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What is the mechanism by which binding of testosterone to the testosterone receptor leads to upregulated gene transcription?


A) 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.
B) 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.
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 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.

E) A) and C)
F) All of the above

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C

In the nitric oxide signaling pathway,nitric oxide activates an enzyme that can convert many molecules of GTP into molecules of cGMP.cGMP is a small molecule that can diffuse through the cytoplasm and bind to an enzyme called protein kinase G (PKG) .Binding of cGMP to PKG leads to a change in the confirmation of PKG that leads to its activation.What type of signaling molecule is cGMP?


A) Scaffold
B) Adapter protein
C) Second messenger
D) Enzyme

E) B) and C)
F) A) and D)

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Using a specific chemical,a cell biologist has blocked one type of channel-linked receptor in a lab rat's liver tissue.What was the likely mechanism of the chemical she used?


A) The chemical prohibits binding of a ligand to the receptor.
B) The chemical prohibits ions from entering the cell via active transport.
C) The chemical causes ions to move in the opposite direction of the ion gradient.
D) The chemical prohibits second messenger signaling.

E) C) and D)
F) A) and B)

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What signaling pathway commonly makes use of a G protein to transduce the signal?


A) Channel-linked receptor pathways
B) Steroid hormone receptor pathways
C) Receptor tyrosine kinase pathways

D) A) and B)
E) None of the above

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Some cancers are caused by the overexpression of receptor tyrosine kinases (RTKs) .It is known that RTK signaling pathways commonly stimulate cell division.Why would the overexpression of receptor tyrosine kinases lead to cancer development?


A) 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.
B) 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.
C) 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.
D) 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.

E) C) and D)
F) A) and D)

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Many receptor tyrosine kinase (RTK) pathways lead to the activation of Ras.To activate Ras,it is necessary to recruit a guanine nucleotide exchange factor to the plasma membrane,because Ras is a membrane associated protein.Guanine nucleotide exchange factors,such as SOS,stimulate the exchange of GDP for GTP.However,SOS cannot bind directly to most RTKs.The protein Grb2 has a domain that can bind to phosphorylated tyrosines,and another domain that can bind to SOS.Therefore,Grb2 can bind to active RTKs and recruit SOS to the plasma membrane.Grb2 is an example of what kind of signaling molecule?


A) Scaffold
B) Adapter protein
C) Second messenger
D) Enzyme

E) A) and B)
F) C) and D)

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How are receptor tyrosine kinases and steroid hormone receptors similar?


A) Both are activated by autophosphorylation
B) Both are transmembrane proteins with a single transmembrane domain
C) Both have a DNA-binding domain
D) Both have a site for binding ligand

E) A) and B)
F) A) and C)

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A researcher is working to generate a new cancer drug.Thus far,he has identified a compound that can reduce the size of tumors in the lung.However,in order for the drug to work,the lung tumor has to be small.In addition,the tumor cannot have metastasized (spread to other areas of the body) .Furthermore,he knows that the drug acts to prohibit the signaling from one tumor cell to another tumor cell.Given the above information,this new drug prohibits:


A) synaptic signaling between tumor cells.
B) autocrine signaling between tumor cells.
C) paracrine signaling between tumor cells.
D) endocrine signaling between tumor cells.

E) A) and B)
F) B) and D)

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C

A mutation in the DNA-binding domain of a steroid hormone receptor is most likely to affect what aspect of receptor function?


A) The conformational change of the receptor
B) The binding of the hormone to the receptor
C) The translocation of the receptor to the nucleus
D) The cellular response to the hormone

E) C) and D)
F) A) and C)

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Leptin is a circulating hormone that is produced by fat cells and plays a role in body metabolism and obesity.It normally binds to receptors in the brain and inhibits appetite.Studies have demonstrated that when obese mice that are leptin deficient are injected with leptin they quickly lose their excess weight.Interestingly,however,many overweight people have high levels of leptin in their bloodstream.Why do you think that the high levels of leptin in obese individuals are insufficient to curb their appetite?


A) Paracrine signaling may be disrupted in obese people with high levels of leptin.
B) Obese people who have high levels of leptin may have a leptin receptor with decreased sensitivity.
C) The form of leptin released by obese people may lack protein kinase activity.
D) In obese people with high levels of leptin,the leptin is a non-functional second messenger.

E) None of the above
F) A) and B)

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What is similar about G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs) ?


A) Both are directly bound to G proteins
B) Both can activate phospholipase C
C) Both are enzymes
D) Both are activated by autophosphorylation

E) A) and B)
F) All of the above

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A mutation that affects Ca++ binding to calmodulin is most likely to interfere with what aspect of a signal transduction pathway?


A) The flow of Ca++ ions through ion channel receptors
B) The cellular response to the second messenger
C) The MAP kinase cascade
D) G protein activity

E) A) and B)
F) A) and C)

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What is the function of a protein kinase?


A) To remove phosphate groups from proteins
B) To cleave membrane phospholipids
C) To phosphorylate GDP to generate GTP
D) To add phosphate groups onto proteins

E) A) and B)
F) All of the above

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In response to injury,cell fragments called platelets get activated to induce clotting.Activated platelets release factors that can in turn bind to specific membrane receptors on nearby cells.What type of signaling would this be considered?


A) Direct contact
B) Paracrine
C) Endocrine
D) Synaptic
E) Autocrine

F) A) and D)
G) B) and D)

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You are interested in developing an inhibitor for the estrogen receptor.You have identified a molecule that is small and hydrophilic.In a test tube,this inhibitor binds tightly to the estrogen receptor,and inhibits the interaction of the receptor with estrogen.Do you think that this molecule will be an effective inhibitor of the estrogen receptor in cells?


A) Yes,because it can prevent estrogen binding.
B) Yes,because it is small.
C) No,because it is hydrophilic.
D) No,because it will need to bind to the DNA-binding domain to act as an inhibitor.

E) None of the above
F) All of the above

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G protein-coupled receptors are the largest family of cell surface receptors.Each receptor passes through the plasma membrane how many times?


A) Once
B) Three times
C) Five times
D) Seven times

E) A) and B)
F) All of the above

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D

Ste5 binds to MAPKKK,MAPKK,and MAPK to organize the kinase cascade.What type of signaling molecule is Ste5?


A) Scaffold
B) Adapter protein
C) Second messenger
D) Enzyme

E) None of the above
F) B) and C)

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These molecules can directly convert extracellular signals into intracellular signals.


A) Second messengers
B) Scaffolds
C) Membrane receptors
D) Adapter proteins
E) G proteins

F) B) and E)
G) A) and B)

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If the effector protein phospholipase C failed to cleave phosphatidylinositol-4,5-bisphosphate (PIP2) ,the action of what enzyme would be affected?


A) cAMP
B) IP3
C) protein kinase A (PKA)
D) protein kinase C (PKC)

E) None of the above
F) B) and C)

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Addison's disease is a disorder that results from a reduction in production of glucocorticoids and mineralocorticoids.Individuals with Addison's disease suffer from a variety of systemic symptoms including: muscle weakness,fever,issues with the gastrointestinal tract,and increased tanning.Considering this information,what type of signaling do you think that glucocorticoids and mineralocorticoids stimulate?


A) Direct contact
B) Paracrine
C) Endocrine
D) Synaptic
E) Autocrine

F) A) and C)
G) A) and E)

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