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- B4bed3c075436ae85b8c7c9c0ab9eb153 NCIT_P378 "NCI" @default.
- B4bed3c075436ae85b8c7c9c0ab9eb153 type Axiom @default.
- B4bed3c075436ae85b8c7c9c0ab9eb153 annotatedProperty IAO_0000115 @default.
- B4bed3c075436ae85b8c7c9c0ab9eb153 annotatedSource NCIT_C19816 @default.
- B4bed3c075436ae85b8c7c9c0ab9eb153 annotatedTarget "G1 Arrest consists of cellular biochemical mechanisms, responsive to diverse governing conditions (DNA damage, contact inhibition, growth factors, etc.), that control cellular progress through the G1 phase of the cell cycle. G1 progress is controlled by de/phosphorylated cyclin/CDK complexes. During G1, cycD/CDK phosphorylation of Rb/HDAC repressor permits E2F/DP1 transcription of genes that promote the G1/S switch and DNA replication. p53 induces p21 inhibition of cycD/CDK; Mdm2 inhibits p53/p21. TGF-b induces p15 inhibition of cycD/CDK. cAMP induces p27 inhibition of cycD/CDK. GSK3b induction of cycD degradation, and INK4, Kip, and Cdc25A regulate cycD/CDK activity." @default.