MAPK8 and TP53 |
mitogen-activated protein kinase 8 |
tumor protein p53 |
- Toll Like Receptor 7/8 (TLR7/8) Cascade
- Cellular Senescence
- Activation of BH3-only proteins
- FCERI mediated MAPK activation
- Toll Like Receptor TLR6:TLR2 Cascade
- Activation of BMF and translocation to mitochondria
- Activated TLR4 signalling
- Toll Like Receptor TLR1:TLR2 Cascade
- Activation of the AP-1 family of transcription factors
- MyD88 cascade initiated on plasma membrane
- Toll Like Receptor 5 (TLR5) Cascade
- Programmed Cell Death
- MyD88 dependent cascade initiated on endosome
- TRAF6 mediated induction of NFkB and MAP kinases upon TLR7/8 or 9 activation
- MyD88:Mal cascade initiated on plasma membrane
- Toll Like Receptor 9 (TLR9) Cascade
- Intrinsic Pathway for Apoptosis
- JNK (c-Jun kinases) phosphorylation and activation mediated by activated human TAK1
- Innate Immune System
- Signalling by NGF
- Cell death signalling via NRAGE, NRIF and NADE
- TRIF-mediated TLR3/TLR4 signaling
- MAP kinase activation in TLR cascade
- p75 NTR receptor-mediated signalling
- MyD88-independent cascade
- Toll Like Receptor 2 (TLR2) Cascade
- Toll-Like Receptors Cascades
- Toll Like Receptor 10 (TLR10) Cascade
- DSCAM interactions
- NRIF signals cell death from the nucleus
- Oxidative Stress Induced Senescence
- Activation of BIM and translocation to mitochondria
- Toll Like Receptor 3 (TLR3) Cascade
- Toll Like Receptor 4 (TLR4) Cascade
- NRAGE signals death through JNK
- Fc epsilon receptor (FCERI) signaling
- MAPK targets/ Nuclear events mediated by MAP kinases
|
- 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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MAPK9 and TP53 |
mitogen-activated protein kinase 9 |
tumor protein p53 |
- Toll Like Receptor 7/8 (TLR7/8) Cascade
- Cellular Senescence
- FCERI mediated MAPK activation
- Toll Like Receptor TLR6:TLR2 Cascade
- Activated TLR4 signalling
- Toll Like Receptor TLR1:TLR2 Cascade
- Activation of the AP-1 family of transcription factors
- MyD88 cascade initiated on plasma membrane
- Toll Like Receptor 5 (TLR5) Cascade
- MyD88 dependent cascade initiated on endosome
- TRAF6 mediated induction of NFkB and MAP kinases upon TLR7/8 or 9 activation
- MyD88:Mal cascade initiated on plasma membrane
- Toll Like Receptor 9 (TLR9) Cascade
- JNK (c-Jun kinases) phosphorylation and activation mediated by activated human TAK1
- Innate Immune System
- TRIF-mediated TLR3/TLR4 signaling
- MAP kinase activation in TLR cascade
- MyD88-independent cascade
- Toll Like Receptor 2 (TLR2) Cascade
- Toll-Like Receptors Cascades
- Toll Like Receptor 10 (TLR10) Cascade
- Oxidative Stress Induced Senescence
- Toll Like Receptor 3 (TLR3) Cascade
- Toll Like Receptor 4 (TLR4) Cascade
- Fc epsilon receptor (FCERI) signaling
- MAPK targets/ Nuclear events mediated by MAP kinases
|
- 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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|
|
|
|
MAPK10 and TP53 |
mitogen-activated protein kinase 10 |
tumor protein p53 |
- Toll Like Receptor 7/8 (TLR7/8) Cascade
- Cellular Senescence
- FCERI mediated MAPK activation
- Toll Like Receptor TLR6:TLR2 Cascade
- Activated TLR4 signalling
- Toll Like Receptor TLR1:TLR2 Cascade
- Activation of the AP-1 family of transcription factors
- MyD88 cascade initiated on plasma membrane
- Toll Like Receptor 5 (TLR5) Cascade
- MyD88 dependent cascade initiated on endosome
- TRAF6 mediated induction of NFkB and MAP kinases upon TLR7/8 or 9 activation
- MyD88:Mal cascade initiated on plasma membrane
- Toll Like Receptor 9 (TLR9) Cascade
