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Which of the following is NOT considered a secondary messenger?
A. diacylglycerol
B. inositol triphosphate
C. CAMP
D.calcium ions
E . GTP
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- An active Gai ultimately prevents production of its pathways second messengers, which means those second messengers are unable to activate the enzyme O phospholipase C O protein kinase A O adenylyl cyclase phosphodiesterase protein kinase CAll of the following molecules can act as second messenger Except: O Enzyme O CAMP O Calcium ions OIP3 and DAG The site where a noncompetitive inhibitorWhich statement best describes the interaction that occurs as a result of the binding of a ligand to a ligand-gated ion channel receptor? A B с D ligand extracellular environment gate closed inactive ligand-gated ion channel receptor ions The process permanently opens or closes the ion channel. cytoplasm The process alters the membrane potential by changing the intracellular ionic concentration. The process causes G proteins to bind with GTP and become activated. The process removes three sodium ions from the cell and brings in two potassium ions.
- Which of the following is false? Steroids do not require a G protein and second messenger. The average pH of blood is 7.4 Increased levels of AMP will cause an increase in enzyme activity A G protein links the first messenger with the second messenger.The drug Buckeyium binds to the NMDA receptor at the orthosteric binding site (were glutamate would normally bind). Assume that glycine is already bound, and that magnesium is not blocking the NMDAR ion channel. If the channel does not open as a result of Buckeyium binding than Buckeyium would be considered aBuckeyium is a medication that binds to the NMDA receptor at the orthosteric binding site (were glutamate would normally bind). Assume glycine is already bonded and magnesium isn't inhibiting the NMDAR ion channel. Buckeyium would be regarded a poison if the channel did not open as a consequence of its binding.
- The figure below shows a signaling pathway activated by the bindiıng of adrehalMNe LU the beta-adrenergic receptor. Binding of adrenaline to the receptor causes GTP-binding and activation of G proteins. Active GTP-bound G protein activates adenylate cyclase to initiate a signaling cascade that affects cellular responses, and includes cellular changes to mediate increased heart rate and accounts for the flight-or-fight response. activated adenylate cyclase adrenaline activated B-adrenergic receptor adenylate cyclase G protein subunit 22 GTP SDP conformational ATP CAMP change in receptor heterotrimeric G protein ACAMP inactive protein kinase A active protein kinase A 4 cellular responses Consider the homozygous mutation in which a cell produces a variant of adenylate cyclase that can no longer be activated Which of the following are true in this cell? Select all that apply. Heart rate increases Protein Kinase A is not activated CAMP levels are lower than normal Heart rate decreaseshe following happens when a G-protein-coupled receptor activates a G protein. OThe alpha subunit exchanges its bound GDP for GTP. OIt activates the alpha subunit and inactivates the beta gamma complex. O The GDP bound to the alpha subunit is phosphorylated to form bound GTP The beta subunit exchanges its bound GDP for GTP.Which of the following is a second messenger signal ? Camp Ip3 DAG G protein coupled receptor A, b and c
- Which of the following is true of signal transduction mediated by protein tyrosine kinases production of cAMP phosphoinositides are activated arrestins compete with G-proteins phosphorylation of tyrosine residuesWhich of the following first messengers is hydrophobic and binds to a nuclear receptor protein inside cells? Oglucagon epinephrine O acetylcholine Oglucocorticoid insulinAlcohol affects the central nervous system by enhancing the effect ofGABA at its receptor. GABA binds to GABA receptors and opensligand-gated Cl–channels. However, chronic consumption of alcoholmakes the GABA receptor less sensitive to both alcohol and GABA,which increases alcohol dependence as well as alcohol withdrawalsymptoms, such as anxiety, tremors, and insomnia. Benzodiazepinesenhance the binding of GABA molecules to their receptors and thus aresometimes used to treat people with alcohol withdrawal symptoms. Forsynapses involving GABA, predict the effect of alcohol on the postsynaptic membranes; compare the effect of chronic alcohol consumption onthe postsynaptic membranes in these synapses; and predict the effect ofbenzodiazepine treatment on the degree of polarization of postsynapticmembranes in people who are experiencing alcohol withdrawalsymptoms.