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A. Name the two proteins that induce a negative feedback in this pathway and explain why both feedback mechanisms exist?
B. Discuss how a mutation resulting in an aberrant protein could cause changes in the cell cycle leading to uncontrolled cell division. Explain what the effect of the mutation would be on the protein’s function and what the effect will be on downstream proteins leading to enhanced cell cycle progression
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- Match the protein on the left with its primary role on the right PINK LAMP2A BCL2 ATF6 [Choose] [Choose] promoting UPR promoting apoptosis inhibiting autophagy inhibiting UPR inhibiting apoptosis mitophagy nonselective autophagy chaperone mediate autophagy [Choose]WRITE ABOUT A THEME: ORGANIZATION The properties oflife emerge at the biological level of the cell. The highly regulated process of apoptosis is not simply the destruction of acell; it is also an emergent property. Write a short essay (about100–150 words) that briefly explains the role of apoptosis inthe development and proper functioning of an animal, and describe how this form of programmed cell death is a process thatemerges from the orderly integration of signaling pathways.At any given time, intestinal crypts of mice com-prise about 15 stem cells and 10 Paneth cells. After celldivision, which occurs about once a day, the daughtercells remain stem cells only if they maintain contact with aPaneth cell. This constant competition for Paneth-cell con-tact raises the possibility that crypts might become mono-clonal over time; that is, the crypt cells at one point in timemight derive from only 1 of the 15 stem cells that existedat some earlier time. To test this possibility, you use theso-called confetti marker that upon activation expressesany one of three fluorescent proteins in the stem cells ofthe crypt. You then examine crypts at various times todetermine whether they contain cells with multiple colorsor only one color (Figure Q22–1). Do the crypts becomemonoclonal over time or not? How can you tell?
- Non-canonical Hedgehog signaling results in actin cytoskeleton rearrangements, leading to cellmovement and changes in cell shape. Describe how changes to the actin cytoskeleton lead to cellmovement and changes in cell shape.You do not need to draw out the signaling pathway again (#1b). Your answer should focus onthe changes to the actin cytoskeleton. Drawings will be helpful!IP3 binds to --- and DAG binds to O Calcium channel of SER/Protein Kinase C O Nucleus/Plasma membrane O G-protein/Protein Kinase C O Phosphatase/Protein Kinase C The inhibition that make permanentFigure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? Signaling molecule binding, dimerization, and the downstream cellular response. Dimerization, and the downstream cellular response. The downstream cellular response. Phosphatase activity, dimerization, and the downsteam cellular response.
- TNF-alpha treatment of prostate carcinoma, LNCAP cells decreases cell survival as shown in the graph below. Which of the following would you observe in these cells treated with TNF- alpha? Select all that apply TNF-a 120 100 80 - 60- 40- 20 - 24 72 (hrs) + Control - TNF-a 10ng + TNF-a 100 ng O Activation of extrinsic pathway of apoptosis O Activation of intrinsic pathway of apoptosis Activation of executioner caspases Recruitment of adapter protein FADD to the TNF-alpha receptor LNCAP cell viability (% of control)explain Mechanism of Myostatin Function & The PI3-K–Akt1 pathwayWhich phase are initially inhibited by Sic1.Phosphorylation marks Sic1 for ubiquitinylation by theSCF ubiquitin-protein ligase and proteosomal degradation,releasing activated S phase CDKs that trigger onset of theS phase
- In the MAPK pathway, GrB2 recruits _____. -GPCR -ERK1 -RTK -SOS# 3 You've engineered a mutant cell where the FADD adapter was truncated. The mutant FADD only contains the Death Domain, and lacks the Death Effector Domain. What is the most likely phenotypic outcome for this mutant cell when presented with the Fas ligand? 20 E O The Fas/FasL oligomer is formed, but apoptosis is blocked O The Fas/FasL oligomer is formed, and apoptosis is hyperactivated O The Fas/FasL oligomer is not formed, and apoptosis is blocked O The Fas/FasL oligomer is not formed, but apoptosis is hyperactivated F3 $ 4 DOD 000 R F4 % 5 F5 T BARAT 6 tv @ MacBook Air F6 Y & 7 F7 U * ➤11 8 F8 · 9 F911. Explain the role of cytochrome c, Bax/Bac, Fas receptor-ligand, caspases, IGFBP3 in causing apoptosis of cells, based on the figures given below. death ligand cytotoxic cell death receptor plasma membrane -granzyme B executioner caspase 3 initiator caspase 8 procaspases caspase 8 caspase 10 tBid executioner Bid cytochrome c procaspases Apaf-1 apoptosome caspase 9 ICAD lamin death substrates vimentin actin etc. Figure 9.34 The Biology of Cancer (O Garland Science 2014)