- JNK (c-Jun kinases) phosphorylation and activation mediated by activated human TAK1
- Innate Immune System
- TRIF-mediated TLR3/TLR4 signaling
- MAP kinase activation in TLR cascade
- MyD88-independent cascade
- Toll Like Receptor 2 (TLR2) Cascade
- Toll-Like Receptors Cascades
- Toll Like Receptor 10 (TLR10) Cascade
- Oxidative Stress Induced Senescence
- Toll Like Receptor 3 (TLR3) Cascade
- Toll Like Receptor 4 (TLR4) Cascade
- Fc epsilon receptor (FCERI) signaling
- MAPK targets/ Nuclear events mediated by MAP kinases
|
- 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
|
- 2,6-Dihydroanthra/1,9-Cd/Pyrazol-6-One
- Cyclohexyl-{4-[5-(3,4-Dichlorophenyl)-2-Piperidin-4-Yl-3-Propyl-3h-Imidazol-4-Yl]-Pyrimidin-2-Yl}Amine
- Cyclopropyl-{4-[5-(3,4-Dichlorophenyl)-2-[(1-Methyl)-Piperidin]-4-Yl-3-Propyl-3h-Imidazol-4-Yl]-Pyrimidin-2-Yl}Amine
- 9-(4-Hydroxyphenyl)-2,7-Phenanthroline
- Phosphoaminophosphonic Acid-Adenylate Ester
- N-(tert-butyl)-4-[5-(pyridin-2-ylamino)quinolin-3-yl]benzenesulfonamide
- N-BENZYL-4-[4-(3-CHLOROPHENYL)-1H-PYRAZOL-3-YL]-1H-PYRROLE-2-CARBOXAMIDE
- N-(3-cyano-4,5,6,7-tetrahydro-1-benzothien-2-yl)-2-fluorobenzamide
- 4-{[5-chloro-4-(1H-indol-3-yl)pyrimidin-2-yl]amino}-N-ethylpiperidine-1-carboxamide
- (3Z)-1-[(6-fluoro-4H-1,3-benzodioxin-8-yl)methyl]-4-[(E)-2-phenylethenyl]-1H-indole-2,3-dione 3-oxime
- (3E)-5-fluoro-1-[(6-fluoro-4H-1,3-benzodioxin-8-yl)methyl]-1H-indole-2,3-dione 3-oxime
- (3Z)-1-[(6-fluoro-4H-1,3-benzodioxin-8-yl)methyl]-4-phenyl-1H-indole-2,3-dione 3-oxime
- 5-bromo-N-(3-chloro-2-(4-(prop-2-ynyl)piperazin-1-yl)phenyl)furan-2-carboxamide
- N-cyclohexyl-4-imidazo[1,2-a]pyridin-3-yl-N-methylpyrimidin-2-amine
- N-{2\'-[(4-FLUOROPHENYL)AMINO]-4,4\'-BIPYRIDIN-2-YL}-4-METHOXYCYCLOHEXANECARBOXAMIDE
- 2-{4-[(4-imidazo[1,2-a]pyridin-3-ylpyrimidin-2-yl)amino]piperidin-1-yl}-N-methylacetamide
- 1-(3-BROMOPHENYL)-7-CHLORO-6-METHOXY-3,4-DIHYDROISOQUINOLINE
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EIF2AK2 and TP53 |
eukaryotic translation initiation factor 2-alpha kinase 2 |
tumor protein p53 |
- ISG15 antiviral mechanism
- Interferon Signaling
- Inhibition of PKR
- Cytokine Signaling in Immune system
- Host Interactions with Influenza Factors
- Influenza Infection
- NS1 Mediated Effects on Host Pathways
- Antiviral mechanism by IFN-stimulated genes
|
- 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
|
|
|
|
|
PRKRIR and TP53 |
protein-kinase, interferon-inducible double stranded RNA dependent inhibitor, repressor of (P58 repressor) |
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
|
|
|
|
|
PSMB3 and TP53 |
proteasome (prosome, macropain) subunit, beta type, 3 |
tumor protein p53 |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- Hh ligand biogenesis disease
- T41 mutants of beta-catenin aren't phosphorylated
- Downstream signaling events of B Cell Receptor (BCR)
- Degradation of beta-catenin by the destruction complex
- Stabilization of p53
- S33 mutants of beta-catenin aren't phosphorylated
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- Removal of licensing factors from origins
- Switching of origins to a post-replicative state
- Mitotic G1-G1/S phases
- Regulation of mRNA stability by proteins that bind AU-rich elements
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- DNA Replication Pre-Initiation
- S45 mutants of beta-catenin aren't phosphorylated
- APC/C:Cdc20 mediated degradation of mitotic proteins
- Regulation of APC/C activators between G1/S and early anaphase
- SCF(Skp2)-mediated degradation of p27/p21
- deletions in the AMER1 gene destabilize the destruction complex
