Chapter 20

Which of the following compounds can act as second messengers in signal transduction pathways? Cyclic AMP Adenylate cyclase Phospholipase C Phosphotidylinositol 4,5-bisphosphate Both A and D

Cyclic AMP

Hormone action is ultimately controlled by the cells that secrete the hormone. True False

False

Most synaptic transmission events are mediated electrically through gap junctions between cells. True False

False

G proteins are membrane-bound proteins that bind GDP when inactive. True False

True

What is the role of activated protein kinases? Phosphorylate ADP to ATP. Phosphorylate proteins. Activate adenylate cyclase. Degrade cAMP to AMP. Convert ATP to cAMP by phosphorylation.

Phosphorylate proteins.

A signal transduction pathway is initiated when a _____ binds to a receptor. G protein tyrosine kinase calmodulin signal molecule cyclic AMP

signal molecule

G proteins __________. 1) are proteins that bind guanine nucleotides 2) can either stimulate or inhibit downstream enzymes such as adenylyl cyclase 3) are activated by hydrolyzing GTP to GDP 4) are in an inactive state when GTP is bound

1,2

Which of the following statements about hormones are correct? 1) Hormones can be peptides, steroids, or amino acid derivatives. 2) Hormones can stimulate the synthesis of target proteins through the activation of specific genes. 3) Hormones can directly activate or inhibit enzymes through the action of signal molecules. 4) Hormones can increase the cellular uptake of metabolites.

1,2,4

Match the correct hormone class (on the left) with the correct protein (on the right) whose synthesis is increased by hormonal stimulation. 1) progesterone A) calcium binding protein 2) 1,25-dihydroxy-vitamin D3 B) phosphoenolpyruvate carboxykinase 3) glucocorticoids C) uteroglobin 4) androgens D) aldolase 1:B; 2:A; 3:D; 4:C 1:D; 2:A; 3:C; 4:B 1:C; 2:B; 3:A; 4:D 1:C; 2:A; 3:B; 4:D

1:C; 2:A; 3:B; 4:D

Which of the following are characteristics of G protein-coupled receptors? 1) They typically have seven transmembrane domains that are embedded in the cell membrane. 2) They carry hydrophilic portions of protein that extend into the extracellular matrix as well as the cytosol. 3) The receptor region is located on the extracellular portion of the protein. 4) Most work in concert with G proteins.

ALL

List factors that make it advantageous for peptide hormones to be synthesized as inactive prohormones that are activated by proteolytic cleavage. Check all that apply. Additional polypeptide sequence may promote correct folding of the polypeptide chain. Signal sequence on the prohormone molecule could direct the protein to the correct subcellular site, then be cleaved off when no longer needed. Protection from premature degradation of the protein by cell proteases. Suppression of the hormonal signal until it is needed. Stabilization of not working folding of protogormone.

Additional polypeptide sequence may promote correct folding of the polypeptide chain. Signal sequence on the prohormone molecule could direct the protein to the correct subcellular site, then be cleaved off when no longer needed. Suppression of the hormonal signal until it is needed.

Oral administration of S-adenosylmethionine has been reported to be effective in treating depression. Suggest a possible explanation. Select all that apply. AdoMet could affect membrane fluidity through effects on phospholipid metabolism. If AdoMet could cross the blood-brain barrier, it might conceivably increase methylation of norepinephrine to give epinephrine. AdoMet could partly compensate for B12 insufficiency. AdoMet could act through folate metabolism, increasing the pool of labile methyl groups. AdoMet could activate the redox-chain components, enhancing cell-respiration processe

AdoMet could act through folate metabolism, increasing the pool of labile methyl groups. AdoMet could affect membrane fluidity through effects on phospholipid metabolism. If AdoMet could cross the blood-brain barrier, it might conceivably increase methylation of norepinephrine to give epinephrine.

