A) Obese people who have high levels of leptin may have a leptin receptor with decreased sensitivity.
B) In obese people with high levels of leptin, the leptin is a non-functional second messenger.
C) Paracrine signaling may be disrupted in obese people with high levels of leptin.
D) The form of leptin released by obese people may lack protein kinase activity.
F) B) and C)
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A
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A) NO inhibits guanylyl cyclase, which allows the build up of cGMP, which acts as an intracellular messenger in a pathway leading to smooth muscle relaxation.
B) NO activates guanylyl cyclase, which catalyzes the synthesis of cGMP, which acts as an intracellular messenger in a pathway leading to smooth muscle relaxation.
C) NO activates cGMP, which catalyzes the synthesis of guanylyl cyclase, which acts as an intracellular messenger in a pathway leading to smooth muscle relaxation.
D) NO activates a protein kinase which catalyzes the synthesis of cGMP, which acts as an intracellular messenger in a pathway leading to smooth muscle relaxation.
F) A) and B)
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A) More phosphorylation of the substrate will be seen in the presence of molecule X.
B) The substrate will be phosphorylated normally in the presence of molecule X.
C) Less phosphorylation of the substrate will be seen in the presence of molecule X.
E) B) and C)
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A) Binding of testosterone to the testosterone receptor leads to the activation of a G protein that stimulates the activation of enzymes that promote gene transcription.
B) Binding of testosterone to the testosterone receptor leads to the opening of an ion channel that leads to an increase in calcium in the cytoplasm. The increased calcium levels activate calmodulin, which can go on to activate other proteins that promote gene transcription.
C) Binding of testosterone to the testosterone receptor leads to a conformational change that allows the receptor to enter the nucleus where it can bind to DNA and promote gene transcription.
D) Binding of testosterone to the testosterone receptor activates guanylyl cyclase, and the resulting cGMP promotes gene transcription.
E) Binding of testosterone to the testosterone receptor leads to the increase in second messengers that activate a kinase cascade, ultimately leading to the activation of transcription factors that promote gene transcription.
G) A) and D)
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C
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A) Scaffold
B) Adapter protein
C) Second messenger
D) Enzyme
F) A) and B)
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A) Try to identify proteins that act downstream of protein X.
B) Try to identify an adapter protein that can interact with both the receptor and protein X.
C) Try to identify a coactivator protein.
D) Confirm the interaction between the receptor tyrosine kinase and its ligand.
F) A) and C)
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A) If there are too many RTKs on the cell surface, it is less likely that inhibitors will bind to all of the available RTKs and block their ability to enter the nucleus. As a result, some of the RTKs will be able to enter the nucleus to stimulate transcription.
B) If there are too many RTKs on the cell surface, this will promote the inhibition of autophosphorylation. In the absence of autophosphorylation, it is more likely that the RTK downstream signaling pathway will be active.
C) RTKs are activated by dimerization, caused by ligand binding. If there are too many receptors on the cell surface, it is possible that these receptors dimerize in the absence of ligand binding, thus stimulating cell division at inappropriate times.
D) If there are too many RTKs on the cell surface, this will tend to allow cells to adhere to each other. Once they adhere, RTKs from one cell can bind to RTKs from another cell, and they can activate each other leading to activation of downstream signaling pathways in both cells.
F) B) and D)
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A) Vasopressin can bind to, and act on, different receptor subtypes, leading to different cellular responses in different tissues.
B) The kidneys have a receptor for vasopressin, but cells in the brain and blood vessels do not have a receptor for vasopressin.
C) Vasopressin binds to the same exact receptor in different tissues, but causes a different conformational change to the receptor in each tissue.
D) Vasopressin can be released at different times to result in different effects.
F) A) and C)
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A
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A) Yes, because it is small.
B) No, because it will need to bind to the DNA-binding domain to act as an inhibitor.
C) No, because it is hydrophilic.
D) Yes, because it can prevent estrogen binding.
F) All of the above
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A) The estrogen receptor is bound to different coactivators in different tissues.
B) Tamoxifen binds different parts of the estrogen receptor in different tissues.
C) Tamoxifen can only enter certain cell types.
D) Bone cells make use of a different type of estrogen receptor that does not bind to Tamoxifen.
F) A) and B)
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A) Both have a DNA-binding domain.
B) Both have a site for binding ligand.
C) Both are activated by autophosphorylation.
D) Both are transmembrane proteins with a single transmembrane domain.
F) B) and D)
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A) autocrine signaling between tumor cells.
B) synaptic signaling between tumor cells.
C) paracrine signaling between tumor cells.
D) endocrine signaling between tumor cells.
F) A) and C)
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