musaww22

musaww22

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Published2110

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Answer:b

Cytosolic Ca2+ causes muscle contraction by______

a. Binding to troponin

b. Binding to tropomyosin

c. Binding to myosin

d. Binding to actin

Muscle contraction is caused by_______

a. The shortening of actin filaments, caused by theATP-dependent action of myosin

b. The shortening of myosin filaments, caused by theATP-dependent action of actin

c. The sliding of myosin and actin filaments, caused by theATP-dependent action of myosin

d. The sliding of myosin and actin filaments, caused by theATP-dependent action of actin

When an action potential reaches a neuromuscular junction theresult is____

a. Acetylcholine binds to receptors on the sarcoplasmicreticulum, causing Ca2+ to flood the cytosol

b. Acetylcholine binds to receptors on the sarcolemma (muscleplasma membrane), causing depolarization of the sarcolemma

c. Ca2+ binds to receptors on the sarcolemma, causingdepolarization of the sarcolemma

d. Acetylcholine binds to troponin, allowing myosin to bind toactin

The step in the contraction cycle at which ATP binds to myosinis___

a. When myosin binds to actin

b. The “power stroke” when myosin slides the actin filamentalong

c. Just after the “power stroke”, in order to release myosinfrom actin

d. Immediately after Ca2+ enters the cytosol

Which of the following statements about the cytoskeleton istrue?

a. The cytoskeleton is made up of four types of proteinfilaments.

b. The bacterial cytoskeleton is important for cell division andDNA segregation.

c. Protein monomers that are held together with covalent bondsform cytoskeletal filaments.

d. The cytoskeleton of a cell can change in response to theenvironment.

Answer: option B
Answer: option B

can i get help in these questions. my answers 6)a 7)c 8)a 9)b 10)e 11)a 12)d- 13)c 14)a 15)b 16)e 17)a 18)d. im unsure of some answers but im wondering if you guys can check if im correct or wrong.thank you

Show transcribed image text
Answer:A
Answer:F
Answer:c
Answer:C) the motor neuron triggers an action potential at the neuromuscular j...
1. The striated appearance ofskeletal muscle is due to the
A. dark color of myosin.
B. multiple nuclei per fiber.
C. regular arrangement of filaments.
D. dense array of microtubules.
E. dense packing of ATP molecules.
Your Response:
2. How do muscle fibersshorten during contraction?
A. Individual protein filaments contract.
B. More cross-bridges are formed betweenfilaments.
C. Arrays of filaments overlap each other.
D. Protein filaments coil more tightly.
E. Subunits of protein polymers detach.
Your Response:
3. How do actin and myosinmolecules interact?
A. Globular myosin heads bind to actin filaments.
B. Globular actin heads bind to myosin filaments.
C. Other proteins connect the two.
D. Myosin filaments bend to connect to actin.
E. Actin filaments bend to connect to myosin.
Your Response:
4. When animals die, musclesstiffen in rigor mortis because
A. muscles cannot contract without ATP.
B. actin and myosin cannot bind without ATP.
C. actin and myosin cannot separate without ATP.
D. ATP is required for synthesis of proteinfilaments.
E. ATP forms cross-bridges between filaments.
Your Response:
5. Vertebrate skeletalmuscles are excitable cells because they
A. can be stimulated by ATP.
B. can be stimulated by an electric charge.
C. can secrete neurotransmitter.
D. possess voltage-gated sodium channels.
E. can attain a high level of activity.
Your Response:
6. Starting with the arrivalof an action potential at the neuromuscular junction, which of thefollowing is the correct order of events?
A. Calcium is released from the sarcoplasmic reticulum,an action potential travels down the T tubules, depolarizationspreads through the T tubule, and myosin binds actin.
B. An action potential travels down the T tubules,depolarization spreads through the T tubule, calcium is releasedfrom the sarcoplasmic reticulum, and myosin binds actin.
C. An action potential travels down the T tubules,depolarization spreads through the T tubule, calcium is taken up bythe sarcoplasmic reticulum, and myosin binds actin.
D. An action potential travels down the T tubules,depolarization spreads through the T tubule, ATP binds to myosin,and myosin binds actin.
E. A T tubule is depolarized, calcium is released fromthe sarcoplasmic reticulum, an action potential is created in themuscle cell, and myosin binds actin.
Your Response:
7. How does tropomyosincontrol muscle contraction?
A. It provides a bridge between actin and myosin.
B. It provides a site where ATP can be utilized.
C. Changes in its position expose actin
Answer: option b
Answer:B)cross bridges have actin binding sites that are normally covered by t...
Answer:depolarization of the T tubules causes calcium channels in the sacropla...
Answer: option 3

