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Lecture 19 - Chapter 17&18 - Mitogens and Apoptosis - March 26.docx

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York University
BIOL 2021
Patricia Lakin- Thomas

March 26, 2013 Lecture 19: Chapter 17 – Cell Cycle Division and growth  Mitogens in G  Mitogen  cell surface receptor such as RTK RasMap Kinase Pathway  gene regulation  “Immediate early” genes – Myc = gene reg protein  Myc = G1 cyclin expression  G1-Cdk activation (brings us to the end of G1  Fig 17-62  G1-cdk phosphorylate Rb (Retinoblastoma protein) o Rb phosphoryltated  E2F protein (gene reg protein) o Activated E2F  increase gene expression (G1/S cyclin and S cyclins, proteins for DNA synthesis, etc)  G1/S phosphorylate and inactivate APC/C-cdk1 and inactivate CKI o S cyclin accumulates  S-cdj activation  S phase  Summary posted on moodle  Fig 17-16*** DNA Damage checkpoint  Late G1 (start) and the G2/M boundary  Detects damaged DNA and unreplicated DNA  Fig 17.63 o P53 – guardian of the genome o If phosphorylated, p21 will be transcribed and inhibit the cycle  ATM/ATRChk1/Chk2phosphorylate p53  Activates and stabalizes p53  transcription of p21 = CKI protein  inhibits cdks  DNA damage  cancer causing mutations  P53 mutations found in half of all cancers  Arrested at the checkpoint o DNA damage repaired  Checkpoint lifted – cell cycle continuous o DNA damage irreparable?  Unicells – will resume cycling anyway  Multicellular – apoptosis Control of Growth  Unicells – nutrients control growth and division  Multicells – growth factors (extracellular signals)  bind to receptors  stimulate synthesis of proteins and other macromolecules o Growth factors  receptor  PI3-Kinase  ToR activations  TOR is a Kinase, activates targets to stimulate metabolism and protein synthesis  Figure 17-65  Ribosome synthesis  activate ribosome protein S6  Activate translation initiation factor eIF4E  Also nutrients ?  Coordinate growth and division  Ras  MAPK  cell division  Ras PI3-Kinase growth Chapter 18: Apoptosis  Regulate division, growth, survival, death  In adult: balance survival and death  Programmed cell death: usually apoptosis Apoptosis  Morphology: o
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