carboxylic Acid
- [2-Amino-6-(2,6-Difluoro-Benzoyl)-Imidazo[1,2-a]Pyridin-3-Yl]-Phenyl-Methanone
- Alsterpaullone
- N-[4-(2,4-Dimethyl-1,3-Thiazol-5-Yl)Pyrimidin-2-Yl]-N\'-Hydroxyimidoformamide
- N\'-(Pyrrolidino[2,1-B]Isoindolin-4-On-8-Yl)-N-(Pyridin-2-Yl)Urea
- 2-[Trans-(4-Aminocyclohexyl)Amino]-6-(Benzyl-Amino)-9-Cyclopentylpurine
- 4-[4-(4-Methyl-2-Methylamino-Thiazol-5-Yl)-Pyrimidin-2-Ylamino]-Phenol
- 3-[4-(2,4-Dimethyl-Thiazol-5-Yl)-Pyrimidin-2-Ylamino]-Phenol
- PHENYLAMINOIMIDAZO(1,2-ALPHA)PYRIDINE
- OLOMOUCINE II
- TRIAZOLOPYRIMIDINE
- Bosutinib
- 4-[(7-OXO-7H-THIAZOLO[5,4-E]INDOL-8-YLMETHYL)-AMINO]-N-PYRIDIN-2-YL-BENZENESULFONAMIDE
- (13R,15S)-13-METHYL-16-OXA-8,9,12,22,24-PENTAAZAHEXACYCLO[15.6.2.16,9.1,12,15.0,2,7.0,21,25]HEPTACOSA-1(24),2,4,6,17(25),18,20-HEPTAENE-23,26-DIONE
- N-(3-CYCLOPROPYL-1H-PYRAZOL-5-YL)-2-(2-NAPHTHYL)ACETAMIDE
- 2-ANILINO-6-CYCLOHEXYLMETHOXYPURINE
- 1-(5-OXO-2,3,5,9B-TETRAHYDRO-1H-PYRROLO[2,1-A]ISOINDOL-9-YL)-3-(5-PYRROLIDIN-2-YL-1H-PYRAZOL-3-YL)-UREA
- (5-phenyl-7-(pyridin-3-ylmethylamino)pyrazolo[1,5-a]pyrimidin-3-yl)methanol
- 2-(3,4-DIHYDROXYPHENYL)-8-(1,1-DIOXIDOISOTHIAZOLIDIN-2-YL)-3-HYDROXY-6-METHYL-4H-CHROMEN-4-ONE
- (2R)-1-(DIMETHYLAMINO)-3-{4-[(6-{[2-FLUORO-5-(TRIFLUOROMETHYL)PHENYL]AMINO}PYRIMIDIN-4-YL)AMINO]PHENOXY}PROPAN-2-OL
- 5-(2,3-dichlorophenyl)-N-(pyridin-4-ylmethyl)-3-thiocyanatopyrazolo[1,5-a]pyrimidin-7-amine
- O6-CYCLOHEXYLMETHOXY-2-(4\'-SULPHAMOYLANILINO) PURINE
- (2S)-N-[(3Z)-5-CYCLOPROPYL-3H-PYRAZOL-3-YLIDENE]-2-[4-(2-OXOIMIDAZOLIDIN-1-YL)PHENYL]PROPANAMIDE
- 5-[(2-AMINOETHYL)AMINO]-6-FLUORO-3-(1H-PYRROL-2-YL)BENZO[CD]INDOL-2(1H)-ONE
- N-cyclopropyl-4-pyrazolo[1,5-b]pyridazin-3-ylpyrimidin-2-amine
- 3-((3-bromo-5-o-tolylpyrazolo[1,5-a]pyrimidin-7-ylamino)methyl)pyridine 1-oxide
- 6-CYCLOHEXYLMETHOXY-2-(3\'-CHLOROANILINO) PURINE
- 3-bromo-5-phenyl-N-(pyridin-4-ylmethyl)pyrazolo[1,5-a]pyrimidin-7-amine
- N-[5-(1,1-DIOXIDOISOTHIAZOLIDIN-2-YL)-1H-INDAZOL-3-YL]-2-(4-PIPERIDIN-1-YLPHENYL)ACETAMIDE
- (3R)-3-(aminomethyl)-9-methoxy-1,2,3,4-tetrahydro-5H-[1]benzothieno[3,2-e][1,4]diazepin-5-one
- 5-[5,6-BIS(METHYLOXY)-1H-BENZIMIDAZOL-1-YL]-3-{[1-(2-CHLOROPHENYL)ETHYL]OXY}-2-THIOPHENECARBOXAMIDE
- (2Z)-5\'-BROMO-2,3\'-BIINDOLE-2\',3(1H,1\'H)-DIONE AMMONIATE
- (2S)-1-{4-[(4-ANILINO-5-BROMOPYRIMIDIN-2-YL)AMINO]PHENOXY}-3-(DIMETHYLAMINO)PROPAN-2-OL
- (2R)-1-{4-[(4-ANILINO-5-BROMOPYRIMIDIN-2-YL)AMINO]PHENOXY}-3-(DIMETHYLAMINO)PROPAN-2-OL
- 2-IMINO-5-(1-PYRIDIN-2-YL-METH-(E)-YLIDENE)-1,3-THIAZOLIDIN-4-ONE
- 4-{5-[(Z)-(2,4-DIOXO-1,3-THIAZOLIDIN-5-YLIDENE)METHYL]FURAN-2-YL}BENZENESULFONAMIDE
- 4-{5-[(Z)-(2-IMINO-4-OXO-1,3-THIAZOLIDIN-5-YLIDENE)METHYL]-2-FURYL}-N-METHYLBENZENESULFONAMIDE
- 4-{5-[(Z)-(2-IMINO-4-OXO-1,3-THIAZOLIDIN-5-YLIDENE)METHYL]FURAN-2-YL}BENZENESULFONAMIDE
- 4-{5-[(Z)-(2-IMINO-4-OXO-1,3-THIAZOLIDIN-5-YLIDENE)METHYL]FURAN-2-YL}-2-(TRIFLUOROMETHYL)BENZENESULFONAMIDE
- 4-{5-[(Z)-(2-IMINO-4-OXO-1,3-THIAZOLIDIN-5-YLIDENE)METHYL]FURAN-2-YL}BENZOIC ACID
- 4-{5-[(1Z)-1-(2-IMINO-4-OXO-1,3-THIAZOLIDIN-5-YLIDENE)ETHYL]-2-FURYL}BENZENESULFONAMIDE
- N-[4-(2,4-DIMETHYL-THIAZOL-5-YL)-PYRIMIDIN-2-YL]-N\',N\'-DIMETHYL-BENZENE-1,4-DIAMINE
- (5Z)-5-(3-BROMOCYCLOHEXA-2,5-DIEN-1-YLIDENE)-N-(PYRIDIN-4-YLMETHYL)-1,5-DIHYDROPYRAZOLO[1,5-A]PYRIMIDIN-7-AMINE
- 6-(3,4-DIHYDROXYBENZYL)-3-ETHYL-1-(2,4,6-TRICHLOROPHENYL)-1H-PYRAZOLO[3,4-D]PYRIMIDIN-4(5H)-ONE
- 6-(3-AMINOPHENYL)-N-(TERT-BUTYL)-2-(TRIFLUOROMETHYL)QUINAZOLIN-4-AMINE