Answer: option C
Answer: option C
Answer: option D
Answer: option C
Answer: option A
Answer: option B

2. Within a single fiber, the tension developed during a twitch depends on:
a. Length of the thick filament
b. Duration of the stimulus
c. Amplitude of the action potential

d. Length of the sarcomeres prior to contraction

c. The speed the action potential is propagated throughout the muscle fiber

3. The two systems that directly control homeostasis:

a. Musculoskeletal and endocrine

b. Nervous and endocrine

c. Cardiovascular and nervous

4. There are 4 primary tissue types, which of these is not a primary tissue type:

a. Connective

d. Blood

b. Neural

e. Muscle

c. Epithelial

None of the above

There are more than two systems that control homeostasis

5. The muscle functional unit responsible for force production is the:

d. Sarcolemma

a. Sarcomere

e. Calcium

Motor unit

Myocyte

6. Choose the true statement(s):
a. Biarticular muscles only produce concentric contractions

b. During an eccentric contraction the muscle neither shortens nor lengthens

C. For a given muscle, it will produce its highest forces during a concentric contraction

d. The primary purpose of concentric contractions is fixation

e. The primary purpose of eccentric contractions is deceleration

7. Homeostasis is the condition in which the body maintains:

A. A dynamic state within an unlimited range, depending on circumstances

B. Static state with little deviation from preset points

C. A relatively stable internal environment, within limits

d. The lowest possible energy usage

8. Osteoclast precursor cells are:

a. Osteocytes

b. Osteoblasts

c. Osteogenic cells (stem cells)

d. None of the above

C. Leukocytes (white blood cells)

Answer: option C
Answer:D. When the myosin molecules of the thick filaments shorten, the muscle...
Answer: option C

1) Binding of ________ to myosin permits cross-bridge _____________ between actin and myosin in skeletal muscle cells.
A) ATP; detachment B actin; detachment C)calcium; attachment D)ATP; attachment E)calcium; detachment

2) What is the definition of a "motor unit"?

A) a pair of antagonistic muscles

B) all of the muscles that affect the movement of any given joint

C) a single motor neuron plus all the muscle fibers it innervates

D) a single muscle fiber plus all of the motor neurons that innervate it

E) all of the motor neurons supplying a single muscle

3) An action potential in the motor end plate rapidly spreads to the interior regions of a muscle cell by means of the: A) Z lines. B) sarcoplasmic reticulum. C) transverse tubules. D) pores in the plasma membrane. E) H zone.

4) Myasthenia gravis is an autoimmune disease in which the immune system gradually destroys the receptors for acetylcholine at the neuromuscular junction. Which of the following drugs might initially be useful in treating the symptoms of this disease?

A)atropine (a muscarinic acetylcholine receptor antagonist)

B)a nicotinic acetylcholine receptor antagonist

C)a drug that inhibits release of acetylcholine

D) curare

E) a drug that inhibits acetylcholinesterase

5) During an isometric twitch in a skeletal muscle:
A)H zones shorten.
B) sarcomeres do not significantly shorten.
C) tension generated by the muscle always exceeds the load on the muscle.
D) the whole muscle shortens.
E)tetanus occurs

These questions were pulled from a Biology/Physiology exam. PLEASE PLEASE PLEASE, Include an explanation of why the correct answer is a specefic one, I really appreciate that.
thanks

Answer: option C
Answer:3 --> 1 ---> 5 --> 4 --> 2
Answer: option C

1. Which of the following structures is NOT a part of the musclefiber?

A. transverse tubule
B. motor end plate
C. sarcolemma
D. synaptic knob
E. sarcoplasmic reticulum

2. You briefly apply a high concentration of acetylcholine (ACh)directly to the motor end plate and observe no contraction of thefiber. Since muscular dysgenesis only affects one type of cell inthe body you would suspect that the motor neurons of dysgenic micework normally. True or False?