- Autodegradation of the E3 ubiquitin ligase COP1
- AMER1 mutants destabilize the destruction complex
- Activation of APC/C and APC/C:Cdc20 mediated degradation of mitotic proteins
- APC:Cdc20 mediated degradation of cell cycle proteins prior to satisfation of the cell cycle checkpoint
- PCP/CE pathway
- Adaptive Immune System
- CDK-mediated phosphorylation and removal of Cdc6
- Hedgehog ligand biogenesis
- APC/C:Cdh1 mediated degradation of Cdc20 and other APC/C:Cdh1 targeted proteins in late mitosis/early G1
- Separation of Sister Chromatids
- HIV Infection
- Ubiquitin-dependent degradation of Cyclin D
- APC truncation mutants have impaired AXIN binding
- Assembly of the pre-replicative complex
- Autodegradation of Cdh1 by Cdh1:APC/C
- p53-Dependent G1 DNA Damage Response
- S37 mutants of beta-catenin aren't phosphorylated
- XAV939 inhibits tankyrase, stabilizing AXIN
- p53-Independent DNA Damage Response
- p53-Independent G1/S DNA damage checkpoint
- G1/S DNA Damage Checkpoints
- Vpu mediated degradation of CD4
- Synthesis of DNA
- M/G1 Transition
- Ubiquitin-dependent degradation of Cyclin D1
- TCF dependent signaling in response to WNT
- SCF-beta-TrCP mediated degradation of Emi1
- degradation of AXIN
- Signaling by Hedgehog
- Regulation of mitotic cell cycle
- Degradation of GLI1 by the proteasome
- degradation of DVL
- Cell Cycle Checkpoints
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Regulation of Apoptosis
- Degradation of GLI2 by the proteasome
- Signaling by the B Cell Receptor (BCR)
- Vif-mediated degradation of APOBEC3G
- Ubiquitin Mediated Degradation of Phosphorylated Cdc25A
- p53-Dependent G1/S DNA damage checkpoint
- truncated APC mutants destabilize the destruction complex
- TCF7L2 mutants don't bind CTBP
- Signaling by Wnt
- Cyclin E associated events during G1/S transition
- APC/C:Cdc20 mediated degradation of Securin
- AUF1 (hnRNP D0) destabilizes mRNA
- CDK-mediated phosphorylation and removal of Cdc6
- RNF mutants show enhanced WNT signaling and proliferation
- G1/S Transition
- truncations of AMER1 destabilize the destruction complex
- Processing-defective Hh variants abrogate ligand secretion
- Host Interactions of HIV factors
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- Regulation of activated PAK-2p34 by proteasome mediated degradation
- AXIN missense mutants destabilize the destruction complex
- S Phase
- APC/C-mediated degradation of cell cycle proteins
- Cyclin A:Cdk2-associated events at S phase entry
- SCF(Skp2)-mediated degradation of p27/p21
- Mitotic Metaphase and Anaphase
- Regulation of ornithine decarboxylase (ODC)
- Antigen processing: Ubiquitination & Proteasome degradation
- Orc1 removal from chromatin
- Mitotic Anaphase
- M Phase
- APC truncation mutants are not K63 polyubiquitinated
- Metabolism of amino acids and derivatives
- Hedgehog 'on' state
- Programmed Cell Death
- Class I MHC mediated antigen processing & presentation
- Regulation of DNA replication
- Cell Cycle, Mitotic
- beta-catenin independent WNT signaling
- Orc1 removal from chromatin
- Activation of NF-kappaB in B cells
- Asymmetric localization of PCP proteins
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Cross-presentation of soluble exogenous antigens (endosomes)
- Antigen processing-Cross presentation
- CDT1 association with the CDC6:ORC:origin complex
- ER-Phagosome 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
|
|
|
|
|
PSMC5 and TP53 |
proteasome (prosome, macropain) 26S subunit, ATPase, 5 |
tumor protein p53 |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- Hh ligand biogenesis disease
