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Various mechanisms that help regulate the cell cycle by down-regulating the s phase cytoplasm. These mechanisms include the unbinding of receptors from ligands, digestion of receptors by proteasomes, dephosphorylation of tyrosine residues on receptors, endocytosis of receptors, slowing ras gtpase activity, and faster ras gtpase activity. Additionally, the document discusses the role of map kinase in initiating s phase by phosphorylating tcf and transcribing the c-fos gene, which ultimately leads to the formation of the ap1 transcription factor and the transcription of e-box proteins.
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RTK III: Mechanisms to Down-regulate Making S Phase Cytoplasm Mechanisms for Down-Regulation of the Cell Cycle
o It is possible for myc to bind to myc or MAX to bind to MAX (homodimers) using the leucine zippers on the molecules o When there is only MAX present, MAX-MAX homodimers are formed and bind to DNA, blocking the transcription of E-box proteins because there is no transcriptional activation domain o When myc is present, the myc-MAX homodimer forms and binds to DNA, transcribing the E-box proteins because myc has a TAD. This heterodimer is also a transcription factor that re-enters the nucleus and binds to the promoters of E box proteins. These proteins include: o elF4e -> promotes protein synthesis o ODC -> (ornithine decarboxylase) takes ornithine (from urea cycle) and produces polyamines (characteristic of S phase cytoplasm; involved in chromosomal condensation) o Cyclins o CDK phosphatase -> an enzyme that removes phosphase from CDK (cyclin dependent kinase) and activates them CyclinD – CDK4 -> phosphorylates Rb protein (retinoblastoma), which is normally bound to E2F. E2F then falls off of Rb and is involved in DNA replication. CyclinG – CDK2 -> phosphorylate histone kinases and p53 (turns on the p53 DNA damage checkpoint) Also involved in turning on molecules needed for chromosome condensation and the phosphorylation of nuclear lamins to change the nuclear shape.