A. True
B. False

3. Arrange the events at the neuromuscular junction in the propersequence from first to last

1. arrival of the action potential at the synaptic knob
2. generation of action potential in sarcolemma
3. binding of ACh to ACh receptors in the motor end plate
4. release of ACh into the synaptic cleft
5. removal of ACh from the cleft by acetylcholinesterase

A. 1, 2, 3, 5, 4
B. 2, 3, 1, 4, 5
C. 1, 4, 3, 2, 5
D. 2, 5, 1, 4, 3

4. After you apply acetylcholine to the muscle fiber you find thatan action potential is generated in the sarcolemma. This resultproves that certain events or conditions occur normally within theneuromuscular junction. Which event or condition is NOT PROVED bythe above result?

A. ACh receptors are present in the membrane of the motor endplate
B. ACh receptors bind to ACh
C. Sodium permeability of the end plate membrane is increased
D. Acetylcholinesterase breaks down ACh

5. Arrange the events of excitation contraction coupling in theproper sequence from first to last

1. cross-bridge cycling
2. action potential in the sarcolemma reaches the triads
3. release of calcium from the sarcoplasmic reticulum
4. exposure of active site on the thin filaments
5. binding of calcium to troponin

A. 2, 3, 5, 4, 1
B. 5, 3, 4, 2, 1
C. 5, 1, 3, 2, 4
D. 3, 5, 2, 4, 1

6. You artificially raise the calcium concentration within thesarcoplasm of the muscle fiber and observe that the cell contractsnormally. From this observation you conclude that the defect inmuscular dysgeny occurs at which step in control of the musclefiber?

A. Exposure of the active site on thin (actin) filaments
B. Binding of calcium to troponin
C. Release of calcium ions from the sarcoplasmic reticulum into thesarcoplasm
D. Repeated cycles of crossbridge binding, pivoting, anddetachment

7. Where in the muscle fiber do you suspect that the normal proteinmade by the mdg gene functions in normal mice?

A. motor end plate
B. triad
C. myofibrils
D. thin filaments

8. All of the following conditions would have same effect onmuscles (flaccid paralysis) as muscular dysgeny with a singleexception. What is the EXCEPTION?

A. botulism
B. poisoning with atropine
C. poisoning with military nerve gas
D. myasthenia gravis

9. You would expect the muscles from an animal afflicted withmuscular dysgenesis to exhibit:

A. hypertrophy
B. atrophy

10. You would expect that a dysgenic mouse dies shortly after birthbecause:

A. the heart fails to beat
B. vasoconstriction of the carotid artery prevents blood flow tothe brain
C. vasodilation of the systemic blood vessels causes the bloodpressure to drop to lethal levels
D. the respiratory muscles are unable to contract

Answer: option C

1. Which of the following structures is NOT a part of the musclefiber?

A. transverse tubule
B. motor end plate
C. sarcolemma
D. synaptic knob
E. sarcoplasmic reticulum

2. You briefly apply a high concentration of acetylcholine (ACh)directly to the motor end plate and observe no contraction of thefiber. Since muscular dysgenesis only affects one type of cell inthe body you would suspect that the motor neurons of dysgenic micework normally. True or False?