- 2-(4-(AMINOMETHYL)PIPERIDIN-1-YL)-N-(3_CYCLOHEXYL-4-OXO-2,4-DIHYDROINDENO[1,2-C]PYRAZOL-5-YL)ACETAMIDE
- 1-(3-(2,4-DIMETHYLTHIAZOL-5-YL)-4-OXO-2,4-DIHYDROINDENO[1,2-C]PYRAZOL-5-YL)-3-(4-METHYLPIPERAZIN-1-YL)UREA
- 4-{[5-(CYCLOHEXYLMETHOXY)[1,2,4]TRIAZOLO[1,5-A]PYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE
- 4-{[5-(CYCLOHEXYLAMINO)[1,2,4]TRIAZOLO[1,5-A]PYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE
- 4-({5-[(4-AMINOCYCLOHEXYL)AMINO][1,2,4]TRIAZOLO[1,5-A]PYRIMIDIN-7-YL}AMINO)BENZENESULFONAMIDE
- 4-{[5-(CYCLOHEXYLOXY)[1,2,4]TRIAZOLO[1,5-A]PYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE
- 4-[(E)-(3,5-DIAMINO-1H-PYRAZOL-4-YL)DIAZENYL]PHENOL
- (2R)-1-[4-({4-[(2,5-DICHLOROPHENYL)AMINO]PYRIMIDIN-2-YL}AMINO)PHENOXY]-3-(DIMETHYLAMINO)PROPAN-2-OL
- (2S)-1-[4-({6-[(2,6-DIFLUOROPHENYL)AMINO]PYRIMIDIN-4-YL}AMINO)PHENOXY]-3-(DIMETHYLAMINO)PROPAN-2-OL
- (2S)-1-[4-({4-[(2,5-DICHLOROPHENYL)AMINO]PYRIMIDIN-2-YL}AMINO)PHENOXY]-3-(DIMETHYLAMINO)PROPAN-2-OL
- (2R)-1-[4-({6-[(2,6-DIFLUOROPHENYL)AMINO]PYRIMIDIN-4-YL}AMINO)PHENOXY]-3-(DIMETHYLAMINO)PROPAN-2-OL
- N-(2-METHOXYETHYL)-4-({4-[2-METHYL-1-(1-METHYLETHYL)-1H-IMIDAZOL-5-YL]PYRIMIDIN-2-YL}AMINO)BENZENESULFONAMIDE
- 4-{[4-(1-CYCLOPROPYL-2-METHYL-1H-IMIDAZOL-5-YL)PYRIMIDIN-2-YL]AMINO}-N-METHYLBENZENESULFONAMIDE
- 1-(3,5-DICHLOROPHENYL)-5-METHYL-1H-1,2,4-TRIAZOLE-3-CARBOXYLIC ACID
- 1-(DIMETHYLAMINO)-3-(4-{{4-(2-METHYLIMIDAZO[1,2-A]PYRIDIN-3-YL)PYRIMIDIN-2-YL]AMINO}PHENOXY)PROPAN-2-OL
- N-(4-{[(3S)-3-(dimethylamino)pyrrolidin-1-yl]carbonyl}phenyl)-5-fluoro-4-[2-methyl-1-(1-methylethyl)-1H-imidazol-5-yl]pyrimidin-2-amine
- 2-{4-[4-({4-[2-methyl-1-(1-methylethyl)-1H-imidazol-5-yl]pyrimidin-2-yl}amino)phenyl]piperazin-1-yl}-2-oxoethanol
- N-[3-(1H-BENZIMIDAZOL-2-YL)-1H-PYRAZOL-4-YL]BENZAMIDE
- (4-AMINO-2-{[1-(METHYLSULFONYL)PIPERIDIN-4-YL]AMINO}PYRIMIDIN-5-YL)(2,3-DIFLUORO-6-METHOXYPHENYL)METHANONE
- N-METHYL-4-{[(2-OXO-1,2-DIHYDRO-3H-INDOL-3-YLIDENE)METHYL]AMINO}BENZENESULFONAMIDE
- N-METHYL-{4-[2-(7-OXO-6,7-DIHYDRO-8H-[1,3]THIAZOLO[5,4-E]INDOL-8-YLIDENE)HYDRAZINO]PHENYL}METHANESULFONAMIDE
- 3-{[(2,2-DIOXIDO-1,3-DIHYDRO-2-BENZOTHIEN-5-YL)AMINO]METHYLENE}-5-(1,3-OXAZOL-5-YL)-1,3-DIHYDRO-2H-INDOL-2-ONE
- 4-{[(2-OXO-1,2-DIHYDRO-3H-INDOL-3-YLIDENE)METHYL]AMINO}-N-(1,3-THIAZOL-2-YL)BENZENESULFONAMIDE
- 3-{[4-([AMINO(IMINO)METHYL]AMINOSULFONYL)ANILINO]METHYLENE}-2-OXO-2,3-DIHYDRO-1H-INDOLE
- 5-hydroxynaphthalene-1-sulfonamide
- N-(4-sulfamoylphenyl)-1H-indazole-3-carboxamide
- 4-[(6-chloropyrazin-2-yl)amino]benzenesulfonamide
- N-phenyl-1H-pyrazole-3-carboxamide
- 4-(acetylamino)-N-(4-fluorophenyl)-1H-pyrazole-3-carboxamide
- (4E)-N-(4-fluorophenyl)-4-[(phenylcarbonyl)imino]-4H-pyrazole-3-carboxamide
- {[(2,6-difluorophenyl)carbonyl]amino}-N-(4-fluorophenyl)-1H-pyrazole-3-carboxamide
- 5-chloro-7-[(1-methylethyl)amino]pyrazolo[1,5-a]pyrimidine-3-carbonitrile
- 5-[(4-AMINOCYCLOHEXYL)AMINO]-7-(PROPAN-2-YLAMINO)PYRAZOLO[1,5-A]PYRIMIDINE-3-CARBONITRILE
- 4-{[(2,6-difluorophenyl)carbonyl]amino}-N-[(3S)-piperidin-3-yl]-1H-pyrazole-3-carboxamide
- 4-{[(2,6-dichlorophenyl)carbonyl]amino}-N-piperidin-4-yl-1H-pyrazole-3-carboxamide
- 4-(4-methoxy-1H-pyrrolo[2,3-b]pyridin-3-yl)pyrimidin-2-amine
- 4-(4-propoxy-1H-pyrrolo[2,3-b]pyridin-3-yl)pyrimidin-2-amine
- HYDROXY(OXO)(3-{[(2Z)-4-[3-(1H-1,2,4-TRIAZOL-1-YLMETHYL)PHENYL]PYRIMIDIN-2(5H)-YLIDENE]AMINO}PHENYL)AMMONIUM