Choose the correct explanation of this apparent paradox. Because inositol trisphosphate is derived from phosphatidylinositol, which in turn is derived from diacylglycerol and inositol, inositol phosphates must be completely dephosphorylated in order to be reincorporated into phosphatidylinositol for another round of synthesis. Because inositol trisphosphate act as an allosteric inhibitor of the enzyme inositol trisphosphate synthetase, excess accumulation of inositol trisphosphate substantially diminishes the activity of the enzyme, reducing the production of new inositol trisphosphate molecules. Because inositol trisphosphate synthetase works both directions, whether synthesis or hydrolysis of inositol trisphosphate prevails depends on the relative concentrations of inositol trisphosphate and its immediate precursor (inositol bisphosphate). By blocking inositol trisphosphate hydrolysis reaction lithium ions prevent accumulation of inositol bisphosphate which will be needed for the reverse reaction of inositol trisphosphate synthesis. Because inositol trisphosphate synthesis occurs in smooth endoplasmic reticulum its precursor (inositol) has to cross the ER membrane, which would be impossible for a molecule bearing charged groups (such as phosphate groups). Thus in order for inositol to permeate into the ER it has to be ripped off of all of its phosphate groups.

Because inositol trisphosphate is derived from phosphatidylinositol, which in turn is derived from diacylglycerol and inositol, inositol phosphates must be completely dephosphorylated in order to be reincorporated into phosphatidylinositol for another round of synthesis.

Botulinum toxin blocks neuromuscular transmission, causing paralysis. How does it do this? Botulinum toxin cleaves the t-SNARE, blocking fusion of the vesicle. Botulinum toxin cleaves the tethering proteins, inhibiting accumulation at the membrane. Botulinum toxin blocks the GTPase activity of Rab. Botulinum toxin inhibits NSF, blocking the regeneration of SNAREs.

Botulinum toxin cleaves the t-SNARE, blocking fusion of the vesicle.

What role does a transcription factor play in a signal transduction pathway? By binding to a plasma membrane receptor it initiates a cascade. It relays a signal from the cytoplasm to the plasma membrane. It activates relay proteins. By binding to DNA it triggers the transcription of a specific gene. It is a plasma membrane protein that binds signal molecules.

By binding to DNA it triggers the transcription of a specific gene.

Which of the following best describes the role of chaperone proteins in the regulation of gene expression by steroid hormones? Chaperone proteins enter the cell and bind receptor molecules. Chaperone proteins activate receptor proteins. Chaperone proteins directly enhance transcription. Chaperone proteins maintain functionality of the receptor.

Chaperone proteins maintain functionality of the receptor.

Choose all the suggestions that correctly describe biochemical experiments that could be done to compare the activity of bisphenol A with that of its estradiol, its structural relative. Select all that apply. Check whether BPA can substitute estrogens in cells that bear mutations affecting estrogen synthesis. Check for competitive or synergistic effects of coadministration of BPA and estradiol. Compare physical properties of estrogens and BPA, such as solubility, rate of diffusion, three-dimensional molecular structure. Compare the effects on transcription of estradiol and bisphenol A in estrogen-responsive cells. Look directly for binding of radiolabeled BPA to receptors for estrogens and related hormones.

Check for competitive or synergistic effects of coadministration of BPA and estradiol. Compare the effects on transcription of estradiol and bisphenol A in estrogen-responsive cells. Look directly for binding of radiolabeled BPA to receptors for estrogens and related hormones.

Which of the following is an extracellular messenger involved in signal transduction? Diacylglycerol Cyclic GMP Rhodopsin Epinephrine Ca2+

Epinephrine

Receptor tyrosine kinases are membrane-spanning proteins with an intrinsic tyrosine kinase domain on the extracellular side of the membrane. True False

False

Part A Part complete Which statement about G proteins is NOT true? Several bacterial toxins, such as that from V. cholerae, can inactivate the GTPase activity of G proteins. Activated G protein moves along the membrane to reach an effector molecule, such as adenylate cyclase. There are some G proteins that have heterotrimeric structure. G proteins possess very active GTPase activity.

