Explain the signaling steps that take place after the EGF receptor is dimerized, up to the poiunt when Ras gets activated. Draw a schematic to make it easier for your classmates to understand.
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5. Explain the signaling steps that take place after the EGF receptor is dimerized, up to the poiunt
when Ras gets activated. Draw a schematic to make it easier for your classmates to understand.
6. Explain why the RTK signaling pathway includes the extra complication of having a protein (Ras)
that switches between GTP- and GDP-bound states.
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- Binding of a ligand (like TGFA) to a receptor tyrosine kinase (RTK) causes all of the following except (can use cell): OA. Dimerization of the receptor B. Auto-phosphorylation of the receptor O C. Activation of Ras through an interction with GRB2 (an adaptor) and SOS (a GEF) proteins. O D. Activation of heterotrimeric G proteinsAberrant 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.)1A. If Creb upregulates gene T with acetylcholine stimulation, what happens to T when cAMP phosphodiesterase is always active compared to normal? 1B. If Creb normally upregulates expression of gene Y with adrenaline stimulation, what happens to gene Y if PKA has a nonfunctional NLS compared to normal signaling? Choices are: A. Stays the same B. Decreased expression C. Increased expression
- 1. Which of the following signaling events is NOT engaged downstream of phospholipase C (PLC)-gamma activation? a. Calcium ion (Ca2+) release from the endoplasmic reticulum (ER) b. Heterodimerization of the subunits c-Fos and c-Jun to form the transcription factor AP-1 c. IkappaB degradation and resulting translocation of NFkappaB into the nucleus d. Recruitment of protein kinase C (PKC)-theta to the plasma membrane e. PIP3 generation at the plasma membrane which recruits and activates Akt, leading to cytoskeletal remodeling8. Explain the steps that lead to phosphorylation (activation) of Akt by EGFR receptor. 9. Explain the difference between the heterotrimeric G-protein of a G-protein coupled receptor and a small G-protein like Ras. 10. Explain how binding of odorants to their receptors triggers activation of adenylate cyclase.G protein coupled receptors play an important role in signal transduction in many cells. Label the four essential components of the G protein coupled receptor signaling system (blanks a-d in the picture) by choosing from the menus below. a b b Each answer will be used at most once, while some will not be used at all (select one for each): Group of answer choices transcription factor с transcription factor Show Transcribed Text d transcription factor B C. transcription factor G protein second messenger G protein second messenger IE G protein second messenger G protein second messenger receptor receptor receptor receptor enzyme enzyme enzyme enzyme steroid hormone steroid hormone steroid hormone steroid hormone
- 10. Explain how scaffold proteins help the efficiency of the AMP kinase cascade. Why is it important that the interaction of the scaffold with the MAP kinases is NOT a very stable interaction?1.Describe in detail the signal transduction pathway that leads to activation of either PKA, Kinase or PC. 2. Describe in detail the signal transduction pathway that leads to activation of MAPKinase or Akt/PKB. 3.Describe the similarities and differences in the structures of GPCRs specific for various ligands including the extracellular , transmembrane , and intracellular domains.1. Based on the following description, draw the cell signaling pathway described (you only need to draw the pathway in one cell, but show the type of signaling described – you may need 2 diagrams). Compound X is released from cells in the pancreas and activates cells in the liver. What general type of cell signaling is this? When compound X binds its receptor on a liver cell, some of the amino acids (Y – one letter amino acid code) on the cytoplasmic side of the receptor are phosphorylated. Label what type of receptor this is. This leads to the receptor activating a cytoplasmic protein F which then activates a kinase K which then activates protein Z (diagram what is happening here – how is protein Z activated). Protein Z activation results in several genes being expressed. Label all your parts (don’t forget to label the ligand). Circle the signal transduction pathway and put a box around the cell response.
- The figure below shows how normal signaling works with a Ras protein acting downstream of a receptor tyrosine kinase. CYTOSOL active receptor tyrosine kinase Taratas THERI signal molecule 00 active signaling Q Search active Ras protein GTP 99+ Į SIGNALING Il app.honorlock.com is sharing your screen. ✡ active signaling protein Y a3) The “Met" receptor is a membrane receptor protein responsible for initiating signal transduction pathways that cause cells to divide, among other things. After the Met receptor has been stimulated by its specific growth factor, another protein called c- Cbl will bind to the Met receptor. C-Cbl will then attach a chain of small proteins called ubiquitin to the Met receptor. These chains of ubiquitin help the cell recognize that the Met receptor should undergo receptor-mediated endocytosis, which eventually leads to the destruction of the Met receptor. Circle any answer or answers that include mutations that could cause the cell to potentially become a cancer cell. A) a mutation causing there to be too much ubiquitin protein produced. B) a mutation causing c-Cbl to be inactivated. C) a mutation causing ubiquitin to be inactivated. D) a mutation causing there to be too few Met receptors produced. E) a mutation causing the Met receptor to no longer be able to bind to its growth factor.…Compare and contrast GPCR and RTK signaling. What role does GTP play in each? What role does phosphorylation play? How do these two signaling types compare to steroid signaling with respect to gene activation?