- 4-METHYL-5-{(2E)-2-[(4-MORPHOLIN-4-YLPHENYL)IMINO]-2,5-DIHYDROPYRIMIDIN-4-YL}-1,3-THIAZOL-2-AMINE
- 6-CYCLOHEXYLMETHYLOXY-2-(4\'-HYDROXYANILINO)PURINE
- 4-(6-CYCLOHEXYLMETHOXY-9H-PURIN-2-YLAMINO)--BENZAMIDE
- 6-(CYCLOHEXYLMETHOXY)-8-ISOPROPYL-9H-PURIN-2-AMINE
- 3-(6-CYCLOHEXYLMETHOXY-9H-PURIN-2-YLAMINO)-BENZENESULFONAMIDE
- (2R)-2-{[4-(benzylamino)-8-(1-methylethyl)pyrazolo[1,5-a][1,3,5]triazin-2-yl]amino}butan-1-ol
- 3-({2-[(4-{[6-(CYCLOHEXYLMETHOXY)-9H-PURIN-2-YL]AMINO}PHENYL)SULFONYL]ETHYL}AMINO)PROPAN-1-OL
- 6-CYCLOHEXYLMETHYLOXY-5-NITROSO-PYRIMIDINE-2,4-DIAMINE
- 1-methyl-8-(phenylamino)-4,5-dihydro-1H-pyrazolo[4,3-h]quinazoline-3-carboxylic acid
- 6-BROMO-13-THIA-2,4,8,12,19-PENTAAZATRICYCLO[12.3.1.1~3,7~]NONADECA-1(18),3(19),4,6,14,16-HEXAENE 13,13-DIOXIDE
- (2R)-2-({9-(1-methylethyl)-6-[(4-pyridin-2-ylbenzyl)amino]-9H-purin-2-yl}amino)butan-1-ol
- 1-[4-(AMINOSULFONYL)PHENYL]-1,6-DIHYDROPYRAZOLO[3,4-E]INDAZOLE-3-CARBOXAMIDE
- 5-(2,3-dichlorophenyl)-N-(pyridin-4-ylmethyl)pyrazolo[1,5-a]pyrimidin-7-amine
- 6-(2-fluorophenyl)-N-(pyridin-3-ylmethyl)imidazo[1,2-a]pyrazin-8-amine
- 3-methyl-N-(pyridin-4-ylmethyl)imidazo[1,2-a]pyrazin-8-amine
- 5-(2-fluorophenyl)-N-(pyridin-4-ylmethyl)pyrazolo[1,5-a]pyrimidin-7-amine
- 3-bromo-5-phenyl-N-(pyridin-3-ylmethyl)pyrazolo[1,5-a]pyrimidin-7-amine
- 3-bromo-5-phenyl-N-(pyrimidin-5-ylmethyl)pyrazolo[1,5-a]pyridin-7-amine
- 3-bromo-6-phenyl-N-(pyrimidin-5-ylmethyl)imidazo[1,2-a]pyridin-8-amine
- N-((2-aminopyrimidin-5-yl)methyl)-5-(2,6-difluorophenyl)-3-ethylpyrazolo[1,5-a]pyrimidin-7-amine
- 3-cyclopropyl-5-phenyl-N-(pyridin-3-ylmethyl)pyrazolo[1,5-a]pyrimidin-7-amine
- 4-{[4-AMINO-6-(CYCLOHEXYLMETHOXY)-5-NITROSOPYRIMIDIN-2-YL]AMINO}BENZAMIDE
- 4-[(5-ISOPROPYL-1,3-THIAZOL-2-YL)AMINO]BENZENESULFONAMIDE
- N-(5-ISOPROPYL-THIAZOL-2-YL)-2-PYRIDIN-3-YL-ACETAMIDE
- 9-amino-5-(2-aminopyrimidin-4-yl)pyrido[3\',2\':4,5]pyrrolo[1,2-c]pyrimidin-4-ol
- N-(3-METHYLBUT-2-EN-1-YL)-9H-PURIN-6-AMINE
|
|
|
|
| CDK5 and TP53 |
cyclin-dependent kinase 5 |
tumor protein p53 |
- Signaling by GPCR
- Axon guidance
- Semaphorin interactions
- Opioid Signalling
- DARPP-32 events
- CRMPs in Sema3A signaling
- Factors involved in megakaryocyte development and platelet production
|
- 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
|
- Indirubin-3\'-Monoxime
- Olomoucine
- Hymenialdisine
- SU9516
- Flavopiridol
- Alsterpaullone
- 6-PHENYL[5H]PYRROLO[2,3-B]PYRAZINE
|
|
|
|
| CDK7 and TP53 |
cyclin-dependent kinase 7 |
tumor protein p53 |
- RNA Polymerase II Promoter Escape
- Formation of HIV-1 elongation complex containing HIV-1 Tat
- RNA Polymerase II Transcription Pre-Initiation And Promoter Opening
- RNA Polymerase I Chain Elongation
- RNA Polymerase I, RNA Polymerase III, and Mitochondrial Transcription
- Tat-mediated elongation of the HIV-1 transcript
- Cyclin E associated events during G1/S transition
- Formation of transcription-coupled NER (TC-NER) repair complex
- Dual incision reaction in TC-NER
- NoRC negatively regulates rRNA expression
- G1/S Transition
- Mitotic G1-G1/S phases
- S Phase
- 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
- Cyclin A:Cdk2-associated events at S phase entry
- Mitotic G2-G2/M phases
- Transcription of the HIV genome
- Nucleotide Excision Repair
- RNA Polymerase II Transcription
- RNA Polymerase I Transcription Initiation
- HIV Infection
- RNA Polymerase I Promoter Clearance
