Exam 3: Ch 15 CLICKER Flashcards

1
Q

Nitric Oxide gas released by endothelial cells in the blood vessels diffuses to induce relaxation of adjacent smooth muscle cells. This is an example of___________ signaling.

A. Endocrine

B. Paracrine

C. Synaptic

D. Contact-dependant

A

B. Paracrine

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2
Q

During nervous-system development in Drosophila, the membrane-bound
protein Delta acts as an inhibitory signal to prevent neighboring cells from developing into neuronal cells. Delta is involved in ______________ signaling.

A. Endocrine

B. Paracrine

C. Synaptic

D. Contact-dependent

A

D. Contact-dependent

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3
Q

If signaling molecules act on the same cells that release them, it is an example of _____________ signaling.

A. Endocrine

B. Autocrine

C. Synaptic

D. Contact-dependent

A

B. Autocrine

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4
Q

Monomeric GTPases are in “ON State(active)” upon binding to:

A. GDP

B. GTP

C. ADP

D. ATP

A

B. GTP

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5
Q

Which of these occur more rapidly in response to a signal?

A- Changes in protein phosphorylation

B- Changes in mRNA synthesis

A

A- Changes in protein phosphorylation

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6
Q

Which of these best describe the GPCRs?

A- All receptors of this class are polypeptides with seven transmembrane segments.

B- Alter the membrane potential directly by changing the permeability
of the plasma membrane.

C- Must be coupled with intracellular monomeric GTP-binding
proteins

A

A- All receptors of this class are polypeptides with seven transmembrane segments.

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7
Q

The length of time a G protein will signal is determined by _______.

A- the activity of phosphatases that turn off G proteins by dephosphorylating Gα.

B- the activity of protein phosphatases that turn GTP into GDP.

C- the GTPase activity of Gα.

A

C- the GTPase activity of Gα.

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8
Q

The two monomers in a receptor tyrosine kinase dimer phosphorylate each other and the process is called………………

A- Nucelotide exchange

B- Ubiquitination

C- Serine Phosphorylation

D- Trans-autophosphorylation

A

D- Trans-autophosphorylation

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9
Q

Which of the following mechanisms is not directly involved in inactivating an activated RTK (Receptor Tyrosine Kinase)?

A- dephosphorylation by serine/threonine phosphatases

B- dephosphorylation by protein tyrosine phosphatases

C- removal of the RTK from the plasma membrane by endocytosis

D- digestion of the RTK in lysosomes

A

A- dephosphorylation by serine/threonine phosphatases

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10
Q

Activation of Notch is irreversible?

A) TRUE

B) FALSE

A

A) TRUE

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11
Q

There is no fundamental chemical distinction between signaling molecules that bind to cell-surface receptors and those that bind to intracellular receptors.

A. True

B. False

A

False. There is a fundamental chemical distinction between signaling molecules that bind to cell-surface receptors and those that bind to intracellular receptors. Cell-surface receptors typically bind to hydrophilic signaling molecules, such as peptides, proteins, and most neurotransmitters, while intracellular receptors usually bind to hydrophobic signaling molecules, such as steroid hormones and thyroid hormones. This difference in chemical nature is due to the location of the receptors and the types of molecules they need to interact with for signaling.

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12
Q

What is the term for the protein that organizes groups of interacting intracellular signaling proteins into signaling complexes?

A. Intracellular receptor

B. Kinase cascade

C. Scaffold protein

D. Interaction domain

A

C. Scaffold protein

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13
Q

What is the term for the compact protein modules found in many intracellular signaling
molecules that bind to a particular structural motif in another protein (or lipid) molecule to
which the signaling protein binds?

A. Cell-surface receptors

B. Ligands

C. Interaction domains

D. Scaffold proteins

A

C. Interaction domains

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14
Q

Negative feedback counteracts the effect of a stimulus and thereby abbreviates and
limits the level of the response, making the system less sensitive to perturbations.

A. True

B. False

A

A. True

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15
Q

Alterations in signaling in the pituitary gland can lead to human disease. The GH-releasing
hormone (GHRH) stimulates release of growth hormone (GH) from the pituitary gland by binding to GHRH receptors, which are G-protein-coupled receptors. Excessive activity of the GHRH signaling leads to excessive release of growth hormone, which can lead to a form of gigantism.

