33.
Upon ingestion of bacteria, white blood cells release a chemical messenger into the blood stream that causes the synthesis of inflammation response proteins by liver cells. What is this is an example of?
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autocrine signaling
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endocrine signaling
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paracrine signaling
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synaptic signaling
34.
Molecules do not flow between the endothelial cells in the brain capillaries. The membranes of the cells must be joined by what?
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gap junctions
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ligand-gated channels
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synapses
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tight junctions
35.
Multicellular organisms employ four different categories of chemical signaling. Analyze the following descriptions to select the benefit provided by autocrine signaling.
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Autocrine signaling helps cells to communicate with distantly located cells.
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Autocrine signaling connects nearby located cells.
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Autocrine signaling helps to amplify the signal by inducing more signaling production from the cell itself.
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Autocrine signaling is specific only for the cell that produced it, giving it a precise means of messaging.
36.
If a chemical is an inhibitor of the enzyme adenylyl cyclase, which of the following steps in the G-protein signaling pathway would be blocked?
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activation of gene transcription
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exchange of GTP for GDP
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ligand bound receptor activation of G-protein
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synthesis of cAMP
37.
Thyroid hormone is a lipid-soluble signal molecule that crosses the membrane of all cells. Why would a cell fail to respond to the thyroid hormone?
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The MAPK cascade leading to cell activation is defective in the target cells.
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The DNA sequence it binds to underwent a mutation.
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There is no intracellular receptor for thyroid hormone in the cell.
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The second messenger does not recognize the signal from the receptor.
38.
The poison from the krait snake’s bungarotoxin binds irreversibly to acetylcholine receptors, interfering with acetylcholine binding at the synapse. What then do you predict is the effect of bungarotoxin binding on the post synaptic cell?
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cAMP production is inhibited.
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Bungarotoxin G-proteins are not activated.
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Ion movement in the cell is inhibited.
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Phosphorylation cascade is inhibited.
39.
In autoimmune lymphoproliferative syndrome (ALPS), lymphocytes which multiplied during an infection persist in the body and damage tissue. The syndrome is caused by a mutation in the FAS gene which encodes a cell surface receptor. Which signaling pathway does the receptor initiate?
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activated metabolism
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apoptosis
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cell division
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cell differentiation
40.
Place the following events in their sequential order:
- protein kinase A is activated
- glycogen breakdown
- epinephrine binds to G-protein-linked receptor
- G-protein activates adenylyl cyclase
- GTP is exchanged for GDP on the G-protein
- ATP is converted to cAMP
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1, 3, 5, 4, 6, 2
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3, 5, 4, 1, 6, 2
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3, 4, 5, 1, 6, 2
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3, 5, 4, 6, 1, 2
41.
The RAS protein is a G-protein connected with the response to receptor tyrosine kinases (RTKs) that initiates the MAPK kinase cascade when GDP is released and GTP uploaded. Mutations in the RAS protein, which interfere with its GTPase activity, are common in cancer. Examine the connection between the inability of RAS to hydrolyze GTP and uncontrolled cell proliferation. Select the best explanation of this connection below.
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RAS, when bound to GTP, becomes permanently inactive even in the presence of the ligand, and no longer regulates cell division.
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RAS, when bound to GTP, becomes permanently active even in the absence of the ligand, and no longer regulates cell division.
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RAS, when bound to GTP, forms a dimer after binding to the ligand, and causes uncontrolled division, but it remains inactive when the ligand is absent.
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RAS, when bound to GTP, does not form a dimer after binding to the ligand but stimulates downstream signaling to occur and causes uncontrolled cell division.
42.
Common medications called β-blockers bind to G-protein-linked receptors in heart muscles, blocking adrenaline. They are prescribed to patients with high blood pressure. Based on your understanding of G-protein-linked receptors, can you formulate a hypothesis on their mechanism of action? Evaluate and select from the options given below.
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Adrenaline has a stimulatory effect on heart rate and blood pressure. β-blockers are antagonistic to adrenaline and produce an inhibitory effect.
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Adrenaline has both a stimulatory and an inhibitory effect on heart rate and blood pressure. β-blockers bind to G-protein-linked receptors and stimulate the inhibitory effect of adrenaline.
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Adrenaline has an inhibitory effect on heart rate and blood pressure. β-blockers have a synergistic effect along with adrenaline, producing an inhibitory effect.
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Adrenaline has both a stimulatory and an inhibitory effect on heart rate and blood pressure. β-blockers bind to G-protein-linked receptors and intervene with the inhibitory effect of adrenaline.