- Formation of the Early Elongation Complex
- G2/M Transition
- RNA Pol II CTD phosphorylation and interaction with CE
- RNA Polymerase II Pre-transcription Events
- HIV Transcription Initiation
- HIV Life Cycle
- RNA Pol II CTD phosphorylation and interaction with CE
- Cyclin A/B1 associated events during G2/M transition
- RNA Polymerase II HIV Promoter Escape
- HIV Transcription Elongation
- Dual incision reaction in GG-NER
- RNA Polymerase I Transcription
- mRNA Capping
- RNA Polymerase I Promoter Escape
- RNA Polymerase I Transcription Termination
- G1 Phase
- Epigenetic regulation of gene expression
- Negative epigenetic regulation of rRNA expression
- Cell Cycle, Mitotic
- Cyclin D associated events in G1
- 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
- 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
|
- Phosphonothreonine
- Flavopiridol
|
|
|
|
| CDK8 and TP53 |
cyclin-dependent kinase 8 |
tumor protein p53 |
- Loss of Function of TGFBR2 in Cancer
- PPARA activates gene expression
- Signaling by NOTCH1 HD Domain Mutants in Cancer
- Metabolism of lipids and lipoproteins
- Signaling by NOTCH1 HD+PEST Domain Mutants in Cancer
- SMAD2/3 MH2 Domain Mutants in Cancer
- TGFBR1 LBD Mutants in Cancer
- SMAD2/SMAD3:SMAD4 heterotrimer regulates transcription
- Transcriptional activity of SMAD2/SMAD3:SMAD4 heterotrimer
- Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant
- Generic Transcription Pathway
- Signaling by NOTCH1
- Transcriptional regulation of white adipocyte differentiation
- Signaling by NOTCH1 in Cancer
- Constitutive Signaling by NOTCH1 HD+PEST Domain Mutants
- FBXW7 Mutants and NOTCH1 in Cancer
- TGFBR2 MSI Frameshift Mutants in Cancer
- Fatty acid, triacylglycerol, and ketone body metabolism
- SMAD2/3 Phosphorylation Motif Mutants in Cancer
- Loss of Function of SMAD2/3 in Cancer
- Signaling by NOTCH
- TGFBR2 Kinase Domain Mutants in Cancer
- Loss of Function of SMAD4 in Cancer
- TGFBR1 KD Mutants in Cancer
- Loss of Function of TGFBR1 in Cancer
- NOTCH1 Intracellular Domain Regulates Transcription
- Signaling by TGF-beta Receptor Complex in Cancer
- Signaling by TGF-beta Receptor Complex
- Signaling by NOTCH1 PEST Domain Mutants in Cancer
- Regulation of lipid metabolism by Peroxisome proliferator-activated receptor alpha (PPARalpha)
- Constitutive Signaling by NOTCH1 PEST Domain Mutants
- 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
|
|
|
|
|
| CDK9 and TP53 |
cyclin-dependent kinase 9 |
tumor protein p53 |
- Loss of Function of TGFBR2 in Cancer
- Formation of HIV-1 elongation complex containing HIV-1 Tat
- RNA Polymerase II Transcription
- HIV Infection
- SMAD2/3 MH2 Domain Mutants in Cancer
- Tat-mediated elongation of the HIV-1 transcript
- Tat-mediated HIV elongation arrest and recovery
- TGFBR1 LBD Mutants in Cancer
- RNA Polymerase II Pre-transcription Events
- SMAD2/SMAD3:SMAD4 heterotrimer regulates transcription
- Transcriptional activity of SMAD2/SMAD3:SMAD4 heterotrimer
- HIV elongation arrest and recovery
- HIV Life Cycle
- Generic Transcription Pathway
- HIV Transcription Elongation
- TGFBR2 MSI Frameshift Mutants in Cancer
- SMAD2/3 Phosphorylation Motif Mutants in Cancer
- Loss of Function of SMAD2/3 in Cancer
- TGFBR2 Kinase Domain Mutants in Cancer
- Host Interactions of HIV factors
- Loss of Function of SMAD4 in Cancer
- Interactions of Tat with host cellular proteins