- T41 mutants of beta-catenin aren't phosphorylated
- Downstream signaling events of B Cell Receptor (BCR)
- Degradation of beta-catenin by the destruction complex
- Stabilization of p53
- S33 mutants of beta-catenin aren't phosphorylated
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- Removal of licensing factors from origins
- Switching of origins to a post-replicative state
- Mitotic G1-G1/S phases
- Regulation of mRNA stability by proteins that bind AU-rich elements
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- DNA Replication Pre-Initiation
- S45 mutants of beta-catenin aren't phosphorylated
- APC/C:Cdc20 mediated degradation of mitotic proteins
- Regulation of APC/C activators between G1/S and early anaphase
- SCF(Skp2)-mediated degradation of p27/p21
- deletions in the AMER1 gene destabilize the destruction complex
- Autodegradation of the E3 ubiquitin ligase COP1
- AMER1 mutants destabilize the destruction complex
- Activation of APC/C and APC/C:Cdc20 mediated degradation of mitotic proteins
- APC:Cdc20 mediated degradation of cell cycle proteins prior to satisfation of the cell cycle checkpoint
- PCP/CE pathway
- Adaptive Immune System
- CDK-mediated phosphorylation and removal of Cdc6
- Hedgehog ligand biogenesis
- APC/C:Cdh1 mediated degradation of Cdc20 and other APC/C:Cdh1 targeted proteins in late mitosis/early G1
- Separation of Sister Chromatids
- HIV Infection
- Ubiquitin-dependent degradation of Cyclin D
- APC truncation mutants have impaired AXIN binding
- Assembly of the pre-replicative complex
- Autodegradation of Cdh1 by Cdh1:APC/C
- p53-Dependent G1 DNA Damage Response
- S37 mutants of beta-catenin aren't phosphorylated
- XAV939 inhibits tankyrase, stabilizing AXIN
- p53-Independent DNA Damage Response
- p53-Independent G1/S DNA damage checkpoint
- G1/S DNA Damage Checkpoints
- Vpu mediated degradation of CD4
- Synthesis of DNA
- M/G1 Transition
- Ubiquitin-dependent degradation of Cyclin D1
- TCF dependent signaling in response to WNT
- SCF-beta-TrCP mediated degradation of Emi1
- degradation of AXIN
- Signaling by Hedgehog
- Regulation of mitotic cell cycle
- Degradation of GLI1 by the proteasome
- degradation of DVL
- Cell Cycle Checkpoints
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Regulation of Apoptosis
- Degradation of GLI2 by the proteasome
- Signaling by the B Cell Receptor (BCR)
- Vif-mediated degradation of APOBEC3G
- Ubiquitin Mediated Degradation of Phosphorylated Cdc25A
- p53-Dependent G1/S DNA damage checkpoint
- truncated APC mutants destabilize the destruction complex
- TCF7L2 mutants don't bind CTBP
- Signaling by Wnt
- Cyclin E associated events during G1/S transition
- APC/C:Cdc20 mediated degradation of Securin
- AUF1 (hnRNP D0) destabilizes mRNA
- CDK-mediated phosphorylation and removal of Cdc6
- RNF mutants show enhanced WNT signaling and proliferation
- G1/S Transition
- truncations of AMER1 destabilize the destruction complex
- Processing-defective Hh variants abrogate ligand secretion
- Host Interactions of HIV factors
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- Regulation of activated PAK-2p34 by proteasome mediated degradation
- AXIN missense mutants destabilize the destruction complex
- S Phase
- APC/C-mediated degradation of cell cycle proteins
- Cyclin A:Cdk2-associated events at S phase entry
- SCF(Skp2)-mediated degradation of p27/p21
- Mitotic Metaphase and Anaphase
- Regulation of ornithine decarboxylase (ODC)
- Antigen processing: Ubiquitination & Proteasome degradation
- Orc1 removal from chromatin
- Mitotic Anaphase
- M Phase
- APC truncation mutants are not K63 polyubiquitinated
