CDKN2A and WRN |
cyclin-dependent kinase inhibitor 2A |
Werner syndrome, RecQ helicase-like |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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CDKN2A and HUWE1 |
cyclin-dependent kinase inhibitor 2A |
HECT, UBA and WWE domain containing 1, E3 ubiquitin protein ligase |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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- Antigen processing: Ubiquitination & Proteasome degradation
- Class I MHC mediated antigen processing & presentation
- Adaptive Immune System
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CDKN2A and ORC4 |
cyclin-dependent kinase inhibitor 2A |
origin recognition complex, subunit 4 |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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- G2/M Checkpoints
- Activation of the pre-replicative complex
- Activation of the pre-replicative complex
- Orc1 removal from chromatin
- Assembly of the pre-replicative complex
- Activation of ATR in response to replication stress
- G1/S Transition
- Assembly of the ORC complex at the origin of replication
- Removal of licensing factors from origins
- Mitotic G1-G1/S phases
- Switching of origins to a post-replicative state
- E2F mediated regulation of DNA replication
- Synthesis of DNA
- DNA Replication Pre-Initiation
- Regulation of DNA replication
- M/G1 Transition
- S Phase
- CDC6 association with the ORC:origin complex
- Cell Cycle, Mitotic
- Orc1 removal from chromatin
- E2F-enabled inhibition of pre-replication complex formation
- Cell Cycle Checkpoints
- Association of licensing factors with the pre-replicative complex
- CDT1 association with the CDC6:ORC:origin complex
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CDKN2A and MTR |
cyclin-dependent kinase inhibitor 2A |
5-methyltetrahydrofolate-homocysteine methyltransferase |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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- Metabolism of vitamins and cofactors
- Defective CD320 causes methylmalonic aciduria
- Defective LMBRD1 causes methylmalonic aciduria and homocystinuria type cblF
- Defective AHCY causes Hypermethioninemia with S-adenosylhomocysteine hydrolase deficiency (HMAHCHD)
- Defective BTD causes biotidinase deficiency
- Defective TPMT causes Thiopurine S-methyltransferase deficiency (TPMT deficiency)
- Defective MMACHC causes methylmalonic aciduria and homocystinuria type cblC
- Defective UGT1A4 causes hyperbilirubinemia
- Sulfur amino acid metabolism
- Defective MTR causes methylmalonic aciduria and homocystinuria type cblG
- Metabolic disorders of biological oxidation enzymes
- Metabolism of amino acids and derivatives
- Defective MTRR causes methylmalonic aciduria and homocystinuria type cblE
- Defective AMN causes hereditary megaloblastic anemia 1
- Defective UGT1A1 causes hyperbilirubinemia
- Defective SLC35D1 causes Schneckenbecken dysplasia (SCHBCKD)
- Biological oxidations
- Defective GCLC causes Hemolytic anemia due to gamma-glutamylcysteine synthetase deficiency (HAGGSD)
- Defective GGT1 causes Glutathionuria (GLUTH)
- Defects in cobalamin (B12) metabolism
- Defective GSS causes Glutathione synthetase deficiency (GSS deficiency)
- Defective GIF causes intrinsic factor deficiency
- Defective OPLAH causes 5-oxoprolinase deficiency (OPLAHD)
- Defective HLCS causes multiple carboxylase deficiency
- Defective MMAB causes methylmalonic aciduria type cblB
- Defective MAT1A causes Methionine adenosyltransferase deficiency (MATD)
- Defective MMADHC causes methylmalonic aciduria and homocystinuria type cblD
- Defective MMAA causes methylmalonic aciduria type cblA
- Defective CUBN causes hereditary megaloblastic anemia 1
- Cobalamin (Cbl, vitamin B12) transport and metabolism
- Phase II conjugation
- Methylation
- Defective MUT causes methylmalonic aciduria mut type
- Metabolism of water-soluble vitamins and cofactors
- Defects in biotin (Btn) metabolism
- Defective TCN2 causes hereditary megaloblastic anemia
- Defects in vitamin and cofactor metabolism
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- Cyanocobalamin
- Tetrahydrofolic acid
- L-Methionine
- Hydroxocobalamin
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CDKN2A and TPI1 |
cyclin-dependent kinase inhibitor 2A |
triosephosphate isomerase 1 |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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- Gluconeogenesis
- Glucose metabolism
- Myoclonic epilepsy of Lafora
- Glycogen storage diseases
- Glycolysis
- Metabolism of carbohydrates
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ACLY and CDKN2A |
ATP citrate lyase |
cyclin-dependent kinase inhibitor 2A |
- Fatty Acyl-CoA Biosynthesis