Consider steps that could be taken to reduce GH release. Select if the following interventions indicated in blue below belong to A or B category.

*Block hydrolysis of GTP by G-alpha.

A. Decreases GH release
B. Increases GH release

A

B. Increases GH release

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16
Q

Alterations in signaling in the pituitary gland can lead to human disease. The GH-releasing
hormone (GHRH) stimulates release of growth hormone (GH) from the pituitary gland by binding to GHRH receptors, which are G-protein-coupled receptors. Excessive activity of the GHRH signaling leads to excessive release of growth hormone, which can lead to a form of gigantism.

Consider steps that could be taken to reduce GH release. Select if the following interventions indicated in blue below belong to A or B category.

*Inhibit interaction of G-alpha with receptor

A. Decreases GH release
B. Increases GH release

A

A. Decreases GH release

17
Q

Alterations in signaling in the pituitary gland can lead to human disease. The GH-releasing
hormone (GHRH) stimulates release of growth hormone (GH) from the pituitary gland by binding to GHRH receptors, which are G-protein-coupled receptors. Excessive activity of the GHRH signaling leads to excessive release of growth hormone, which can lead to a form of gigantism.

Consider steps that could be taken to reduce GH release. Select if the following interventions indicated in blue below belong to A or B category.

*Activate phosphorylation of the receptor by GRK kinase
A. Decreases GH release
B. Increases GH release

A

A. Decreases GH release

18
Q

Alterations in signaling in the pituitary gland can lead to human disease. The GH-releasing
hormone (GHRH) stimulates release of growth hormone (GH) from the pituitary gland by binding to GHRH receptors, which are G-protein-coupled receptors. Excessive activity of the GHRH signaling leads to excessive release of growth hormone, which can lead to a form of gigantism.

Consider steps that could be taken to reduce GH release. Select if the following interventions indicated in blue below belong to A or B category.

*Block binding of arrestin to the receptor
A. Decreases GH release
B. Increases GH release

A

B. Increases GH release

19
Q

Which of the following would increase phosphorylation of CREB by PKA?

A. blocking binding of the regulatory subunits to the catalytic subunits of PKA

B. blocking nuclear entry of PKA.

C. blocking ATP binding to the active site of PKA

D. blocking cAMP binding to the regulatory subunits of PKA

A

A. blocking binding of the regulatory subunits to the catalytic subunits of PKA

20
Q

The mechanism of how Gator 2 inhibits
Gator 1 has remained unknown.
However, in 2023, researchers found that the E3 ligase subunit of Gator2 ubiquitinates a subunit of Gator1 and inhibits its GAP activity. What is the expected effect of this inhibition?

A. Rag remains bound to GDP

B. Ragulator activity is inhibited

C. mTORC1 kinase is activated

A

C. mTORC1 kinase is activated

21
Q

Imagine that two protein kinases, PK1 and PK2, act sequentially in a kinase cascade that
activates a set of target proteins bringing about a growth response.

When either kinase is inactivated, cells do not respond to the extracellular signal.

By contrast, cells containing a mutant form of PK1 that is permanently active respond even
in the absence of an extracellular signal. Cells that contain both an inactivated PK2 and a
permanently active PK1 respond in the absence of a signal.

Given these data, what is the order of action of PK1 and PK2?

A. PK1 activates PK2.
B. PK2 activates PK1.

A

B. PK2 activates PK1.

22
Q

Imagine that two protein kinases, PK1 and PK2, act sequentially in a kinase cascade that
activates a set of target proteins bringing about a growth response.

When either kinase is inactivated, cells do not respond to the extracellular signal.

By contrast, cells containing a mutant form of PK1 that is permanently active respond even
in the absence of an extracellular signal. Cells that contain both an inactivated PK2 and a
permanently active PK1 respond in the absence of a signal.

What outcome would you predict for a doubly mutant cell line with an activating mutation
in PK2 and an inactivating mutation in PK1?

A. The doubly mutant cells would grow in the absence of signal.

B. The doubly mutant cells would not grow even in the presence of signal

A

B. The doubly mutant cells would not grow even in the presence of signal