- Metabolism of amino acids and derivatives
- Hedgehog 'on' state
- Programmed Cell Death
- Class I MHC mediated antigen processing & presentation
- Regulation of DNA replication
- Cell Cycle, Mitotic
- beta-catenin independent WNT signaling
- Orc1 removal from chromatin
- Activation of NF-kappaB in B cells
- Asymmetric localization of PCP proteins
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Cross-presentation of soluble exogenous antigens (endosomes)
- Antigen processing-Cross presentation
- CDT1 association with the CDC6:ORC:origin complex
- ER-Phagosome 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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PSMD11 and TP53 |
proteasome (prosome, macropain) 26S subunit, non-ATPase, 11 |
tumor protein p53 |
- Hedgehog 'off' state
- misspliced GSK3beta mutants stabilize beta-catenin
- Hh ligand biogenesis disease
- T41 mutants of beta-catenin aren't phosphorylated
- Downstream signaling events of B Cell Receptor (BCR)
- Degradation of beta-catenin by the destruction complex
- Stabilization of p53
- S33 mutants of beta-catenin aren't phosphorylated
- AXIN mutants destabilize the destruction complex, activating WNT signaling
- Removal of licensing factors from origins
- Switching of origins to a post-replicative state
- Mitotic G1-G1/S phases
- Regulation of mRNA stability by proteins that bind AU-rich elements
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- DNA Replication Pre-Initiation
- S45 mutants of beta-catenin aren't phosphorylated
- APC/C:Cdc20 mediated degradation of mitotic proteins
- Regulation of APC/C activators between G1/S and early anaphase
- SCF(Skp2)-mediated degradation of p27/p21
- deletions in the AMER1 gene destabilize the destruction complex
- Autodegradation of the E3 ubiquitin ligase COP1
- AMER1 mutants destabilize the destruction complex
- Activation of APC/C and APC/C:Cdc20 mediated degradation of mitotic proteins
- APC:Cdc20 mediated degradation of cell cycle proteins prior to satisfation of the cell cycle checkpoint
- PCP/CE pathway
- Adaptive Immune System
- CDK-mediated phosphorylation and removal of Cdc6
- Hedgehog ligand biogenesis
- APC/C:Cdh1 mediated degradation of Cdc20 and other APC/C:Cdh1 targeted proteins in late mitosis/early G1
- Separation of Sister Chromatids
- HIV Infection
- Ubiquitin-dependent degradation of Cyclin D
- APC truncation mutants have impaired AXIN binding
- Assembly of the pre-replicative complex
- Autodegradation of Cdh1 by Cdh1:APC/C
- p53-Dependent G1 DNA Damage Response
- S37 mutants of beta-catenin aren't phosphorylated
- XAV939 inhibits tankyrase, stabilizing AXIN
- p53-Independent DNA Damage Response
- p53-Independent G1/S DNA damage checkpoint
- G1/S DNA Damage Checkpoints
- Vpu mediated degradation of CD4
- Synthesis of DNA
- M/G1 Transition
- Ubiquitin-dependent degradation of Cyclin D1
- TCF dependent signaling in response to WNT
- SCF-beta-TrCP mediated degradation of Emi1
- degradation of AXIN
- Signaling by Hedgehog
- Regulation of mitotic cell cycle
- Degradation of GLI1 by the proteasome
- degradation of DVL
- Cell Cycle Checkpoints
- Signaling by WNT in cancer
- GLI3 is processed to GLI3R by the proteasome
- Regulation of Apoptosis
- Degradation of GLI2 by the proteasome
- Signaling by the B Cell Receptor (BCR)
- Vif-mediated degradation of APOBEC3G
- Ubiquitin Mediated Degradation of Phosphorylated Cdc25A
- p53-Dependent G1/S DNA damage checkpoint
- truncated APC mutants destabilize the destruction complex
- TCF7L2 mutants don't bind CTBP
- Signaling by Wnt
- Cyclin E associated events during G1/S transition