G proteins possess very active GTPase activity.

How do endocrine hormones reach their target cells? Select the best answer. Hormones travel through the lymphatic system to target cells. Hormones are produced by endocrine cells that are adjacent to target cells. Ducts transport hormones directly to target cells. Hormones are transported through the blood stream to target cells. Hormones are released at synapses adjacent to target cells.

Hormones are transported through the blood stream to target cells.

How might it affect lipid metabolism? Lypolysis would be promoted. Lipid biosynthesis would be promoted. Lipid metabolism would not be changed.

Lypolysis would be promoted.

A β-adrenergic response can be modulated through the actions of a receptor kinase and arrestin, because phosphorylation by the kinase desensitizes the receptor. How might signaling by a tyrosine receptor kinase, such as the insulin receptor, be modulated? Modulation occurs through action of protein tyrosine phosphatases on phosphorylated tyrosine residues. Modulation occurs through action of insulin receptor substrate-1 (IRS-1), a protein that binds to the kinase domain of the insulin receptor via its SH2 domains and prevents tyrosine residues from phosphorylation. Modulation occurs through action of insulin receptor substrate-1 (IRS-1), a protein that binds to the kinase domain of the insulin receptor via its SH2 domains and prevents phosphorilated tyrosine residues from dephosphorylation. Modulation occurs through action of protein tyrosine kinases on dephosphorylated tyrosine residues.

Modulation occurs through action of protein tyrosine phosphatases on phosphorylated tyrosine residues.

How would drinking several cups of coffee affect muscle function? Muscle function would be enhanced. Muscle function would be diminished. Muscle function would not be changed. It depends on the person.

Muscle function would be enhanced.

Why is this structural modification necessary? Addition of butyrate chains renders cAMP more active because of increased ability to bind to target proteins through ionic and hydrophobic interactions in which butyrate chains participate. Thus, the effects caused by such modified cAMP are more prominent and easily detectable than those caused by original compound. Negative charge on the phosphate of cAMP prevents its passage through cell membranes. The butyrate chains make the molecule more lipophilic, although the negative charge on the phosphate is unaffected. Membrane-bound phosphodiesterase degrades external cAMP just after it enters the cell through the cell membrane. In order to protect phosphodiester bonds from phosphodiesterase they are covered with butyrate chains. The phosphodiester bonds in cAMP are highly unstable in solutions with low salt concentrations, such as those surrounding cells in cell cultures. Two butyrate chains are introduced into cAMP molecule so as to make it less prone to self-decay before it enters the cell.

Negative charge on the phosphate of cAMP prevents its passage through cell membranes. The butyrate chains make the molecule more lipophilic, although the negative charge on the phosphate is unaffected.

Would you expect the binding curve to be hyperbolic? Yes, the binding curve will be hyperbolic. No, the binding curve will not be hyperbolic.

No, the binding curve will not be hyperbolic.

How could you test the premise that di-Bu-cAMP has the same biochemical effects as cAMP? Select all that apply. One could determine whether the butyryl chains are cleaved from the molecule after uptake into cells. One could compare the actions of cAMP and dibutyryl-cAMP in cells whose plasma membrane had been treated with an agent to increase its permeability. One could assess the effect of dibutyryl-cAMP on purified cAMP target proteins. One could identify whether dibutyryl-cAMP occurs naturally in cells and what proteins it binds to.

One could compare the actions of cAMP and dibutyryl-cAMP in cells whose plasma membrane had been treated with an agent to increase its permeability. One could assess the effect of dibutyryl-cAMP on purified cAMP target proteins.