- TGFBR1 KD Mutants in Cancer
- Pausing and recovery of Tat-mediated HIV elongation
- Loss of Function of TGFBR1 in Cancer
- Late Phase of HIV Life Cycle
- Formation of RNA Pol II elongation complex
- Signaling by TGF-beta Receptor Complex
- Signaling by TGF-beta Receptor Complex in Cancer
- Pausing and recovery of HIV elongation
- Formation of HIV elongation complex in the absence of HIV Tat
- Transcription of the HIV genome
- SMAD4 MH2 Domain Mutants in Cancer
- 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
|
|
|
|
|
| CDKN2C and TP53 |
cyclin-dependent kinase inhibitor 2C (p18, inhibits CDK4) |
tumor protein p53 |
- Cyclin D associated events in G1
- Oxidative Stress Induced Senescence
- G1 Phase
- Cellular Senescence
- Senescence-Associated Secretory Phenotype (SASP)
- Oncogene Induced Senescence
- Mitotic G1-G1/S phases
- Cell Cycle, Mitotic
|
- 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
|
|
|
|
|
| RCC1 and TP53 |
regulator of chromosome condensation 1 |
tumor protein p53 |
- HIV Life Cycle
- Rev-mediated nuclear export of HIV RNA
- HIV Infection
- Nuclear import of Rev protein
- Rev-mediated nuclear export of HIV RNA
- Host Interactions of HIV factors
- Interactions of Rev with host cellular proteins
- Late Phase of HIV Life Cycle
|
- 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
|
|
|
|
|
| CHD3 and TP53 |
chromodomain helicase DNA binding protein 3 |
tumor protein p53 |
- Chromatin modifying enzymes
- Chromatin organization
- HDACs deacetylate histones
- RNA Polymerase I, RNA Polymerase III, and Mitochondrial Transcription
- RNA Polymerase I Transcription
- RNA Polymerase I Transcription Initiation
- RNA Polymerase I Promoter Clearance
|
- 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
|
|
|
|
|
| CHEK1 and TP53 |
checkpoint kinase 1 |
tumor protein p53 |
- Signaling by SCF-KIT
- Ubiquitin Mediated Degradation of Phosphorylated Cdc25A
- G2/M DNA damage checkpoint
- G2/M Checkpoints
- Activation of ATR in response to replication stress
- Chk1/Chk2(Cds1) mediated inactivation of Cyclin B:Cdk1 complex
- p53-Independent DNA Damage Response
- Cell Cycle Checkpoints
- p53-Independent G1/S DNA damage checkpoint
- G1/S DNA Damage 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
|
|
|
|
|
| PLK3 and TP53 |
polo-like kinase 3 |
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
|
|
|
|
|
| KLF6 and TP53 |
Kruppel-like factor 6 |
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
|
|
|
|
|
| CR2 and TP53 |
complement component (3d/Epstein Barr virus) receptor 2 |
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
|
|
|
|
|
| MAPK14 and TP53 |
mitogen-activated protein kinase 14 |
tumor protein p53 |
- ADP signalling through P2Y purinoceptor 1
- Cellular Senescence
- Toll Like Receptor TLR1:TLR2 Cascade
- Toll Like Receptor 5 (TLR5) Cascade
- NOD1/2 Signaling Pathway
- p38MAPK events
- MyD88 dependent cascade initiated on endosome
- Toll Like Receptor 9 (TLR9) Cascade
- ERK/MAPK targets
- activated TAK1 mediates p38 MAPK activation
- Regulation of mRNA stability by proteins that bind AU-rich elements
- CDO in myogenesis
- TRIF-mediated TLR3/TLR4 signaling
- Toll Like Receptor 2 (TLR2) Cascade
- Platelet homeostasis
- Activation of PPARGC1A (PGC-1alpha) by phosphorylation
- Myogenesis
- Signaling by VEGF
- Platelet sensitization by LDL
- Signalling to RAS
- Toll Like Receptor 4 (TLR4) Cascade