A. True
B. False

3. Arrange the events at the neuromuscular junction in the propersequence from first to last

1. arrival of the action potential at the synaptic knob
2. generation of action potential in sarcolemma
3. binding of ACh to ACh receptors in the motor end plate
4. release of ACh into the synaptic cleft
5. removal of ACh from the cleft by acetylcholinesterase

A. 1, 2, 3, 5, 4
B. 2, 3, 1, 4, 5
C. 1, 4, 3, 2, 5
D. 2, 5, 1, 4, 3

4. After you apply acetylcholine to the muscle fiber you find thatan action potential is generated in the sarcolemma. This resultproves that certain events or conditions occur normally within theneuromuscular junction. Which event or condition is NOT PROVED bythe above result?

A. ACh receptors are present in the membrane of the motor endplate
B. ACh receptors bind to ACh
C. Sodium permeability of the end plate membrane is increased
D. Acetylcholinesterase breaks down ACh

5. Arrange the events of excitation contraction coupling in theproper sequence from first to last

1. cross-bridge cycling
2. action potential in the sarcolemma reaches the triads
3. release of calcium from the sarcoplasmic reticulum
4. exposure of active site on the thin filaments
5. binding of calcium to troponin

A. 2, 3, 5, 4, 1
B. 5, 3, 4, 2, 1
C. 5, 1, 3, 2, 4
D. 3, 5, 2, 4, 1

6. You artificially raise the calcium concentration within thesarcoplasm of the muscle fiber and observe that the cell contractsnormally. From this observation you conclude that the defect inmuscular dysgeny occurs at which step in control of the musclefiber?

A. Exposure of the active site on thin (actin) filaments
B. Binding of calcium to troponin
C. Release of calcium ions from the sarcoplasmic reticulum into thesarcoplasm
D. Repeated cycles of crossbridge binding, pivoting, anddetachment

7. Where in the muscle fiber do you suspect that the normal proteinmade by the mdg gene functions in normal mice?

A. motor end plate
B. triad
C. myofibrils
D. thin filaments

8. All of the following conditions would have same effect onmuscles (flaccid paralysis) as muscular dysgeny with a singleexception. What is the EXCEPTION?

A. botulism
B. poisoning with atropine
C. poisoning with military nerve gas
D. myasthenia gravis

9. You would expect the muscles from an animal afflicted withmuscular dysgenesis to exhibit:

A. hypertrophy
B. atrophy

10. You would expect that a dysgenic mouse dies shortly after birthbecause:

A. the heart fails to beat
B. vasoconstriction of the carotid artery prevents blood flow tothe brain
C. vasodilation of the systemic blood vessels causes the bloodpressure to drop to lethal levels
D. the respiratory muscles are unable to contract

Answer: option A

1. Which of the following structures is NOT a part of the musclefiber?

A. transverse tubule
B. motor end plate
C. sarcolemma
D. synaptic knob
E. sarcoplasmic reticulum

2. You briefly apply a high concentration of acetylcholine (ACh)directly to the motor end plate and observe no contraction of thefiber. Since muscular dysgenesis only affects one type of cell inthe body you would suspect that the motor neurons of dysgenic micework normally. True or False?

A. True
B. False

3. Arrange the events at the neuromuscular junction in the propersequence from first to last

1. arrival of the action potential at the synaptic knob
2. generation of action potential in sarcolemma
3. binding of ACh to ACh receptors in the motor end plate
4. release of ACh into the synaptic cleft
5. removal of ACh from the cleft by acetylcholinesterase

A. 1, 2, 3, 5, 4
B. 2, 3, 1, 4, 5
C. 1, 4, 3, 2, 5
D. 2, 5, 1, 4, 3

4. After you apply acetylcholine to the muscle fiber you find thatan action potential is generated in the sarcolemma. This resultproves that certain events or conditions occur normally within theneuromuscular junction. Which event or condition is NOT PROVED bythe above result?