Choose correct statements describing features of insulin signaling that affect glucose utilization. Select all that apply. Glucose uptake into cells is stimulated through mobilization of glucose transporters to the membrane. Glucose metabolism is activated by phosphorylation of the key enzymes of phosphofructokinase and isocitrate dehydrogenase - the key enzymes of glycolisis and citric cycle, respectively. Membrane synthesis is stimulated through the signal cascade that results in activation of fat acid synthase complex. Over the long term insulin receptor activation stimulates protein synthesis and cell division. The action of phosphoinositide 3-kinase stimulates an enzyme phosphorylation cascade that results in enhanced glycogen synthesis. Over the long term insulin receptor activation stimulates cell apoptosis.

Over the long term insulin receptor activation stimulates protein synthesis and cell division. The action of phosphoinositide 3-kinase stimulates an enzyme phosphorylation cascade that results in enhanced glycogen synthesis. Glucose uptake into cells is stimulated through mobilization of glucose transporters to the membrane.

_____ catalyzes the production of _____, which then opens an ion channel that releases _____ into the cell's cytoplasm. Adenylyl cyclase ... IP3 .... Ca2+ Adenylyl cyclase ... cyclic AMP ... Ca2+ Phospholipase C ... cyclic AMP ... Ca2+ Protein kinase ... PIP2 ... Na+ Phospholipase C ... IP3 .... Ca2+

Phospholipase C ... IP3 .... Ca2+

Which of the following statements about the adrenergic receptor is NOT true? Beta-blockers work as antagonists for this receptor, thereby controlling heartbeat rate. Propranolol is an agonist for this receptor. Isoproterenol is an agonist for this receptor. The responses to the stimulation of some of these receptors include smooth muscle contraction, increased heart rate, and increased lipolysis.

Propranolol is an agonist for this receptor.

What kind of evidence would prove otherwise? Protein sequencing could be used to demonstrate that adenylate cyclase activity and epinephrine-binding activity are carried out by different proteins. Protein fractionation, with a demonstration that epinephrine-binding activity and adenylate cyclase activity could be physically separated from one another can be done. Mutational analysis, with a demonstration that epinephrine-binding activity and adenylate cyclase activity are encoded by different genes can be done. Adenylate cyclase inhibitors or hormone binding competitive inhibitors can be used to demonstrate that adenylate cyclase activity and epinephrine-binding activity are inhibited independently.

Protein fractionation, with a demonstration that epinephrine-binding activity and adenylate cyclase activity could be physically separated from one another can be done.

What is the biochemical basis for the action of Prozac? Prozac selectively inhibits the hydrolysis of serotonin by synaptic cleft enzymes, thereby increasing the amount of the neurotransmitter that reaches the postsynaptic cell, stimulating synaptic transmission in areas related to regulation of mood. Prozac selectively inhibits reuptake of serotonin by presynaptic neurons, thereby increasing the amount of the neurotransmitter that reaches the postsynaptic cell, stimulating synaptic transmission in areas related to regulation of mood. Prozac selectively stimulates reuptake of serotonin by presynaptic neurons, thereby decreasing the amount of the neurotransmitter that reaches the postsynaptic cell, inhibiting synaptic transmission in areas related to regulation of mood. Prozac selectively stimulates the hydrolysis of serotonin by synaptic cleft enzymes, thereby decreasing the amount of the neurotransmitter that reaches the postsynaptic cell, stimulating synaptic transmission in areas related to regulation of mood.

Prozac selectively inhibits reuptake of serotonin by presynaptic neurons, thereby increasing the amount of the neurotransmitter that reaches the postsynaptic cell, stimulating synaptic transmission in areas related to regulation of mood.

What is the role of Rab GTPase in the process? Rab GTPase facilitates the initial binding of t-SNARE to v-SNARE. Rab GTPase locks the t-SNARE and v-SNARE together, facilitating fusion of the vesicle. Rab GTPase causes the fusion of the vesicle to the target membrane. Rab GTPase helps to disconnect t-SNARE and v-SNARE after fusion has occurred.

Rab GTPase locks the t-SNARE and v-SNARE together, facilitating fusion of the vesicle.

