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1a. Contrast the activation of cytokine receptors to the activation of receptor threonine kinases.
b. We discovered a new cytokine that stimulates cancer cell growth. Now we want to determine if the JAK/STAT pathway is activated after stimulation. In the lab we have a small molecule that can competitively bind to SH2 domains. Explain where and how in the pathway this inhibitor would be effective.
Step by step
Solved in 3 steps
- a.What would happen if IKKbeta did not phosphorylate IkappaB? b.Why is it so hard to make cytokine therapies? c.Why would you use the MyD88 independent pathway versus the MyD88 dependent pathway?RTK: What would the following double mutations mean for the status of the signaling pathway, and the phosphorylation of MAPKK (MEK)? 1. Ligand is bound to the receptor; MAPK T120A mutation (T120 is normally phosphorylated by MAPKK) a) Pathway ON (final output is achieved) b) Pathway OFF (no final output) c) Phosphorylation of MAPKK MEK d) NO Phosphorylation of MAPKK MEK 2) Ligand is not bound to the receptor; MAPKKK T132E mutation (T132 is normally phosphorylated by Ras) a) Pathway ON (final output is achieved) b) Pathway OFF (no final output) c) Phosphorylation of MAPKK MEK d) NO Phosphorylation of MAPKK MEKActivation of certain GPCRs triggers an intracellular signaling mechanism that involves activation of adenlyl cyclase and an increase of cAMP. Which of the following statements best describes the the events that follow such a cAMP increase? a.) The cAMP increase leads to activation of protein kinase C. b.) The cAMP increase leads to activation of the release of the gamma subunit from the GPCR. c.) The cAMP increase leads to activation of protein kinase A.
- 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 expression47. 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-> i1.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.
- You are studying the role of CAMP in cell signaling. You hypothesize that 2 intracellular signaling proteins, named GO and TIGERS, interact with each other when cells are treated with an extracellular source of CAMP. The two proteins were tagged with CFP or YFP (CFP = cyan fluorescent protein; YFP = yellow fluorescent protein). CFP is excited by 435 nm light and emits lights at 480 nm. YFP is excited by 480 nm light and emits light at 535 nm. 400 500 Wavelength of Emitted Light 400 500 Wavelength of Emitted Light 600 600 Fluorescence 400 400 500 Wavelength of Emitted Light 600 500 Wavelength of Emitted Light 600 Fluorescence Intensity 400 500 Wavelength of Emitted Light 600 Figure Legend. A. Cells expressing GO-CFP irradiate with 435 nm light. B. Cells expressing TIGERS-YFP and irradiated with 435 nm light. C. Cells expressing TIGERS- YFP and irradiated with 480 nm light. D. Cells expressing GO-CFP and TIGERS-YFP and irradiated with 435 nm light. E. Cells expressing GO-CFP and…The hypothesis for the experiment shown in the picture  is that the TamC3 and TamR3 cell lines function, and grow the absence of estrogen, receptor function. Reduced reliance on estrogen, receptor signaling alters mTOR pathway activity. If this hypothesis is true, then mediators of mTOR signaling (Akt or p70S6K) should have reduced levels of phosphorylation . A. Where would you look to see this? B. To what degree does the data in the picture support the hypothesis?Researchers have found that a certain signal transduction pathway, illustrated in the figure below, may be responsible for the development of cancer in pancreatic cells. In normal pancreatic cells, where the pathway remains inactive, a membrane-bound receptor called Ptc inhibits a downstream protein known as Smo. The inhibition of Smo blocks the activa- tion of a complex of proteins known as the HSC, which results in the cleaving of one of its proteins called Ci. The cleaving of Ci, in turn, prevents the pathway from initiating the syn- thesis of division-facilitating enzymes. A Ptc B Smo с inhibition D A model of a Ptc signal transduction pathway under normal conditions. HSC Ci cleavage A certain protein called the Hedgehog protein (Hh) is found to activate this signal transduction pathway and trigger uninterruptable cell division. cell division not initiated Which of the following describes the most plausible mechanism by which Hh triggers uninterruptable cell division? Hh binds to…
- This is a tyrosine kinase receptor. a. Briefly describe the action of the receptor upon binding to the logand. b. There are several intracellular pathway possibilities for downstream responses. How might this receptor be able to selectively activate one particular pathway over another?Put the following steps for the outline of the growth factor signaling pathway in order: Map Kinase Kinase is Phosphorylated Proteins involved in gene transcription are activated Growth factor binds to its receptor in the cytoplasmic membrane Receptor recruits adaptor protein and GEF Autophosphorylation of tyrosine residues on the receptor Structural change of the receptor activates Tyrosine Kinase Map Kinase Kinase Kinase is phosphorylated Ras, a small GTPase, is activated by the exchange of GTP for GDP Map Kinase is Phosphorylated Map Kinase enters the nucleusPathway analysis: Link the protein names to the correct statements by interrogating the depicted pathway. Options: A. RTK Receptor Threonine Kinase B. GEF Guanidine Exchange Factor C. PLC Phospholipase C D. GAP GTPase Activating Protein E. Gαi F. Raf Rapidly Accelerated Fibrosarcoma G. PAK1 p21 Activated Kinase H. WASP Wiscott Aldrich syndrome protein I. RTK Receptor Tyrosine Kinase J. GPCR G-protein Coupled Receptor K. Steroid Receptor L. Phosphatase M. MEK1 (Mitogen-Activated Protein) Kinase/ERK (Extracellular Signal-Regulated Kinase) Kinase 1 N. AC Adenylyl cyclase O. IP3R IP3 Receptor P. ERK1/2 Extracellular Signal-Regulated Kinase