- Toll Like Receptor 3 (TLR3) Cascade
- Platelet activation, signaling and aggregation
- Signalling to ERKs
- Organelle biogenesis and maintenance
- Toll Like Receptor 7/8 (TLR7/8) Cascade
- Signal amplification
- VEGFA-VEGFR2 Pathway
- Toll Like Receptor TLR6:TLR2 Cascade
- Activated TLR4 signalling
- Activation of the AP-1 family of transcription factors
- MyD88 cascade initiated on plasma membrane
- 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
- MAP kinase activation in TLR cascade
- NGF signalling via TRKA from the plasma membrane
- MyD88-independent cascade
- Mitochondrial biogenesis
- Toll-Like Receptors Cascades
- Toll Like Receptor 10 (TLR10) Cascade
- DSCAM interactions
- KSRP destabilizes mRNA
- Oxidative Stress Induced Senescence
- Nucleotide-binding domain, leucine rich repeat containing receptor (NLR) signaling pathways
- ERK/MAPK targets
- MAPK targets/ Nuclear events mediated by MAP kinases
- Nuclear Events (kinase and transcription factor activation)
|
- 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
|
- 4-[5-[2-(1-Phenyl-Ethylamino)-Pyrimidin-4-Yl]-1-Methyl-4-(3-Trifluoromethylphenyl)-1h-Imidazol-2-Yl]-Piperidine
- N-[(3z)-5-Tert-Butyl-2-Phenyl-1,2-Dihydro-3h-Pyrazol-3-Ylidene]-N\'-(4-Chlorophenyl)Urea
- 1-(2,6-Dichlorophenyl)-5-(2,4-Difluorophenyl)-7-Piperidin-4-Yl-3,4-Dihydroquinolin-2(1h)-One
- Inhibitor of P38 Kinase
- 6((S)-3-Benzylpiperazin-1-Yl)-3-(Naphthalen-2-Yl)-4-(Pyridin-4-Yl)Pyrazine
- 3-(4-Fluorophenyl)-1-Hydroxy-2-(Pyridin-4-Yl)-1h-Pyrrolo[3,2-B]Pyridine
- 1-(5-Tert-Butyl-2-Methyl-2h-Pyrazol-3-Yl)-3-(4-Chloro-Phenyl)-Urea
- 3-(Benzyloxy)Pyridin-2-Amine
- 1-(2,6-Dichlorophenyl)-5-(2,4-Difluorophenyl)-7-Piperazin-1-Yl-3,4-Dihydroquinazolin-2(1h)-One
- 4-[3-Methylsulfanylanilino]-6,7-Dimethoxyquinazoline
- 1-(5-Tert-Butyl-2-P-Tolyl-2h-Pyrazol-3-Yl)-3-[4-(2-Morpholin-4-Yl-Ethoxy)-Naphthalen-1-Yl]-Urea
- 2-Chlorophenol
- 4-(Fluorophenyl)-1-Cyclopropylmethyl-5-(2-Amino-4-Pyrimidinyl)Imidazole
- SB220025
- 4-(2-HYDROXYBENZYLAMINO)-N-(3-(4-FLUOROPHENOXY)PHENYL)PIPERIDINE-1-SULFONAMIDE
- Triazolopyridine
- 1-[1-(3-aminophenyl)-3-tert-butyl-1H-pyrazol-5-yl]-3-naphthalen-1-ylurea
- N-ethyl-4-{[5-(methoxycarbamoyl)-2-methylphenyl]amino}-5-methylpyrrolo[2,1-f][1,2,4]triazine-6-carboxamide
- N-[2-methyl-5-(methylcarbamoyl)phenyl]-2-{[(1R)-1-methylpropyl]amino}-1,3-thiazole-5-carboxamide
- 5-(2,6-dichlorophenyl)-2-[(2,4-difluorophenyl)sulfanyl]-6H-pyrimido[1,6-b]pyridazin-6-one
- N-cyclopropyl-4-methyl-3-[1-(2-methylphenyl)phthalazin-6-yl]benzamide
- 4-PHENOXY-N-(PYRIDIN-2-YLMETHYL)BENZAMIDE
- 4-[5-(3-IODO-PHENYL)-2-(4-METHANESULFINYL-PHENYL)-1H-IMIDAZOL-4-YL]-PYRIDINE
- N-cyclopropyl-2\',6-dimethyl-4\'-(5-methyl-1,3,4-oxadiazol-2-yl)biphenyl-3-carboxamide
- 4-[3-(4-FLUOROPHENYL)-1H-PYRAZOL-4-YL]PYRIDINE
- 4-{4-[(5-hydroxy-2-methylphenyl)amino]quinolin-7-yl}-1,3-thiazole-2-carbaldehyde
- N-(3-cyanophenyl)-2\'-methyl-5\'-(5-methyl-1,3,4-oxadiazol-2-yl)-4-biphenylcarboxamide
- N-(cyclopropylmethyl)-2\'-methyl-5\'-(5-methyl-1,3,4-oxadiazol-2-yl)biphenyl-4-carboxamide
- N~3~-cyclopropyl-N~4~\'-(cyclopropylmethyl)-6-methylbiphenyl-3,4\'-dicarboxamide
- 3-{3-bromo-4-[(2,4-difluorobenzyl)oxy]-6-methyl-2-oxopyridin-1(2H)-yl}-N,4-dimethylbenzamide
- 2-fluoro-4-[4-(4-fluorophenyl)-1H-pyrazol-3-yl]pyridine
- 2-{4-[5-(4-chlorophenyl)-4-pyrimidin-4-yl-1H-pyrazol-3-yl]piperidin-1-yl}-2-oxoethanol