The membrane-bound receptor in G protein-coupled signal transduction is quite separate to the effector enzyme which catalyses the formation of an intracellular ________.

Second Messenger

In the late 1980s, Robert Weinberg isolated DNA from bladder cancer cells and used this to transfect normal mouse fibroblasts. Which of the following statements is NOT true of this experiment? Altered forms of oncogenes already present in humans contribute to tumorigenesis. Sequence analysis of the transforming gene H-ras was found to contain multiple mutations. The DNA recovered from transformed mouse cells contained human sequences. The transforming gene was nearly identical with the oncogene derived from Harvey rat sarcoma virus, known as H-ras.

Sequence analysis of the transforming gene H-ras was found to contain multiple mutations.

Which of the following best describes the mechanism by which steroid hormones control gene expression? Chaperone proteins transport steroid hormones into the cell and guide them to their target genes. Steroid hormones transport mRNA from the nucleus into the cytoplasm, where it is translated into protein. Steroid hormones enter a cell, bind directly to hormone response elements (HREs), and enhance transcription. Steroid hormones that enter the cell activate receptors. These hormone-receptor complexes then bind HREs and influence gene expression.

Steroid hormones that enter the cell activate receptors. These hormone-receptor complexes then bind HREs and influence gene expression.

What consequences would you expect? Stimulation of adenylate cyclase is lost much faster than in case of GTP. Stimulation of adenylate cyclase is reached much faster than in case of GTP. Stimulation of adenylate cyclase is reached much slower than in case of GTP. Stimulation of adenylate cyclase is lost much slower than in case of GTP.

Stimulation of adenylate cyclase is lost much slower than in case of GTP.

How might this mutation affect signaling involving a GPCR? Such a mutation would cause the block of downstream signaling. Such a mutation would cause desensibilization of the GPCR. Such a mutation would cause hypersensibilization of the GPCR. Such a mutation would cause hyperactivation of downstream signaling.

Such a mutation would cause hyperactivation of downstream signaling.

Describe a mechanism by which a steroid hormone might act to increase intracellular levels of cyclic AMP. Check all that apply. The mechanism could include induced synthesis of a phosphodiesterase inhibitor or repressed synthesis of cAMP phosphodiesterase. Steroid hormones could inhibit transcription of the gene for adenylate cyclase and, hence, increase the steady-state level of this enzyme. Steroid hormones could activate transcription of the gene for adenylate cyclase and, hence, increase the steady-state level of this enzyme. Steroid hormone receptors could launch gene transcription pathways associated with the destruction of cAMP. Steroid hormones could allosterically inhibit the cAMP phosphodiesterase active site. The mechanism could include destruction by a steroid hormone of intermediates in the pathway of cAMP synthesis.

The mechanism could include induced synthesis of a phosphodiesterase inhibitor or repressed synthesis of cAMP phosphodiesterase. Steroid hormones could activate transcription of the gene for adenylate cyclase and, hence, increase the steady-state level of this enzyme.

Autophosphorylation is an important part of the mechanism of the receptor tyrosine kinases. Why is this? The phosphorylation provides sites for recruitment of other signal transduction molecules. The phosphorylation causes the receptors to dimerize. The phosphorylation activates the kinase domain. The phosphorylation causes down regulation of the receptors.

The phosphorylation provides sites for recruitment of other signal transduction molecules.

Choose the correct explanation of your answer. The reaction of EGF with its receptor should be trimolecular at low EGFR concentrations, because EGF binding should promote dimerization of the monomeric receptor. The reaction of EGF with its receptor should be bimolecular at high EGFR concentrations, because EGF binding should promote dimerization of the monomeric receptor. The reaction of EGF with its receptor should be bimolecular at low EGFR concentrations, because EGF binding should promote dimerization of the monomeric receptor. The reaction of EGF with its receptor should be trimolecular at high EGFR concentrations, because EGF binding should promote dimerization of the monomeric receptor.