- APC/C:Cdc20 mediated degradation of Securin
- AUF1 (hnRNP D0) destabilizes mRNA
- CDK-mediated phosphorylation and removal of Cdc6
- RNF mutants show enhanced WNT signaling and proliferation
- G1/S Transition
- truncations of AMER1 destabilize the destruction complex
- Processing-defective Hh variants abrogate ligand secretion
- Host Interactions of HIV factors
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex
- Regulation of activated PAK-2p34 by proteasome mediated degradation
- AXIN missense mutants destabilize the destruction complex
- S Phase
- APC/C-mediated degradation of cell cycle proteins
- Cyclin A:Cdk2-associated events at S phase entry
- SCF(Skp2)-mediated degradation of p27/p21
- Mitotic Metaphase and Anaphase
- Regulation of ornithine decarboxylase (ODC)
- Antigen processing: Ubiquitination & Proteasome degradation
- Orc1 removal from chromatin
- Mitotic Anaphase
- M Phase
- APC truncation mutants are not K63 polyubiquitinated
- Metabolism of amino acids and derivatives
- Hedgehog 'on' state
- Programmed Cell Death
- Class I MHC mediated antigen processing & presentation
- Regulation of DNA replication
- Cell Cycle, Mitotic
- beta-catenin independent WNT signaling
- Orc1 removal from chromatin
- Activation of NF-kappaB in B cells
- Asymmetric localization of PCP proteins
- deletions in the AXIN genes in hepatocellular carcinoma result in elevated WNT signaling
- Cross-presentation of soluble exogenous antigens (endosomes)
- Antigen processing-Cross presentation
- CDT1 association with the CDC6:ORC:origin complex
- ER-Phagosome 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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PTK2 and TP53 |
protein tyrosine kinase 2 |
tumor protein p53 |
- Axon guidance
- DCC mediated attractive signaling
- Netrin mediated repulsion signals
- Platelet Aggregation (Plug Formation)
- VEGFA-VEGFR2 Pathway
- EPHB-mediated forward signaling
- EPHA-mediated growth cone collapse
- Programmed Cell Death
- EPH-Ephrin signaling
- NCAM signaling for neurite out-growth
- Netrin-1 signaling
- Fcgamma receptor (FCGR) dependent phagocytosis
- Regulation of actin dynamics for phagocytic cup formation
- Innate Immune System
- Apoptotic cleavage of cellular proteins
- Apoptotic execution phase
- p130Cas linkage to MAPK signaling for integrins
- Integrin alphaIIb beta3 signaling
- Signal regulatory protein (SIRP) family interactions
- GRB2:SOS provides linkage to MAPK signaling for Integrins
- Signaling by VEGF
- Platelet activation, signaling and aggregation
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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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RAB4A and TP53 |
RAB4A, member RAS oncogene family |
tumor protein p53 |
- Translocation of GLUT4 to the plasma membrane
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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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RAD51 and TP53 |
RAD51 recombinase |
tumor protein p53 |
- Assembly of the RAD51-ssDNA nucleoprotein complex
- Homologous DNA pairing and strand exchange
- Meiotic recombination
- 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
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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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RANBP2 and TP53 |
RAN binding protein 2 |
tumor protein p53 |
- Mitotic Prometaphase
- Separation of Sister Chromatids
- Mitotic Prophase
- HIV Infection
- Nuclear import of Rev protein
- Regulatory RNA pathways
