To examine: whether the statement “in theregulation of molecular switches, protein kinases andguanine nucleotide exchange factors (GEFS) alwaysturn proteins on, whereas protein phosphatases andGTPase-activating proteins (GAPS) always turnproteins off" is true or false.

Small intracellular signalling molecules called second messengers are released in response to…

Answered: To examine: Whether the statement “in…

To examine: Whether the statement “in the regulation of molecular switches, protein kinases and guanine nucleotide exchange factors (GEFS) always

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter4: Principles Of Neural And Hormonal Communication

Section: Chapter Questions

Problem 5RE: Second-messenger systems ultimately bring about the desired cell response by inducing a change in...

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Please note whether each protein is either a Kinase (K), ATPase (A), GTPase (G), Membrane protein (M). Some proteins may need more than one letter: Dynamin [Choose ] Porin [Choose ] EGF Receptor [Choose ] CD4 [Choose ] P-glycoprotein [Choose ] Rho [Choose ] <
"In the regulation of molecular switches, protein kinases and guanine nucleotide exchange factors (GEFs) always turn proteins on, whereas protein phosphatases and GTPase activating proteins (GAPS) always turn proteins off" is true or false.
To examine: Whether the statement "protein tyrosine phosphatases display exquisite specificity for their substrates, unlike most serine/threonine protein phosphatases, which have rather broad specificity" is true or false.
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 MEK
When a trimeric G protein is activated by GPCR? The three subunit of the G protein remain tightly associated with each other; the GDP bound to the a subunit is phosphorylated to form bound GTP; it dissociates into a free B subunit and an ay subunit Options: hydrolyzed, cleaves, phosphorylate, dephosphorylates, folds, glycosates; gtp, gdp, cgmp, atp, adp, camp; cleaves, phosphorylation, dephosphorylation, unfolds, glcosylates, deglycosylate; leucine kinases, glycine kinase, Tyrosine kinases, valine kinase; triimetization, dimerization, monomerization
GTP binding proteins are molecular switches. How do GTP binding proteins work? Provide two examples of GTP binding proteins that function in intracellular protein transport. Make a drawing that illustrates the function of each of these proteins in their respective roles. Predict the direct outcome of a mutation that: Inhibits GTPase activity Inhibits interaction with the GEF
Although purified actin can assemble reversibly in vitro, various actin-binding proteins regulate the assembly of actin filaments in the cell. Predict the effect on a cell’s actin cytoskeleton if function-blocking antibodies against each of the following were independently microinjected into cells: profilin, thymosin-β4, CapZ, and the Arp2/3 complex.
. which of the following statements about heterotrimetric G proteins and their receptors is incorrect? A: when GTP binds to the alpha subunit of the G protein, the beta-gamma subunit dissociates from the alpha subunit B: G-protein coupled receptors contain nine transmembrane alpha helices C: binding of arrestin causes removal of the receptor from the membrane D: G protein- coupled receptors may be desensitized by serine phosphorylation I had chosen option A and got it wrong. What is the Correct answer and explain how it is. Also, where did i go wrong in choosing option A?
Please asap
Atherosclerosis can obstruct or block flow in arteries, including those that provide oxygenated blood to the heart. Elevated levels of [ Select ] ["LDL, and VLDL", "HDL"] are associated with atherosclerosis, most likely because of their role in delivery of lipids to peripheral tissues and cells. Smooth muscle cells are recruited to the site of damage, where they [ Select ] ["induce apoptosis of endothelial cells", "proliferate"] , hence expanding the extent of the lesion.
An SH2-containing protein contains a mutation that changes its binding pocket such that tyrosine and phosphotyrosine bind with equal afﬁnity. As a result, MEK activity: does not change with receptor dimerization and transautophosphorylation decreases due to changes in Raf activation increases with ligand binding-induced dimerization decreases due to allosteric inhibition of SH2-domain binding
For each of the following, describe the path the protein takes to its final destination in the cell.Drawings are strongly recommended!Proteins: 1) Hedgehog (released from the signaling cell), 2) Smoothened, 3) Ci/GliYour answers should include the following if they apply for each protein:o Sorting sequences and how the protein knows where to go at each step (what recognizesdifferent sorting sequences/tags)o How/when the protein is inserted into the membrane (if it is a membrane protein)o What organelles the protein passes through on its way to its final destinationo How the protein is transported (vesicles? translocons? etc.), including a role for microtubuleso How the protein might be modified in each organelle it passes througho What other proteins are involved in transport and how the system is reset to allow for otherproteins to be transported