The reaction of EGF with its receptor should be trimolecular at low EGFR concentrations, because EGF binding should promote dimerization of the monomeric receptor.

What do you think might be the purpose of these modifications? These processes are triggered in response to unfavorable conditions or extensive DNA damage and render β-adrenergic receptors indifferent to extracellular growth factors, which leads to cell cycle arrest. These processes are required to sensibilize β-adrenergic receptors, thus creating a positive feedback loop which facilitates rapid signal transduction. These processes is an important stage in signal cascade that conducts extracellular signals into the cell. These processes control receptor activity and modulate the adrenergic response.

These processes control receptor activity and modulate the adrenergic response.

Which of the following does NOT belong to a receptor tyrosine kinase family? Insulin receptor Epidermal growth factor receptor Fibroblast growth factor receptor Thyroid receptor Platelet-derived growth factor receptor

Thyroid receptor

The end result of a signal transduction pathway is often a change in gene expression. True False

True

Would you expect an inhibitor of this enzyme to potentiate or antagonize the action of Viagra? Choose the correct explanation. Viagra acts by inhibiting this reaction, any other compound acting similarly should potentiate the effect of Viagra. Viagra acts as an antagonist of 5'-GMP, any compound that inhibits the converting of cGMP to 5'-GMP should potentiate the effect of Viagra. Viagra acts to stimulate the synthesis of cGMP, any compound that inhibits the hydrolysis of cGMP should potentiate the effect of Viagra. Viagra acts to convert cGMP into an active derivative, any compound that inhibits the hydrolysis of cGMP should increase the amount of cGMP for conversion and thus potentiate the effect of Viagra.

Viagra acts by inhibiting this reaction, any other compound acting similarly should potentiate the effect of Viagra.

What is the biochemical basis for the action of Viagra? Viagra molecule contains a nitro group which is cleaved off by the enzyme nitric oxide synthase and released in the form of NO⋅ that in turn activates guanylate cyclase and stimulates cGMP formation. Viagra inhibits cyclic GMP phosphodiesterase, so cGMP levels remain high, thereby prolonging the effects of nitric oxide on regional blood flow. Viagra mimics cGMP but is not readily degraded in human cells and thus it provides prolonged allosteric activation of cGMP-stimulated protein kinase that acts to yield vasodilation of endothelial vascular cells and the underlying smooth muscle. Viagra activates cAMP phosphodiesterase thus lowering the level of cAMP, which is the antagonist of cGMP. This leads to vasodilatation of endothelial vascular cells and the underlying smooth muscle.

Viagra inhibits cyclic GMP phosphodiesterase, so cGMP levels remain high, thereby prolonging the effects of nitric oxide on regional blood flow.

Consider the mechanism of Botulinum toxin. Is this toxin reversible? No, Botulinum toxin damage results in atrophy of the neuron and neuron death. Yes, it will reverse when the concentration of Botulinum toxin decreases. No, Botulinum toxin causes permanent damage to the nerve terminal. Yes, however the cell must regenerate new t-SNAREs.

Yes, however the cell must regenerate new t-SNAREs.

Receptor tyrosine kinases are activated by hormones that cause cell division (mitogens). Which of the following describes a way that a protein in the pathway could be mutated to result in its constitutive activation causing unregulated cell division? a mutation in Grb2 that changes its SH2 binding domain a mutation in the receptor that removes an important tyrosine from the cytoplasmic tail a mutation in Ras that makes it unable to hydrolyze GTP a mutation in MAPK that removes one of its phosphorylation domains

a mutation in Ras that makes it unable to hydrolyze GTP

Part I Part complete A protein kinase activating many other protein kinases is an example of _____. amplification a cellular response sensitization deactivation mutualism

amplification

Nuclear receptors: are DNA rather than proteins. reside on the nuclear membrane. do not bind to hormones. are transcriptional regulators. reside only within the nucleus of a cell.

are transcriptional regulators.