A. ACh receptors are present in the membrane of the motor endplate
B. ACh receptors bind to ACh
C. Sodium permeability of the end plate membrane is increased
D. Acetylcholinesterase breaks down ACh

5. Arrange the events of excitation contraction coupling in theproper sequence from first to last

1. cross-bridge cycling
2. action potential in the sarcolemma reaches the triads
3. release of calcium from the sarcoplasmic reticulum
4. exposure of active site on the thin filaments
5. binding of calcium to troponin

A. 2, 3, 5, 4, 1
B. 5, 3, 4, 2, 1
C. 5, 1, 3, 2, 4
D. 3, 5, 2, 4, 1

6. You artificially raise the calcium concentration within thesarcoplasm of the muscle fiber and observe that the cell contractsnormally. From this observation you conclude that the defect inmuscular dysgeny occurs at which step in control of the musclefiber?

A. Exposure of the active site on thin (actin) filaments
B. Binding of calcium to troponin
C. Release of calcium ions from the sarcoplasmic reticulum into thesarcoplasm
D. Repeated cycles of crossbridge binding, pivoting, anddetachment

7. Where in the muscle fiber do you suspect that the normal proteinmade by the mdg gene functions in normal mice?

A. motor end plate
B. triad
C. myofibrils
D. thin filaments

8. All of the following conditions would have same effect onmuscles (flaccid paralysis) as muscular dysgeny with a singleexception. What is the EXCEPTION?

A. botulism
B. poisoning with atropine
C. poisoning with military nerve gas
D. myasthenia gravis

9. You would expect the muscles from an animal afflicted withmuscular dysgenesis to exhibit:

A. hypertrophy
B. atrophy

10. You would expect that a dysgenic mouse dies shortly after birthbecause:

A. the heart fails to beat
B. vasoconstriction of the carotid artery prevents blood flow tothe brain
C. vasodilation of the systemic blood vessels causes the bloodpressure to drop to lethal levels
D. the respiratory muscles are unable to contract

Answer: option B

1. Which of the following structures is NOT a part of the musclefiber?

A. transverse tubule
B. motor end plate
C. sarcolemma
D. synaptic knob
E. sarcoplasmic reticulum

2. You briefly apply a high concentration of acetylcholine (ACh)directly to the motor end plate and observe no contraction of thefiber. Since muscular dysgenesis only affects one type of cell inthe body you would suspect that the motor neurons of dysgenic micework normally. True or False?

A. True
B. False

3. Arrange the events at the neuromuscular junction in the propersequence from first to last

1. arrival of the action potential at the synaptic knob
2. generation of action potential in sarcolemma
3. binding of ACh to ACh receptors in the motor end plate
4. release of ACh into the synaptic cleft
5. removal of ACh from the cleft by acetylcholinesterase

A. 1, 2, 3, 5, 4
B. 2, 3, 1, 4, 5
C. 1, 4, 3, 2, 5
D. 2, 5, 1, 4, 3

4. After you apply acetylcholine to the muscle fiber you find thatan action potential is generated in the sarcolemma. This resultproves that certain events or conditions occur normally within theneuromuscular junction. Which event or condition is NOT PROVED bythe above result?

A. ACh receptors are present in the membrane of the motor endplate
B. ACh receptors bind to ACh
C. Sodium permeability of the end plate membrane is increased
D. Acetylcholinesterase breaks down ACh

5. Arrange the events of excitation contraction coupling in theproper sequence from first to last

1. cross-bridge cycling
2. action potential in the sarcolemma reaches the triads
3. release of calcium from the sarcoplasmic reticulum
4. exposure of active site on the thin filaments
5. binding of calcium to troponin

A. 2, 3, 5, 4, 1
B. 5, 3, 4, 2, 1
C. 5, 1, 3, 2, 4
D. 3, 5, 2, 4, 1

6. You artificially raise the calcium concentration within thesarcoplasm of the muscle fiber and observe that the cell contractsnormally. From this observation you conclude that the defect inmuscular dysgeny occurs at which step in control of the musclefiber?