- N-(3-TERT-BUTYL-1H-PYRAZOL-5-YL)-N\'-{4-CHLORO-3-[(PYRIDIN-3-YLOXY)METHYL]PHENYL}UREA
- N-[4-CHLORO-3-(PYRIDIN-3-YLOXYMETHYL)-PHENYL]-3-FLUORO-
- 3-FLUORO-5-MORPHOLIN-4-YL-N-[3-(2-PYRIDIN-4-YLETHYL)-1H-INDOL-5-YL]BENZAMIDE
- 3-FLUORO-N-1H-INDOL-5-YL-5-MORPHOLIN-4-YLBENZAMIDE
- 3-(1-NAPHTHYLMETHOXY)PYRIDIN-2-AMINE
- 3-(2-CHLOROPHENYL)-1-(2-{[(1S)-2-HYDROXY-1,2-DIMETHYLPROPYL]AMINO}PYRIMIDIN-4-YL)-1-(4-METHOXYPHENYL)UREA
- 8-(2-CHLOROPHENYLAMINO)-2-(2,6-DIFLUOROPHENYLAMINO)-9-ETHYL-9H-PURINE-1,7-DIIUM
- 2-(2,6-DIFLUOROPHENOXY)-N-(2-FLUOROPHENYL)-9-ISOPROPYL-9H-PURIN-8-AMINE
- N,4-dimethyl-3-[(1-phenyl-1H-pyrazolo[3,4-d]pyrimidin-4-yl)amino]benzamide
- N-cyclopropyl-3-{[1-(2,4-difluorophenyl)-7-methyl-6-oxo-6,7-dihydro-1H-pyrazolo[3,4-b]pyridin-4-yl]amino}-4-methylbenzamide
- N-cyclopropyl-4-methyl-3-{2-[(2-morpholin-4-ylethyl)amino]quinazolin-6-yl}benzamide
- 6-[4-(2-fluorophenyl)-1,3-oxazol-5-yl]-N-(1-methylethyl)-1,3-benzothiazol-2-amine
- 2-(ETHOXYMETHYL)-4-(4-FLUOROPHENYL)-3-[2-(2-HYDROXYPHENOXY)PYRIMIDIN-4-YL]ISOXAZOL-5(2H)-ONE
- [5-AMINO-1-(4-FLUOROPHENYL)-1H-PYRAZOL-4-YL][3-(PIPERIDIN-4-YLOXY)PHENYL]METHANONE
- [5-AMINO-1-(4-FLUOROPHENYL)-1H-PYRAZOL-4-YL](3-{[(2R)-2,3-DIHYDROXYPROPYL]OXY}PHENYL)METHANONE
- 4-[5-(4-FLUORO-PHENYL)-2-(4-METHANESULFINYL-PHENYL)-3H-IMIDAZOL-4-YL]-PYRIDINE
- 4-(4-FLUOROPHENYL)-1-CYCLOROPROPYLMETHYL-5-(4-PYRIDYL)-IMIDAZOLE
- 3-FLUORO-5-MORPHOLIN-4-YL-N-[1-(2-PYRIDIN-4-YLETHYL)-1H-INDOL-6-YL]BENZAMIDE
|
|
|
|
| CSNK1A1 and TP53 |
casein kinase 1, alpha 1 |
tumor protein p53 |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- APC truncation mutants have impaired AXIN binding
- T41 mutants of beta-catenin aren't phosphorylated
- TCF7L2 mutants don't bind CTBP
- truncated APC mutants destabilize the destruction complex
- Signaling by Wnt
- APC truncation mutants are not K63 polyubiquitinated
- disassembly of the destruction complex and recruitment of AXIN to the membrane
- S37 mutants of beta-catenin aren't phosphorylated
- Degradation of beta-catenin by the destruction complex
- RNF mutants show enhanced WNT signaling and proliferation
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- S33 mutants of beta-catenin aren't phosphorylated
- Hedgehog 'on' state
- XAV939 inhibits tankyrase, stabilizing AXIN
- Beta-catenin phosphorylation cascade
- truncations of AMER1 destabilize the destruction complex
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- AXIN missense mutants destabilize the destruction complex
- S45 mutants of beta-catenin aren't phosphorylated
- deletions in the AMER1 gene destabilize the destruction complex
- TCF dependent signaling in response to WNT
- AMER1 mutants destabilize the destruction complex
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Signaling by Hedgehog
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Degradation of GLI2 by the proteasome
- Activation of SMO
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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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| CSNK1D and TP53 |
casein kinase 1, delta |
tumor protein p53 |
- Organelle biogenesis and maintenance
- Assembly of the primary cilium
- G2/M Transition
- Anchoring of the basal body to the plasma membrane
- Regulation of PLK1 Activity at G2/M Transition
- Cell Cycle, Mitotic
- Loss of proteins required for interphase microtubule organization from the centrosome