- Rev-mediated nuclear export of HIV RNA
- Nuclear Envelope Breakdown
- Mitotic Anaphase
- SLC-mediated transmembrane transport
- M Phase
- Influenza Life Cycle
- HIV Life Cycle
- Influenza Viral RNA Transcription and Replication
- Rev-mediated nuclear export of HIV RNA
- Myoclonic epilepsy of Lafora
- Glycogen storage diseases
- Transcriptional regulation by small RNAs
- Vpr-mediated nuclear import of PICs
- ISG15 antiviral mechanism
- Interferon Signaling
- Host Interactions of HIV factors
- Regulation of Glucokinase by Glucokinase Regulatory Protein
- Nuclear Pore Complex (NPC) Disassembly
- Cytokine Signaling in Immune system
- Interactions of Vpr with host cellular proteins
- Interactions of Rev with host cellular proteins
- Influenza Infection
- Hexose transport
- Cell Cycle, Mitotic
- Late Phase of HIV Life Cycle
- Antiviral mechanism by IFN-stimulated genes
- Resolution of Sister Chromatid Cohesion
- Viral Messenger RNA Synthesis
- Metabolism of carbohydrates
- Glucose transport
- Mitotic Metaphase and Anaphase
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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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RAP1B and TP53 |
RAP1B, member of RAS oncogene family |
tumor protein p53 |
- Rap1 signalling
- p130Cas linkage to MAPK signaling for integrins
- Integrin alphaIIb beta3 signaling
- GRB2:SOS provides linkage to MAPK signaling for Integrins
- Platelet activation, signaling and aggregation
- Platelet Aggregation (Plug Formation)
- Adaptive Immune System
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- Cellular Senescence
- Activation of BH3-only proteins
- p53-Dependent G1/S DNA damage checkpoint
- Oncogene Induced Senescence
- p53-Dependent G1 DNA Damage Response
- Formation of Senescence-Associated Heterochromatin Foci (SAHF)
- Pre-NOTCH Transcription and Translation
- Stabilization of p53
- Transcriptional activation of p53 responsive genes
- Programmed Cell Death
- Pre-NOTCH Expression and Processing
- G1/S DNA Damage Checkpoints
- Intrinsic Pathway for Apoptosis
- Transcriptional activation of cell cycle inhibitor p21
- DNA Damage/Telomere Stress Induced Senescence
- Signaling by NOTCH
- Factors involved in megakaryocyte development and platelet production
- Activation of NOXA and translocation to mitochondria
- Oxidative Stress Induced Senescence
- Autodegradation of the E3 ubiquitin ligase COP1
- Activation of PUMA and translocation to mitochondria
- Cell Cycle Checkpoints
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RBBP5 and TP53 |
retinoblastoma binding protein 5 |
tumor protein p53 |
- Chromatin organization
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- formation of the beta-catenin:TCF transactivating complex
- PKMTs methylate histone lysines
- Signaling by Wnt
- deactivation of the beta-catenin transactivating complex
- Chromatin modifying enzymes
- 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
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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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TRIM27 and TP53 |
tripartite motif containing 27 |
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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RPA1 and TP53 |
replication protein A1, 70kDa |
tumor protein p53 |
- HSF1 activation
- Gap-filling DNA repair synthesis and ligation in TC-NER
- G2/M Checkpoints
- Repair synthesis for gap-filling by DNA polymerase in TC-NER
- Activation of the pre-replicative complex
- DNA strand elongation
- Mismatch Repair
- G1/S Transition