A. Exposure of the active site on thin (actin) filaments
B. Binding of calcium to troponin
C. Release of calcium ions from the sarcoplasmic reticulum into thesarcoplasm
D. Repeated cycles of crossbridge binding, pivoting, anddetachment

7. Where in the muscle fiber do you suspect that the normal proteinmade by the mdg gene functions in normal mice?

A. motor end plate
B. triad
C. myofibrils
D. thin filaments

8. All of the following conditions would have same effect onmuscles (flaccid paralysis) as muscular dysgeny with a singleexception. What is the EXCEPTION?

A. botulism
B. poisoning with atropine
C. poisoning with military nerve gas
D. myasthenia gravis

9. You would expect the muscles from an animal afflicted withmuscular dysgenesis to exhibit:

A. hypertrophy
B. atrophy

10. You would expect that a dysgenic mouse dies shortly after birthbecause:

A. the heart fails to beat
B. vasoconstriction of the carotid artery prevents blood flow tothe brain
C. vasodilation of the systemic blood vessels causes the bloodpressure to drop to lethal levels
D. the respiratory muscles are unable to contract

Answer: option A

Skeletal Muscle is innervate by axons from motor neurons whose main body is located in the spinal cord. At its termination, the motor neuron lacks a myelin sheath & divides into a number of terminals, synapsing with several muscle fibers. Impulses arriving at the terminal stumulate the realease of the neurotransmitter acetylcholine (ACh). ACh, in turn, binds to specific receptors located on the adjacent muscle membrane, causing depolarization & subsequent contraction of the muscle. The Ach receptor is a protein with a molecular weight of about 250,000. It is made up of 5 subunits which extend through the cell membrane.

Myasthenia gravis is a debilitating & sometimes fatal, autoimmune disease that causes progressive weakening of muscles. Antibodies specific to the ACh receptor on the postsynaptic membrane of the neuralmuscular junction (the motor end plate) interrupt synapatic transmission by increasing endocytosis of ACh receptors. They also form immune complexes, which causes further distruction of the post-synaptic membrane.

1. In response to bound a ACh, the ACh receptor.....

a) release calcium ions into the cytoplasm

b) hydrolyzes ATP to pump sodium ions into the cell

c) allows chloride ions to passively diffuse into the cell

d) allows sodium ions to passively diffuse into the cell

2. The antibody & the ACh receptor both.....

a) bind acetylcholine

b) are secreted proteins

c) are synthesized primarily by cells of the immune system

d) are composed of multiple polypeptides

3. Aceytcholinesterase inhibitors, such as pyridostigmine & neostigmine, increase the duration of action of released ACh, & thus are beneficial to patients with myasthenia gravis. They function by....

I. Removing anti-acetylcholine receptor antibodies

II. Preventing the degradation of acetylcholine

III. Substituting for acetylcholine in its action at the neuromuscular junction

a) I only

b ) II only

c) II & III only

d) none of the above

Answer:allows chloride ions to passively diffuse into the cell
Answer: option A
Answer:3.) Muscle fiber 4.) Myofibril

Which of the following would be an effector protein at the end of a signaling pathway?

A transcription factor that blocks the promoter region of a kinase

A cytoskeletal anchor protein that when phosphorylated is localized to the leading edge of a migrating cell to direct movement

A protein that breaks down dietary fat to Acetyl CoA for use in the TCA/Krebs/Citric Acid cycle.

All of the above

----------------------------------------------------------------------------------------------------

Match the following membrane receptor types with their characteristics

- A. B. C. D.

Opens in response to ligand binding, turns a chemical signal into an electrical one.

- A. B. C. D.

Contains intrinsic GTPase activity

- A. B. C. D.

Is a 7 pass transmembrane protein

- A. B. C. D.

Associate with enzymes in the cell , such as kinases

- A. B. C. D.

Can as a molecular switch through phosphorylation and dephosphorylation

- A. B. C. D.

Act as a molecular switch through GTP hydrolysis

- A. B. C. D.

1/3 of all drugs target these

A.

Enzyme-Coupled Receptors

B.

ion-channel-coupled receptor

C.

G-Protein coupled receptor

D.