- Loss of Nlp from mitotic centrosomes
- Centrosome maturation
- Mitotic G2-G2/M phases
- Recruitment of mitotic centrosome proteins and complexes
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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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| CSNK2A1 and TP53 |
casein kinase 2, alpha 1 polypeptide |
tumor protein p53 |
- Mitotic Prometaphase
- Signal transduction by L1
- Axon guidance
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- L1CAM interactions
- Signaling by Wnt
- Cell Cycle, Mitotic
- M Phase
- WNT mediated activation of DVL
- TCF dependent signaling in response to WNT
- RNF mutants show enhanced WNT signaling and proliferation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Signaling by WNT in cancer
- Condensation of Prometaphase Chromosomes
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- 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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- (5-Oxo-5,6-Dihydro-Indolo[1,2-a]Quinazolin-7-Yl)-Acetic Acid
- 1,8-Di-Hydroxy-4-Nitro-Xanthen-9-One
- Resveratrol
- 1,8-Di-Hydroxy-4-Nitro-Anthraquinone
- Benzamidine
- 5,8-Di-Amino-1,4-Dihydroxy-Anthraquinone
- Phosphoaminophosphonic Acid-Adenylate Ester
- Tetrabromo-2-Benzotriazole
- DIMETHYL-(4,5,6,7-TETRABROMO-1H-BENZOIMIDAZOL-2-YL)-AMINE
- S-METHYL-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- N1,N2-ETHYLENE-2-METHYLAMINO-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- 3-METHYL-1,6,8-TRIHYDROXYANTHRAQUINONE
- 3,8-DIBROMO-7-HYDROXY-4-METHYL-2H-CHROMEN-2-ONE
- 19-(cyclopropylamino)-4,6,7,15-tetrahydro-5H-16,1-(azenometheno)-10,14-(metheno)pyrazolo[4,3-o][1,3,9]triazacyclohexadecin-8(9H)-one
- N,N\'-DIPHENYLPYRAZOLO[1,5-A][1,3,5]TRIAZINE-2,4-DIAMINE
- 4-(2-(1H-IMIDAZOL-4-YL)ETHYLAMINO)-2-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(CYCLOHEXYLMETHYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-CHLOROBENZYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-ETHYLPIPERAZIN-1-YL)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- N-(3-(8-CYANO-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZIN-2-YLAMINO)PHENYL)ACETAMIDE
- 2,3,7,8-tetrahydroxychromeno[5,4,3-cde]chromene-5,10-dione
- 5,6-dichloro-1-beta-D-ribofuranosyl-1H-benzimidazole
- 1,2,5,8-tetrahydroxyanthracene-9,10-dione
- Ellagic Acid
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| CSNK2B and TP53 |
casein kinase 2, beta polypeptide |
tumor protein p53 |
- Mitotic Prometaphase
- Signal transduction by L1
- Axon guidance
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- L1CAM interactions
- Signaling by Wnt
- Cell Cycle, Mitotic
- M Phase
- WNT mediated activation of DVL
- TCF dependent signaling in response to WNT
- RNF mutants show enhanced WNT signaling and proliferation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Signaling by WNT in cancer
- Condensation of Prometaphase Chromosomes
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- 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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| DAPK3 and TP53 |
death-associated protein kinase 3 |
tumor protein p53 |
- Programmed Cell Death
- Role of DCC in regulating apoptosis
- Extrinsic Pathway
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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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