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Function
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47 Pathways
- Evasion of Oncogene Induced Senescence Due to Defective p16INK4A binding to CDK4 and CDK6,
- Mitotic G1 phase and G1/S transition,
- RNA Polymerase II Transcription,
- Transcriptional regulation of granulopoiesis,
- Disease,
- Cyclin A:Cdk2-associated events at S phase entry,
- Signaling by PTK6,
- Defective binding of RB1 mutants to E2F1,(E2F2, E2F3),
- G1/S Transition,
- Cell Cycle, Mitotic,
- Evasion of Oncogene Induced Senescence Due to Defective p16INK4A binding to CDK4,
- Signaling by Non-Receptor Tyrosine Kinases,
- Gene expression (Transcription),
- Diseases of Cellular Senescence,
- Diseases of mitotic cell cycle,
- Transcriptional regulation by RUNX2,
- Developmental Biology,
- Chromatin modifying enzymes,
- G1 Phase,
- Senescence-Associated Secretory Phenotype (SASP),
- RMTs methylate histone arginines,
- Diseases of cellular response to stress,
- Oxidative Stress Induced Senescence,
- Cellular responses to external stimuli,
- Evasion of Oncogene Induced Senescence Due to p16INK4A Defects,
- Cell Cycle,
- Chromatin organization,
- S Phase,
- Cyclin D associated events in G1,
- Cyclin E associated events during G1/S transition ,
- Transcriptional regulation of white adipocyte differentiation,
- PTK6 Regulates Cell Cycle,
- SCF(Skp2)-mediated degradation of p27/p21,
- Signal Transduction,
- Ubiquitin-dependent degradation of Cyclin D,
- Evasion of Oxidative Stress Induced Senescence Due to Defective p16INK4A binding to CDK4,
- Cellular responses to stress,
- Evasion of Oxidative Stress Induced Senescence Due to p16INK4A Defects,
- Oncogene Induced Senescence,
- Reproduction,
- Cellular Senescence,
- Evasion of Oxidative Stress Induced Senescence Due to Defective p16INK4A binding to CDK4 and CDK6,
- Meiosis,
- Aberrant regulation of mitotic cell cycle due to RB1 defects,
- Generic Transcription Pathway,
- Meiotic recombination,
- Aberrant regulation of mitotic G1/S transition in cancer due to RB1 defects
Gene --> GO terms.
Gene -> HPO annotation (Human Phenotype Ontology)
Mouse Gene --> Allele [Phenotype]
Genomics
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Gene --> Chromosomal location.
Gene --> GO terms.
Gene --> Overlapping genes.
Disease
Gene (Hum OR Rat) --> Mouse Allele (Phenotype)
Gene --> Alleles and Disease (clinVar data)
Gene -> HPO annotation (Human Phenotype Ontology)
Mouse Gene --> Allele [Phenotype]
Other
47 Pathways
- Evasion of Oncogene Induced Senescence Due to Defective p16INK4A binding to CDK4 and CDK6,
- Mitotic G1 phase and G1/S transition,
- RNA Polymerase II Transcription,
- Transcriptional regulation of granulopoiesis,
- Disease,
- Cyclin A:Cdk2-associated events at S phase entry,
- Signaling by PTK6,
- Defective binding of RB1 mutants to E2F1,(E2F2, E2F3),
- G1/S Transition,
- Cell Cycle, Mitotic,
- Evasion of Oncogene Induced Senescence Due to Defective p16INK4A binding to CDK4,
- Signaling by Non-Receptor Tyrosine Kinases,
- Gene expression (Transcription),
- Diseases of Cellular Senescence,
- Diseases of mitotic cell cycle,
- Transcriptional regulation by RUNX2,
- Developmental Biology,
- Chromatin modifying enzymes,
- G1 Phase,
- Senescence-Associated Secretory Phenotype (SASP),
- RMTs methylate histone arginines,
- Diseases of cellular response to stress,
- Oxidative Stress Induced Senescence,
- Cellular responses to external stimuli,
- Evasion of Oncogene Induced Senescence Due to p16INK4A Defects,
- Cell Cycle,
- Chromatin organization,
- S Phase,
- Cyclin D associated events in G1,
- Cyclin E associated events during G1/S transition ,
- Transcriptional regulation of white adipocyte differentiation,
- PTK6 Regulates Cell Cycle,
- SCF(Skp2)-mediated degradation of p27/p21,
- Signal Transduction,
- Ubiquitin-dependent degradation of Cyclin D,
- Evasion of Oxidative Stress Induced Senescence Due to Defective p16INK4A binding to CDK4,
- Cellular responses to stress,
- Evasion of Oxidative Stress Induced Senescence Due to p16INK4A Defects,
- Oncogene Induced Senescence,
- Reproduction,
- Cellular Senescence,
- Evasion of Oxidative Stress Induced Senescence Due to Defective p16INK4A binding to CDK4 and CDK6,
- Meiosis,
- Aberrant regulation of mitotic cell cycle due to RB1 defects,
- Generic Transcription Pathway,
- Meiotic recombination,
- Aberrant regulation of mitotic G1/S transition in cancer due to RB1 defects
