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- Use the SGF-signaling pathway image as a reference, to answer the following questions. Use the data provided to EXPLAIN if the cell will get to the response step or not. Keep in mind the purpose of this pathway is to cause skin cell division Growth Factor (GF-signal) Activation of GF Receptor (RTK-receptor) To cause Cell proliferation/cell division (Response) Plasma membrane Sos Grb2 (Ras GEF) (adapter) Raf МАРКK Mek МАРКK Activation of target genes that stimulate proliferation Erk МАРК You have a skin cell in a dish and have added Neural Growth Factor (NGF) to the cell media (the liquid the cell needs to live).A tumor cannot grow to be very large without the development of new blood vessels (angiogenesis) to provide access to oxygen and nutrients. During the 1990s, it was discovered that Factor X stimulates the proliferation and migration of the cells that form blood vessels, thereby inducing the formation of new blood vessels. Factor X binds to specific receptor tyrosine kinases (RTKs) on the cell surface and causes the RTKs to dimerize and become active, initiating an intracellular signaling cascade that stimulates cell division and inhibits apoptosis. Many cancer cells secrete high levels of Factor X, and increased Factor X expression in a tumor is correlated with a poor medical outcome for the patient. Some evidence suggests that blocking Factor X-dependent signaling may prevent the formation of new blood vessels and lead to the death of immature blood vessels without disturbing mature blood vessels. You work for a biotechnology company that seeks to create anticancer drugs that…Because of oxygen and nutrient requirements, cells in a tissue must reside within 100 μm of a blood vessel. Based on this information, explain why many malignant tumors often possess gain-of-function mutations in one of the following genes: βFGF, TGF-α, and VEGF.
- Explain with specific examples how oncogenic receptors would promote cellular proliferation in the absence of external growth factorsDistinguish between What is known of CD105 (endoglin) as an hepatcellular carcinoma marker and it’s potential as a drug target. Discuss: - Is anything known about its biology? E.g does it have known ligands and normal functions? - if you were to target it would you just use it to get growth inhibiting compound into the new blood vessels or is CD105 required for neovascularization?Use the SGF-signaling pathway image as a reference, to answer the following questions. Use the data provided to EXPLAIN if the cell will get to the response step or not. Keep in mind the purpose of this pathway is to cause skin cell division Growth Factor (GF-signal) Activation of GF Receptor (RTK-receptor) To cause Cell proliferation/cell division (Response) Plasma membrane Ras GEF ladapter) MAPIKK Mek MAPIK MAPK You have a skin cell that inject SGF protein directly into the cytoplasm but you do NOT put SGF in the media (the liquid the cell needs to live).
- Put the following steps for the outline of the growth factor signaling pathway in order: Map Kinase Kinase is Phosphorylated Proteins involved in gene transcription are activated Growth factor binds to its receptor in the cytoplasmic membrane Receptor recruits adaptor protein and GEF Autophosphorylation of tyrosine residues on the receptor Structural change of the receptor activates Tyrosine Kinase Map Kinase Kinase Kinase is phosphorylated Ras, a small GTPase, is activated by the exchange of GTP for GDP Map Kinase is Phosphorylated Map Kinase enters the nucleusIn the light of the mechanisms of signal transduction pathways, describe how: 1. the immune system is alerted and responds 2. immune responses against infected cells can lead to organ failureDescribe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.
- Aberrant signaling through the EGF receptor signal transduction pathway drives many forms of breast cancer, while misregulation of PI3K drives many prostate cancers. PI3K is one of MANY downstream effectors of EGF receptor signaling, and there are several known activating mutations of PI3K. Would a small molecule that targets PI3K be an effective treatment for a breast cancer that is driven by aberrant signaling through the EGF receptor? Briefly explain your choice. (THIS CAN BE DONE IN LESS THAN TWO SENTENCES, AND MINIMALLY IN ABOUT EIGHT WORDS.)Once an activated signaling pathway has elicited the proper changes in target gene expression, the pathway must be inactivated. Otherwise, pathological consequences may result, as exemplified by persistent growth factor initiated signaling in many cancers. Many signaling pathways possess intrinsic negative feedback by which a downstream event in a pathway turns off an upstream event. Describe the negative feedback that down-regulates signals induced by (a) erythropoietin and (b) TGF-β.E: Using either GPCRs (G-protein couples receptors) or RTKs (Receptor tyrosine kinases), describe: 1. How ligand binding activates the receptor. Ex: which proteins are involved? what changes can occur to the receptor after binding the ligand? 2. A signal transduction pathway that occurs due to the ligand binding (must include a secondary messenger). 3. Any cellular response due to the ligand binding. 4. A way that the signal pathway is regulated.