A mutated form of the a subunit of the heterotrimeric G protein has been identified. It isfound to readily exchange GDP for GTP even the absence of an activated receptor.a. What would be the effect on a signaling pathway containing the mutated protein? And in light ofyour answer would this protein more likely to function as an oncogene or as a tumor suppressor.Briefly explain your answer.b. A paper finds an interesting study where an analog of GTP (GTPYS,guanosine 5'-0-[gamma-thio]triphosphate) is used to alter G-proteinactivity. The authors claim that the data below suggest that it couldperhaps be used as a treatment for patients with the mutated a subunitas described above. What do you think?HO[P]OH OH ONOH OHGTPYSRate of HydrolysisTimeGTPI GTPYS

Heterotrimeric G proteins have 3 subunits; , and . GPCRs (G protein coupled receptors) are…

Answered: A mutated form of the a subunit of the…

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 1VCQ: Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is...

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I just read an abstract of the paper “Disulfide bond-disrupting agents activate the tumor necrosis family-related apoptosis-inducing ligand/death receptor 5 pathway” and noted that “DDAs and TRAIL synergize to kill cancer cells and are cytotoxic to HER2+ cancer cells with acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib.” For the last sentence, I am not sure the meaning of the “acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib”. Is the “acquired resistance ... to inhibitor” a good thing or bad thing, as far as the synergize effect of DDAs and TRAIL”? Hope that expert can help.
a. A typical cellular response of a mammary epithelial cell to EGF signal is proliferation. the Kd for the interaction between EGF and its receptor is 1x10^-10 M. Lets imagine that at least 25% of the receptors on a normal cell must be engaged by EGD in order to trigger the cellular proliferation response. What minimum concentration of EGF is required to reduce cell proliferation? (Show calculation). b. Mammary epithelial cancer cells have amplified levels of EGF receptors on their surface. If such a cell has 1000 EGF receptors, as compared to 200 receptors on a normal cell, what minimum concentration of EGF is required to induce cell proliferation in the cancer cell? [Show calculation]. Note that the same number of receptors (not percentage of receptors) must be activated to promote proliferation in normal cells and cancer cell. c. The ambient (unstimulated) concentration of EGF in mammary epithelial tissue is 1x10^-11 M. Will this level of EGF stimulate proliferation in normal…
TSC acts as a tumor suppressor by continually suppressing mTOR and must be inhibited in order for mTOR to be active. True or false, explain why
Signaling pathways often require receptor dimers to become active. What would be an advantage of the extrinsic apoptosis pathway requiring a trimer? I note from the article "Nature Reviews, Cancer 16:539, 2016" the following: The extrinsic apoptotic pathway, upon binding to their cognate ligand, death receptors such as tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor (TRAILR) and FAS can activate initiator caspases (caspase-8 and caspase-10) through dimerization mediated by adaptor proteins such as FAS-associated death domain protein (FADD). Active caspase-8 and caspase-10 then cleave and activate the effector caspase-3 and caspase-7, leading to apoptosis. I can't think of any other pathway that uses a trimer, so there must be a reason. Glad an exprt can help.
Explain why in cells that are genetically NF1–/–, basal levels of GTP-bound activated Ras are higher than normal and respond to growth factor stimulation by increasing rapidly to far higher levels.
Steroid hormones are required by the body at puberty and into adolescence to regulate growth and cell division at more rapid pace than in later life. This regulation occurs via their interaction with cellular receptors and the signaling cascades/pathways that follow. Describe for me the difference between the two major classes of steroids, anabolic and catabolic steroids. What might you expect the result of signaling cascades to be in cells receiving either anabolic or catabolic “signals”? (B) At some point in late adolescence, steroid production decreases by almost 100 fold, as we transition into “adulthood”. Why might we wish to stop these signals from constantly being in our blood stream, (like, Say, between 17-24 years of age)? What result might these steroids have on cancer cells where abhorrent signaling is already causing an increased rate of cell division/growth? Could steroid use result in Cancer?
Many malignant tumors are characterized by the activation of one or more growth-factor receptors. What is the catalytic activity associated with transmembrane growth factor receptors such as the EGF receptor?
''In the cellular regulatory pathways that controlcell growth and proliferation, the products of oncogenesare stimulatory components and the products of tumorsuppressor genes are inhibitory components.'' 'Is this statement true? Explain why or why not.
Describe 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.
which of hthe following would result in a persisting proliferation response to growth factor receptor activation after the ligand is no longer binding to its rceptor kinase? 1. Both a mutation that blocks the GTPas activity of Ras and a mutation that blocks the exchange of GDP with GTP would cause the response to persist. 2. a mutation that blocks the GTPas activity of Ras 3. neither a mutation that blocks the GTPas activity of Ras nor a mutation that blocks the exchange of GDP with GTP would cause the response to persist 4. a mutatiaon that blocks the exchange of GDP with GTP
Figure 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.
Studies suggest that the presence of oncogenic Ras is not sufficient to drive tumorigenesis. Instead, the activity of Ras needs to be amplified and sustained to induce pathological consequences. Recent studies have suggested a role for inflammatory stimuli on tumor development in the context of oncogenic Ras. Is the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?

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