he magnification of the signal from a water-soluble hormone is achieved through an increase in _______. cAMP in the cytoplasm adenylate cyclase in the plasma membrane plasma membrane receptors phosphodiesterase in the cytoplasm water-soluble hormone in the blood

cAMP in the cytoplasm

What would be the effects on cAMP levels? cAMP levels should be the same cAMP levels should increase cAMP levels should decrease

cAMP levels should increase

Choose the correct balanced equation for the hydrolysis of cGMP, catalyzed by cGMP phosphodiesterase. cGMP + H2O⟶5'-GMP cGMP + H2O⟶guanosine+Pi cGMP + H2O⟶3'-GMP cGMP + H2O⟶ guanine+Pi

cGMP + H2O⟶5'-GMP

Hormones that use the tyrosine kinase receptor mechanism as shown in the animation are important for cellular growth and survival. paracrine control of one cell by an adjacent cell. rapid adaptation to physiological changes. regulation of cellular calcium levels.

cellular growth and survival.

Name the amino acid residue that is used to complex zinc ions in the zinc finger motif of steroid receptors.

cysteine

Calcium ions that act as second messengers are stored in _____. lysosomes mitochondria chloroplasts peroxisomes endoplasmic reticula

endoplasmic reticula

Sos activates Ras. Sos is an example of a protein with an SH2 domain. tyrosine kinase. guanine-nucleotide exchange factor (GEF). GTPase-activating protein (GAP).

guanine-nucleotide exchange factor (GEF).

What is another likely role of the SNARE mechanism of vesicle fusion, in addition to secretion of material? sorting of material into secretory vesicles segregation of acid hydrolases into early endosomes insertion of membrane proteins into the plasma membrane endocytosing material via pinocytosis

insertion of membrane proteins into the plasma membrane

The dominant negative mutation of the receptor in the animation is effective in blocking the hormone signal because it blocks binding of Grb2/Sos to the normal receptors by competing for its binding. it blocks the binding of the hormone with normal receptors. it is able to dimerize with a functional receptor without the activation of autophosphorylation. it activates an alternate pathway that physiologically antagonizes the Ras pathway.

it is able to dimerize with a functional receptor without the activation of autophosphorylation.

A signal molecule is also known as a(n) _____. protein initiator key receptor ligand

ligand

What protein complex or complexes provide initial recognition of the vesicle with the target membrane? NSF and SNAPs Rab GTPase multisubunit tethering proteins and coiled-coil tethering proteins t-SNAREs and v-SNAREs

multisubunit tethering proteins and coiled-coil tethering proteins

Which of the following is NOT a secondary messenger? inositol 1,4,5-trisphosphate sn-1,2-diacylglycerol nitric oxide cAMP

nitric oxide

Cyclic AMP is degraded by __________. phosphodiesterase protein kinase G proteins AMP adenylate cyclase

phosphodiesterase

Water-soluble hormones affect target cells by binding to __________. adenylate cyclase plasma membrane receptors cAMP protein kinases cytoplasmic receptors

plasma membrane receptors

A signal transduction pathway is initiated when a _____ binds to a receptor. cyclic AMP tyrosine kinase calmodulin G protein signal molecule

signal molecule

The reason some cells respond to the presence of a steroid hormone while others do not is that _______. the receptors necessary for regulation differ among cells of various types chaperone proteins block the hormone response elements (HREs) in some cells the specific HRE is present only in certain cells only certain cells contain the gene that is targeted by a given steroid hormone

the receptors necessary for regulation differ among cells of various types

Which of these is the second of the three stages of cell signaling? gene activation reception binding of a neurotransmitter to a plasma membrane receptor transduction cell response

transduction

Which subunit of the G protein is most likely affected by the mutation? α-subunit is most likely to be affected by mutation β-subunit is most likely to be affected by mutation γ-subunit is most likely to be affected by mutation

α-subunit is most likely to be affected by mutation