Chapter 13: Problem 14
How do excitatory and inhibitory neurotransmitters differ in their effects on ligand-gated ion channels?
Chapter 13: Problem 14
How do excitatory and inhibitory neurotransmitters differ in their effects on ligand-gated ion channels?
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Get started for freeIntracellular receptors A. usually bind hydrophobic ligands. B. may be located either in the cytosol or nucleus in unbound state. C. when bound to their ligand, regulate gene transcription. D. when bound to their ligand, function as dimeric complexes binding to specific DNA sequences. E. all of the above.
Cells can terminate signal transduction by cell surface receptors by A. reducing agonist availability in the vicinity of the target cell. B. internalizing and degrading the receptor-agonist complex. C. modifying the receptor so that it is inactive or desensitized. D. all of the above. E. none of the above.
The ErbB/HER family of receptor tyrosine kinase genes are linked to many different types of human cancers. Overexpression of any of these genes would lead to an increase in the various receptors. ErbB2 encodes the HER2 protcin. This receptor does not bind any known extracellular growth factor, but it does form dimers with other growth-factor-bound HER receptors. Even modest overexpression of HER2 can alter normal cell growth regulation. Ras protein is a critical regulator in cell proliferation, and its activity is enhanced by activated tyrosine kinase. Elements of its action include all of the following except A. formation of cyclic GMP. B. adaptor proteins binding to phosphorylated ryrosines on receptor tyrosine kinase. C. recruitment and stimulation of Ras-activating protein. D. exchange of GDP for GTP on the Ras protein. E. initiation of a cascade in which several kinases are activated sequentially by phosphorylation.
Growth hormone releasing hormone (GHRH) produced by the hypothalamus binds to its pituitary receptor and leads to the production of growth hormone (GH) because of increase in cyclic AMP. Certain pituitary tumors result in hypersecretion of GH because of a mutation that produces a \(G_{s}-\alpha\) protein with a greatly diminished GTPase activity. Elements leading to increased cyclic AMP in response to GHRH binding to its receptor include A. activation of a monomeric G prorein. B. activation of adenylate cyclase by \(\alpha_{s}\) -subunit of a \(\mathrm{G}_{s}\) protein. C. activation of cyclic nucleotide phosphodiesterase. D. activation of protein kinase A. E. $ all of the above.
Manic depression may be caused by overactiviry of certain central nervous system cells, perhaps caused by abnormally high levels of hormones or neurotransmitters which stimulate phospholipidbased signal transduction (c.g., from phosphatidylinositol [PI]). Lithium has been used for many years to treat manic depression. In the presence of \(\mathrm{Li}^{*}\), the PI system is slowed despite continued stimulation and cells become less sensitive to these stimuli. Li \(^{+}\) may have two functions, inhibition of the phosphatase that dephosphorylates inositol trisphosphate and direct interference with the function of G proteins. Which of the following statements concerning G proteins is correct? A. G proteins bind the appropriate hormone at the cell surface. B. GTP is bound to G protein in the resting state. C. \(\alpha\) -Subunit may be cither stimulatory or inhibitory because it has two forms. D. Adenylate cyclase can be activated only if \(\alpha\) - and \(\beta\) -subunits of \(G\) protein are associated with each other. E. Hydrolysis of GTP is necessary for G protein subunits to separate.
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