5 Results in 8 T cell receptor complex 19 10 Binds to Results in HH Activated ZAP-70 phosphorylates adaptor proteins •1,2,3,4 = Components •5= this binds to '6' along with "I' • 6= what does 'I' and 's bind to •7,8,9,10 = Signal transduction steps
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- 47. Order the sequence of Canonical signaling via Frizzled receptors. i) β-catenin can now promote proliferation and stem cell state ii) Frizzled receptor signals for dishevelled and axin binding to itself iii) LRP assisted with Wnt binding to frizzled receptor iv) Preventing the activation of GSK-β which signals for phosphorylation A. iii ->ii-> iv-> i B. iv-> iii -> ii-> i C. i-> ii-> iv-> iii D. iii-> iv-> ii-> iMAKE CONNECTIONSPDGF signals cells by binding toa cell-surface receptor tyrosinekinase. If you added a chemicalthat blocked phosphorylation,how would the results differ?(See Figure 11.8.)3. The role of the cytoskeleton in Hedgehog signaling (actin rearrangements, microtubules)a. The Smoothened protein localizes to the primary cilium of the target cells. Suppose there is amutation that impairs a protein involved in basal body formation. How do you think would thisaffect signaling through Smoothened? Make sure to define basal body, explain its function, andrelate it to Smoothened signaling. b. Cos2 and Fu bind to microtubules, localizing Ci/Gli to the cytoplasm. How do you think a mutationin a microtubule associated protein (MAP) that functions to stabilize microtubules would affectboth the microtubules and Hedgehog signaling? Make sure to describe the role of the protein,regulation of microtubule dynamics, and how this might affect cells when Hedgehog is bothpresent and absent.
- 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.Where do DAG and IP3 originate? They are formed by phosphorylation of cAMP.' They are ligands expressed by signaling cells. They are hormones that diffuse through the plasma membrane to stimulate protein production. They are the cleavage products of the inositol phospholipid, PIP2.Cite evidence supporting a long evolutionary history for cell signaling molecules.
- In what important way does receptor-mediated endocytosis differ from phagocytosis? It transports only small amounts of fluid It does not involve the pinching off of membrane It brings in only a specifically targeted substance It brings substances into the cell, while phagocytosis removes substances.What property prevents the ligands of cell-surface receptors from entering the cell? The molecules bind to the extracellular domain. The molecules are hydrophilic and cannot penetrate the hydrophobic inferior of the plasma membrane. The molecules are attached to transport proteins that deliver them through the bloodstream to target cells. The ligands are able to penetrate the membrane and directly influence gene expression upon receptor binding.Name and define (briefly) the four different types of receptors involved in Cellsignaling. Give an example of a ligand and specific type of receptor (where would you find the receptor?) for one of the receptors defined.
- ), 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?).One important role of Fas and Fas ligand is to medi-ate the elimination of tumor cells by killer lymphocytes.In a study of 35 primary lung and colon tumors, half thetumors were found to have amplified and overexpressed agene for a secreted protein that binds to Fas ligand. How doyou suppose that overexpression of this protein might con-tribute to the survival of these tumor cells? Explain yourreasoning.Define Transmembrane JAK-STAT binding receptors?