- Homologous recombination repair of replication-independent double-strand breaks
- Mitotic G1-G1/S phases
- Removal of the Flap Intermediate from the C-strand
- Chromosome Maintenance
- DNA Replication Pre-Initiation
- S Phase
- Removal of the Flap Intermediate
- Global Genomic NER (GG-NER)
- Nucleotide Excision Repair
- Activation of the pre-replicative complex
- Extension of Telomeres
- Mismatch repair (MMR) directed by MSH2:MSH6 (MutSalpha)
- Assembly of the RAD51-ssDNA nucleoprotein complex
- Telomere Maintenance
- Activation of ATR in response to replication stress
- Processing of DNA double-strand break ends
- Double-Strand Break Repair
- Dual incision reaction in GG-NER
- Meiotic recombination
- Synthesis of DNA
- Lagging Strand Synthesis
- Processive synthesis on the C-strand of the telomere
- Processive synthesis on the lagging strand
- M/G1 Transition
- Cellular response to heat stress
- Regulation of HSF1-mediated heat shock response
- Telomere C-strand (Lagging Strand) Synthesis
- Presynaptic phase of homologous DNA pairing and strand exchange
- Repair synthesis of patch ~27-30 bases long by DNA polymerase
- Cell Cycle, Mitotic
- Gap-filling DNA repair synthesis and ligation in GG-NER
- Homologous DNA pairing and strand exchange
- Mismatch repair (MMR) directed by MSH2:MSH3 (MutSbeta)
- Transcription-coupled NER (TC-NER)
- Homologous Recombination Repair
- Formation of incision complex in GG-NER
- Cell Cycle Checkpoints
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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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RPS3 and TP53 |
ribosomal protein S3 |
tumor protein p53 |
- Nonsense-Mediated Decay (NMD)
- Translation initiation complex formation
- Translation
- SRP-dependent cotranslational protein targeting to membrane
- Eukaryotic Translation Termination
- Peptide chain elongation
- Influenza Infection
- Viral mRNA Translation
- L13a-mediated translational silencing of Ceruloplasmin expression
- Influenza Life Cycle
- Nonsense Mediated Decay (NMD) enhanced by the Exon Junction Complex (EJC)
- Ribosomal scanning and start codon recognition
- Formation of the ternary complex, and subsequently, the 43S complex
- Influenza Viral RNA Transcription and Replication
- GTP hydrolysis and joining of the 60S ribosomal subunit
- Eukaryotic Translation Initiation
- Activation of the mRNA upon binding of the cap-binding complex and eIFs, and subsequent binding to 43S
- Formation of a pool of free 40S subunits
- Eukaryotic Translation Elongation
- Cap-dependent Translation Initiation
- Nonsense Mediated Decay (NMD) independent of the Exon Junction Complex (EJC)
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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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RRM2 and TP53 |
ribonucleotide reductase M2 |
tumor protein p53 |
- E2F mediated regulation of DNA replication
- G1/S Transition
- G1/S-Specific Transcription
- Metabolism of nucleotides
- Synthesis and interconversion of nucleotide di- and triphosphates
- Mitotic G1-G1/S phases
- Cell Cycle, Mitotic
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- 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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S100A2 and TP53 |
S100 calcium binding protein A2 |
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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S100A4 and TP53 |
S100 calcium binding protein A4 |
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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