- Fatty acid, triacylglycerol, and ketone body metabolism
- Metabolism of lipids and lipoproteins
- Integration of energy metabolism
- ChREBP activates metabolic gene expression
- Triglyceride Biosynthesis
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- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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ACTG1 and CDKN2A |
actin gamma 1 |
cyclin-dependent kinase inhibitor 2A |
- Axon guidance
- Gap junction degradation
- Adherens junctions interactions
- Translocation of GLUT4 to the plasma membrane
- L1CAM interactions
- Recycling pathway of L1
- VEGFA-VEGFR2 Pathway
- EPHB-mediated forward signaling
- Interaction between L1 and Ankyrins
- Cell-cell junction organization
- EPH-ephrin mediated repulsion of cells
- Gap junction trafficking and regulation
- EPH-Ephrin signaling
- Fcgamma receptor (FCGR) dependent phagocytosis
- Regulation of actin dynamics for phagocytic cup formation
- Innate Immune System
- Cell junction organization
- Formation of annular gap junctions
- Gap junction trafficking
- Signaling by VEGF
- Cell-extracellular matrix interactions
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- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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BCL2L1 and CDKN2A |
BCL2-like 1 |
cyclin-dependent kinase inhibitor 2A |
- Inflammasomes
- The NLRP1 inflammasome
- Nucleotide-binding domain, leucine rich repeat containing receptor (NLR) signaling pathways
- Programmed Cell Death
- BH3-only proteins associate with and inactivate anti-apoptotic BCL-2 members
- Innate Immune System
- Intrinsic Pathway for Apoptosis
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- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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CCNG1 and CDKN2A |
cyclin G1 |
cyclin-dependent kinase inhibitor 2A |
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- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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CDC5L and CDKN2A |
cell division cycle 5-like |
cyclin-dependent kinase inhibitor 2A |
- Processing of Capped Intron-Containing Pre-mRNA
- mRNA Splicing
- mRNA Splicing - Major Pathway
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- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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CDC6 and CDKN2A |
cell division cycle 6 |
cyclin-dependent kinase inhibitor 2A |
- CDK-mediated phosphorylation and removal of Cdc6
- G2/M Checkpoints
- Activation of the pre-replicative complex
- Activation of the pre-replicative complex
- Orc1 removal from chromatin
- CDK-mediated phosphorylation and removal of Cdc6
- Assembly of the pre-replicative complex
- Activation of ATR in response to replication stress
- G1/S Transition
- G1/S-Specific Transcription
- Removal of licensing factors from origins
- Mitotic G1-G1/S phases
- Switching of origins to a post-replicative state
- E2F mediated regulation of DNA replication
- Synthesis of DNA
- DNA Replication Pre-Initiation
- Regulation of DNA replication
- M/G1 Transition
- G0 and Early G1
- S Phase
- CDC6 association with the ORC:origin complex
- Cell Cycle, Mitotic
- Orc1 removal from chromatin
- Cell Cycle Checkpoints
- CDT1 association with the CDC6:ORC:origin complex
- Association of licensing factors with the pre-replicative complex
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- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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CDK6 and CDKN2A |
cyclin-dependent kinase 6 |
cyclin-dependent kinase inhibitor 2A |
- 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
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- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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CDKN2A and ZNF410 |
cyclin-dependent kinase inhibitor 2A |
zinc finger protein 410 |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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CDKN2A and CDKN2C |
cyclin-dependent kinase inhibitor 2A |
cyclin-dependent kinase inhibitor 2C (p18, inhibits CDK4) |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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- 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
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CDKN2A and ZFP91 |
cyclin-dependent kinase inhibitor 2A |
ZFP91 zinc finger protein |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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CDKN2A and HIF1A |
cyclin-dependent kinase inhibitor 2A |
hypoxia inducible factor 1, alpha subunit (basic helix-loop-helix transcription factor) |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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- Signaling by NOTCH1 HD Domain Mutants in Cancer
