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19 Cards in this Set
- Front
- Back
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What are the characteristics of Cell Transformation?
How is Rous Sarcoma Virus relevant? |
Cell transformation = cells going from normal to malignant
Characterized by: Loss of contact inhibition Immortilization Serum Independence Anchorage independence Increased Glycolysis All of these chacteristics can be induced by Rous Sarcoma Virus (virus can cause tumors) |
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What is the action of pp60src?
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Phosphorylates at tyrosine residues
IT'S A TYROSINE KINASE! |
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How does the viral version (v-src) of pp60src differ from the cellular version (c-src)?
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Viral version can't be shut off. Lacks a phosphorylation site required for it to become inactive. When this site is phosphorylated, the kinase shuts off.
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What is a proto-oncogene?
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Normal gene that can becomes an oncogene after spontaneous mutation (NO VIRUS REQUIRED)
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What are the effects of Epidermal GF?
Describe what happens when EGF binds its receptor. |
Growth stimulation
Activation of Glycolysis Increased Nutrient Transport Cell Differentiation EGF binds receptor, forms dimer with another receptor. Tyrosine Kinase Domain changes shape to bind ATP. Auto-phosphorylates at TYROSINE sites Then phosphorylates exogenous substrates |
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Describe how EGFr activity is regulated.
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Receptor activity occurs in proportion to amount of hormone present
Thus, allosteric regulation by EGF |
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How does the erythroblastosis virus differ from EGFr?
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It's missing ligand binding domain (part that binds EGF); doesn't need EGF to turn on. It's on ALL the time.
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What is the EGF receptor family? What do they all have in common? Difference?
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HER1, 2, etc.
All have tyrosine kinase domains; all dimerize; can dimerize with each other All bind different ligands! |
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What is the effect of trastuzumab on HER receptors?
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Trastuzumab is monoclonal antibody that interacts with HER2 receptor to inhibit cleavage/dimerization.
Can bring immune cells to surface of cancer cells. Can promote degradation of receptor. |
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How does Receptor Tyr Kinase interact with PLC-gamma?
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RTK phosphorylates and activates enzyme DIRECTLY.
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How does Receptor Tyrosine Kinase interact with Phophoinositides (p85/p110)?
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RTK Serves as docking site for enzyme, changes conformation of enzyme to active it.
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How does Receptor Tyrosine Kinase interact with Shc?
What are the consequences of this? What are the clinical applications of this? |
RTK phosphorlates Shc
Shc (adaptor protein) recruits proteins (Grb2, SOS) to interact with RAS-GTP RAS is a small G protein RAS-GTP-proteins then recruit Raf Then recruits MEK then Recruits MAPK Can go on to phosphorylate other stuff Known as TRIPLE KINASE CASCADE! Clinical application: EVERY constituent of this pathway is a target for anti-cancer therapies (they're all vulnerable to mutations resulting in cancer) |
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What does the SRC gene have in common with the p85, phospholipase-C, and Shc genes?
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They share common domains (SH domains) which are all targets for cancer drugs.
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Describe Receptor Tyrosine Kinase interaction with JAK.
What are the consequences of this? |
Hormone binds RTK
RTK is already bound to JAK RTK directly activates JAK JAK phosphorylates STAT STAT-Pi forms dimer with another STAT-Pi STAT dimer moves to nucleus, binds DNA STAT is a transcription factor |
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Describe the steps requires in insulin signaling.
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Insulin signaling intitiated by activation of insulin RTK!
Insulin binds Insulin RTK RTK auto-pi, then activates IRS-1 IRS-1 is docked with PI-3 kinase PI-3 kinase is activated Pi-3 kinase actives protein phosphatases; de-pi enzymes |
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How is the glucose lowering effect of insulin mediated? What does this require?
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Activation of skeletal muscle glucose transporters
Requires translocation of glucose transporters to cell surface |
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What is the effect of [glucose] on glucose transport?
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Glucose transport is independent of glucose transportation. Relies on number of glucose transporters AVAILABLE!
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How does impaired glucose absorption arise in Diabetes Mellitus II?
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Limited translocation of glucose receptors to cell surface.
Scientists unsure how insulin causes translocation. |
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What a mutation in STAT result in? Why?
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STAT is required for growth hormone signaling.
Mutated STAT would be associated with short stature, impaired immune function. |
