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Lecture

Biol 314 - Definitions (Ursini Section)

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Department
Biology (Sci)
Course
BIOL 314
Professor
Thomas Duchaine
Semester
Fall

Description
Definitions: Signal transduction: When a cell receives an extracellular cue which ittransduces into the cell to affect intracellular signaling pathways. End results: Affected gene expression. Tumor Virus: A cell-free filtrate held to be a virus that is responsible for a specific neoplasm in humans or animals. A virus may be tumor forming depending on species (Cold virus causes tumor in mice). Neoplasm: Tumor Mitogenesis: Induction of mitosis. c-Src: Src Kinase promotes mitogenesis. Off state: On State: - CSK phosphorylates - Protein Tyrosine Phosphatase Y527. dephosphorylates Y527 - Y527 binds Src SH2 - Release Kinase domain domain (Active site exposed) (intramolecular) - Tyrosine Kinases - Active site closed phosphorylate Y416 in active (Inaccessible to site tyrosine residues) (Increases Src kinase activity) v-Src: An analog of c-Src found in tumors. Y527 domain is absent. Kinase domain is constitutively active in the absence of external mitogenic stimuli. v-Src is an oncogene. MMTV Mouse Mammary tumor virus Milk-transmitted retrovirus. MMTV promoter Highly associated with the mammary gland, but doesnot depend on pregnancy/lactating. Facilitates experiments on the mammary-epithelial specific expression of genes in transgenic mouse models. Murine Polyomavirus Transforms numerous epithelial cells in mice. Middle T antigen Prominent oncogene. Induces fast transformation by recruiting c-Src andkeeping it active. Src phosphorylates 2 tyrosine, Activating pl3 kinase & Ras. ~~> Tumor! Phenocopying Epigenetics mimics genotype. P53 Induced by DNA damage or viral infection that blocks cell cycle progression (G1 or G2) until DNA is repaired or itinduces apoptosis of virally infected cells. P53 is NOT an oncogene! P53 inactivating Their action results in loss of p53 cell cycle checkpoint. proteins Virally infected cells evade cell cycle arrest andapoptosis. - Increased genomic instability, accumulation of mutations in daughter cells. Work by: 1. Sequestering p53 o Large T antigen (SV40) o E6 (HPV) o E1B (EBV) 2. Inducing degradation via MDM2 by sequestering USPs(De- ubiquinating enzymes) o EBNA1 (EBV) 3. Blocking p53 DNA-binding activity o NS5A (HCV) pRB A tumor suppressor that mediates G1 checkpoint controls Rb=retinoblastoma Activation of Cyclin CDK leads to phospholytation of Rb Off: On: - Underphosphorilated - Phosphorylated Rb releases E2F. Rb binds & - E2F is active. inactivates E2F TFs. - E2F an induce transcription of - Cell remains in G1. genes required for progression into S phase (fos, myc, cyclin E, cyclin A) Tumor Viruses & Rb Tumor viruses will block Rb, leading to loss of G1checkpoint. HPV: Oncovirus expresses proteins that bind to Rb, releasing E2F EBV: Oncovirus express proteins reducing p16 expression.P16 turns off CDK. CDK cannot phosphorylate E2F. Activate E2F Cell procedes into S-phase. Cyclin/CDK complexes Viruses affect Cyclin CDK complexes to highjack cell cycle checkpoints. EBV EBV (BHRF1) protein is a viral BCl2 homologue. Cannot be inactivated by BH3 containing protens. Increases cellular BCL2 expression. Binds Cyclin A/CDK 2 and stimulates its Kinase activity. HTLV Increases Cellular Cyclin D1 expression KSHV KSHV protein (v-FLIP) encodes a viral protein thatinhibits FAS- mediated apoptosis. Expresses v-Cyclin, Cyclin D1 homologue. Cytotoxic genes Genes toxic to a cell Definitions: Phosphatidylinositol A negatively charged phospholipid that is found inall eukaryotic membranes Phosphatic acid backbone, linked to an inositol molecule via phosphate head group. Unlikely to have a structural role in membrane because present at low level. Steady state maintained. Myoinositol A six carbon carbohydrate molecule with OH groups on each carbon. Inositol Kinases Add Phosphate groups to carbons. Activity regulatedby intracellular signaling pathways. Inositol Phosphatase Removes phosphates on carbon. Activity regulated byintracellular signaling pathways. Phosphatidylinositol Signaling pathway activated by Phosphatidylinositol(PI) which Signaling regulates numerous biological processes including: - Proliferation - Survival - Cell motility Mediated by switches from PI to PI 4-Phosphate to PI 4- bisphosphate. PLC/Phospholipase C Cleaves PIP to generate IP and DAG 2 3 IP3 Second messenger, potentiates calcium signaling. - Opens IP R3channel, calcium leaves ER. - STIM1 then goes to ER/plasma membrane contact sitesand 2+ opens ICRAC(Ca channel). Extracellular Ca enters cytoplasm. Increased calcium levels in cell regulates large amount DAG Second messenger GPCR G protein coupled receptors Seven-trans membrane domain receptors located on plasma membrane. Undergo a conformational change upon ligand binding, alpha subunit dissociates, can activate genes. Activates many PLC family members PLCγ Only member with SH2 domain Amplify Binds to phospho-tyrosine on RTK PLC RTK Phosphorylates tyrosine, activating PLCγ and bringing it signaling clo
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