G-protein

--------------------------------------------------------------------------------------------------

Place the following steps of GPCR signaling in order

(A) The active beta gamma subunit is bound by inactive alpha subunits, inactivating beta-gamma

(B) The activated alpha subunit binds target proteins until hydrolysis of the GTP inactivates the subunit

(C) The alpha subunit dissociates from the beta and gamma subunits

(D) GTP binds the alpha subunit of the G-Protein

(E) ligand binds to GPCR

(F)GPCR changes conformation

(G)G Protein is recruited to the activated receptor

(H)GDP is dissociated from G Protein complex

Answer:A protein that breaks down dietary fat to Acetyl CoA for use in the TCA...
Answer: option A

QUESTION 1

Many mutations in receptor kinases that lead to cancer allow the dimerization and activation of the receptor, even in the absence of signaling molecule. An example of this is a mutant form of the EGF receptor kinase called Her2/neu. An antibody that prevents dimerization of Her2/neu receptor kinases is being tested for its effectiveness in stopping cancer. At which stage would this drug work?

A.
It would prevent the signaling cell from producing the signal.

B.
It would prevent the receptor from binding to the signal.

C.
It would prevent the receptor from becoming activated.

D.
It would prevent the termination of the signal.

1 points
QUESTION 2

Which type of cell signaling does not rely on the diffusion of a chemical signal
molecule?

A.
juxtacrine

B.
paracrine

C.
autocrine

D.
endocrine

E.
All of these choices are correct.

1 points
QUESTION 3

Steroid hormones:

A.
have the same effect on different types of cells.

B.
bind to cell-surface receptors.

C.
bind intracellular receptors to form complexes that migrate to the nucleus.

D.
facilitate the initiation of translation by ribosomes.

1 points
QUESTION 4

Which type of signal receptor dimerizes upon ligand binding, leading to phosphorylation of the receptor dimer?

A.
G protein-coupled receptor

B.
receptor tyrosine kinase

C.
ligand-gated ion channel

D.
nuclear receptor

1 points
QUESTION 5

Which of the following is a part of the MAP kinase pathway?

A.
A receptor kinase is activated by binding to a growth factor and phosphorylates receptor cytoplasmic domains.

B.
phosphorylated sites on the receptor dimer recruit a signaling complex that stimulates Ras to release GDP and bind GTP

C.
The activated RAS protein activates a protein kinase in the signal-transduction pathway.

D.
A series of protein kinases amplify the signal to the nucleus where a transcription factor causes increased transcription of genes involved in the cell division cycle

E.
all of the above

1 points
QUESTION 6

An increased heart rate caused by the release of epinephrine from the adrenal glands and movement of the epinephrine through the blood stream to the heart is an example of _______________________________.

A.
autocrine signaling

B.
juxtacrine signaling

C.
paracrine signaling

D.
endocrine signaling

1 points
QUESTION 7

At the neuromuscular junction, acetylcholine released from a motor neuron

A.
binds to and opens Na+ channels on skeletal muscle cells

B.
causes an action potential in the motor neuron

C.
causes hyperpolarization of skeletal muscle cells

1 points
QUESTION 8

A mutated ras allele encodes Ras protein that is unable to hydrolyze GTP to GDP. What does this do?

A.
keeps Ras permanently active

B.
prevents Ras activity

C.
Neither

1 points
QUESTION 9

Phosphatases are a family of enzymes that specifically remove phosphate groups from proteins that were added by protein kinases. Vanadate is an inhibitor of tyrosine phosphatases in eukaryotic cells. What effect would vanadate have on the response of cells to signals received by receptor tyrosine kinases?

