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Hedgehog - Cell signaling pathway
1) describe its normal function and mechanism, and 2) predict what may happen if certain proteins in the pathway become mutated to be constitutively active (activated even in the absence of the preceding step in the pathway) or inactivated. It will be clearest to include a drawing of the pathway.
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- 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.Cell signaling The maximum secretion rates of proteins are one type of limiting constraint on signal-ing processes since a cell cannot send a signal faster than it can secrete it. These maximum signalingrates can be estimated with maximum rates of transcription and translation. Consequently, proteins withstrong promoters can be synthesized at much higher rates. Immunoglobulins, which are important signal-ing molecules, have very strong promoters. Their maximum secretion rate is on the order of 2000 to 8000antibody molecules/cell/second, which corresponds to approximately 1 pg/cell/hr. Part AWhat would be the maximum signal (in pg/cell/hr) that a cell could send for the following situations: (1)Signal molecule A has a MW = 100,000 daltons and is secreted at a rate of 1000 molecules/cell/second. (2)Signal molecule B has a MW = 50,000 daltons and is secreted at 5000 molecules/cell/second.Part BWhich molecule is secreted at a higher rate? By how much?Part CIf equivalent fluxes of both…The output of RTK pathways is often the activation of MAP Kinase. Explain how MAPK can lead to activation of a specific subset of proteins, leading to distinct effects in different cell types in response to the same growth signal.
- Cancers are often caused by overactive growth factor receptor signaling (remember growth factor receptors are enzyme-linked receptor pathways). If you were able to use gene therapy to overexpress a particular protein in a cancer cell, which of the following might be useful to overexpress in order to combatt cancer? a GAP that acts on Ras a phosphatase that acts on GPCR a protein that enhances the activity of Akt a ubiqtuin ligase that acts on the MAPK phophataseI 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.Part A (Short Response): You are developing a TGF-β agonist, but you don’t yet know which specific proteins it is signaling through. You want to do a single Western blot to measure changes in signaling activity, regardless of which pathway is being activated. For which protein involved in these pathways could you measure the levels in the nucleus of cells and be confident in your results? Why? This part was already posted on chegg, but I didn't understand the answer. I need a thorough explanation, so I can fully understand. Part B (Short Response): There have been many attempts to block TGF-β signaling in cancer through many different mechanisms, but none of been very successful. Why do you think this is? I know they have gotten close to being successful, but I don't know what preventing their success.
- 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 GTPYou work for a large biotechnology company that is studying viruses, vaccines, and small molecule inhibitors. You are asked to give an overview of cell signaling as it relates to the coronavirus and young adults. a) Describe cell signaling pathways (e.g., at least 3) that are likely manipulated during a coronavirus infection. In your description, include how the pathways are involved in antagonizing the host antiviral response.), create a simple flowchart depicting the MC1R pathway. There should be a minimum of five steps in the pathway. Be sure to include reception (protein binding to its ligand), a portion of the transduction pathway (what’s the intracellular reaction? What molecule works intracellularly?), and the cellular response (What’s produced from the cell?).
- 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.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.Help constructing a concept map? Example provided below. Many studies have indicated that autophagy and apoptosis play an important role in the pathogenesis of spinal cord injury. In recent years, research on autophagy-related signal transduction pathways has demonstrated that the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway is closely associated with the initiation of autophagy. However, the mechanism of the pathological relationship between this signaling pathway and apoptosis in spinal cord injury is unclear. In this study, we used an in vitro model of spinal cord injury to observe the mechanism of the PI3K/Akt/mTOR signaling pathway and the apoptosis of neurons via the mitochondrial pathway. Mitochondrial pathway apoptosis-related proteins were detected by western blot. Akt and mTOR phosphorylation levels peaked 4 h after mechanical damage and then decreased. Following administration of the PI3K-specific…