- Cellular response to hypoxia
- Regulation of Hypoxia-inducible Factor (HIF) by oxygen
- Signaling by NOTCH1 HD+PEST Domain Mutants in Cancer
- Oxygen-dependent proline hydroxylation of Hypoxia-inducible Factor Alpha
- Signaling by NOTCH
- Regulation of gene expression by Hypoxia-inducible Factor
- Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant
- NOTCH1 Intracellular Domain Regulates Transcription
- Oxygen-dependent asparagine hydroxylation of Hypoxia-inducible Factor Alpha
- Signaling by NOTCH1
- Signaling by NOTCH1 PEST Domain Mutants in Cancer
- Signaling by NOTCH1 in Cancer
- FBXW7 Mutants and NOTCH1 in Cancer
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CDKN2A and HSP90AB1 |
cyclin-dependent kinase inhibitor 2A |
heat shock protein 90kDa alpha (cytosolic), class B member 1 |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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- HSF1 activation
- Axon guidance
- Semaphorin interactions
- Inflammasomes
- Attenuation phase
- Cellular response to heat stress
- HSF1-dependent transactivation
- Uptake and actions of bacterial toxins
- The NLRP3 inflammasome
- Nucleotide-binding domain, leucine rich repeat containing receptor (NLR) signaling pathways
- Sema3A PAK dependent Axon repulsion
- Fcgamma receptor (FCGR) dependent phagocytosis
- Regulation of actin dynamics for phagocytic cup formation
- Uptake and function of diphtheria toxin
- Innate Immune System
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- Geldanamycin
- 9-Butyl-8-(3,4,5-Trimethoxybenzyl)-9h-Purin-6-Amine
- Adenosine-5\'-Diphosphate
- Radicicol
- 4-[4-(2,3-DIHYDRO-1,4-BENZODIOXIN-6-YL)-3-METHYL-1H-PYRAZOL-5-YL]-6-ETHYLBENZENE-1,3-DIOL
- 8-(6-BROMO-BENZO[1,3]DIOXOL-5-YLSULFANYL)-9-(3-ISOPROPYLAMINO-PROPYL)-ADENINE
- 4-{4-[4-(3-AMINOPROPOXY)PHENYL]-1H-PYRAZOL-5-YL}-6-CHLOROBENZENE-1,3-DIOL
- (5E)-14-CHLORO-15,17-DIHYDROXY-4,7,8,9,10,11-HEXAHYDRO-2-BENZOXACYCLOPENTADECINE-1,12(3H,13H)-DIONE
- (5Z)-12-CHLORO-13,15-DIHYDROXY-4,7,8,9-TETRAHYDRO-2-BENZOXACYCLOTRIDECINE-1,10(3H,11H)-DIONE
- (5E)-12-CHLORO-13,15-DIHYDROXY-4,7,8,9-TETRAHYDRO-2-BENZOXACYCLOTRIDECINE-1,10(3H,11H)-DIONE
- (5Z)-13-CHLORO-14,16-DIHYDROXY-3,4,7,8,9,10-HEXAHYDRO-1H-2-BENZOXACYCLOTETRADECINE-1,11(12H)-DIONE
- METHYL 3-CHLORO-2-{3-[(2,5-DIHYDROXY-4-METHOXYPHENYL)AMINO]-3-OXOPROPYL}-4,6-DIHYDROXYBENZOATE
- 2-(3-AMINO-2,5,6-TRIMETHOXYPHENYL)ETHYL 5-CHLORO-2,4-DIHYDROXYBENZOATE
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CDKN2A and PSMC3 |
cyclin-dependent kinase inhibitor 2A |
proteasome (prosome, macropain) 26S subunit, ATPase, 3 |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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- 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
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CDKN2A and MCM2 |
cyclin-dependent kinase inhibitor 2A |
minichromosome maintenance complex component 2 |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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- Synthesis of DNA
- G2/M Checkpoints
- Activation of the pre-replicative complex
- DNA Replication Pre-Initiation
- M/G1 Transition
- Regulation of DNA replication
- Activation of the pre-replicative complex
- Orc1 removal from chromatin
- S Phase
- DNA strand elongation
- Cell Cycle, Mitotic
- Assembly of the pre-replicative complex
- Orc1 removal from chromatin
- G1/S Transition
- Activation of ATR in response to replication stress
- Cell Cycle Checkpoints
- Removal of licensing factors from origins
- Mitotic G1-G1/S phases
- Switching of origins to a post-replicative state
- Unwinding of DNA
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CDKN2A and MCM5 |
cyclin-dependent kinase inhibitor 2A |
minichromosome maintenance complex component 5 |
- 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
- Oxidative Stress Induced Senescence
- Cellular Senescence
- Oncogene Induced Senescence
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- Synthesis of DNA
- G2/M Checkpoints
- Activation of the pre-replicative complex
- DNA Replication Pre-Initiation
- M/G1 Transition
- Regulation of DNA replication
- Activation of the pre-replicative complex
- Orc1 removal from chromatin
- S Phase
- DNA strand elongation
- Cell Cycle, Mitotic
- Assembly of the pre-replicative complex
- Orc1 removal from chromatin
- G1/S Transition
- Activation of ATR in response to replication stress
- Cell Cycle Checkpoints
- Removal of licensing factors from origins
- Mitotic G1-G1/S phases
- Switching of origins to a post-replicative state
- Unwinding of DNA
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