A.
The response of the cell would last longer than it normally would.

B.
The response of the cell would be shorter than it normally would.

C.
The signal would still bind the receptor, so there would be no effect.

1 points
QUESTION 10

A cellular response to a signal can be terminated by:

A.
disassociation of the ligand from the receptor.

B.
inactivation of intracellular signal transduction proteins.

C.
endocytosis of the receptor

D.
depletion of a second messenger.

E.
All of these choices are correct.

1 points
QUESTION 11

The type of cellular response to a signal depends on:

A.
the type of receptor being expressed in the cell.

B.
the type of intracellular signal transduction proteins being expressed in the cell.

C.
other signals to which the cell is concurrently responding.

D.
All of these choices are correct.

1 points
QUESTION 12

Cell-to-cell signaling involves

A.
a ligand

B.
a signaling cell

C.
a receptor

D.
a responding cell

E.
all of the above

1 points
QUESTION 13

An important signaling event that determines whether or not a cell will become a neuron involves binding of a transmembrane protein in one cell directly to a transmembrane protein of another cells, initiating intracellular signaling in one of the cells. This is an example of ___________ signaling.

A.
juxtacrine

B.
paracrine

C.
autocrine

D.
endocrine

E.
All of these choices are correct.

1 points
QUESTION 14

Which type of receptor is an intracellular receptor (i.e. not an integral plasma membrane protein)?

A.
G protein-coupled receptor

B.
receptor tyrosine kinase

C.
ligand-gated ion channel

D.
nuclear receptor

1 points
QUESTION 15

After acetylcholine is secreted by a motor neuron and stimulates initiation of an action potential in skeletal muscle, the signal is reversed by:

A.
depletion of acetylcholine, which returns the ligand-gated ion channel to the resting, closed conformation, preventing further transport of sodium ions.

B.
an ATP-powered sodium pump in the plasma membrane that continuously works to set up a sodium concentration gradient.

C.
an enzyme that degrades and removes acetylcholine from the neuromuscular junction.

D.
a resting neuron that stops releasing acetylcholine into the neuromuscular junction.

E.
All of these choices are correct.

1 points
QUESTION 16

Which of the following scenarios would result in a proliferation signal via the MAP kinase cascade in the absence of ligand binding to its receptor tyrosine kinase?

A.
a continuously active MAP kinase kinase

B.
a Ras molecule that has no GTPase activity

C.
a continuously inactive MAP kinase pathway and an inactive Ras

D.
prevention of activity of phosphatases that would normally dephosphorylate kinases in the MAPK cascade or the transcription factors phosphorylated by MAPK

E.
all of the above

1 points
QUESTION 17

Which of these is NOT a protein?

A.
receptor tyrosine kinase

B.
Ras

C.
transcription factor

D.
cAMP

E.
ligand gated ion channel

1 points
QUESTION 18

Ras is a cytosolic protein. Where is the mRNA for Ras translated?

A.
a ribosome in the cytosol

B.
a ribosome in the cytosol that has been directed to the surface of the rough ER

C.
nucleus

1 points
QUESTION 19

Activation of MAPK leads to phosphorylation of transcription factors. What is a DIRECT (i.e. occurring before any of the others on the list) result of this?

A.
change in rates of transcription of specific genes involved in regulation of the cell cycle

B.
increased synthesis of proteins

C.
cell division

1 points
QUESTION 20

A GPCR is a plasma membrane protein. Where is the mRNA for this GPCR translated?

A.
a ribosome in the cytosol

B.
a ribosome in the cytosol that has been directed to the surface of the rough ER

C.
nucleus

1 points
QUESTION 21

What is the monomer that is polymerized to synthesize a GPCR protein?

A.
epinephrine

B.
amino acid

C.
ribonucleotide

D.
deoxyribonucleotide

E.
monosaccharide

1 points
QUESTION 22

What is the monomer that is polymerized to form the mRNA for a GPCR?

A.
epinephrine

B.
amino acid

C.
ribonucleotide

D.
deoxyribonucleotide

E.
monosaccharide

1 points
QUESTION 23

The gene for a GPCR is a segment of a polymer composed of which monomer?

A.
epinephrine

B.
amino acid

C.
ribonucleotide

D.
deoxyribonucleotide

E.
monosaccharide

Answer:C. It would prevent the receptor from becoming activated
Answer:b

Show transcribed image text
Answer:c
Answer:b
Answer:contact-dependent K+ channel receptor
Answer: option c
Answer: option b
Answer: option b

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