Which of the following is not an example of an ion transporter?

TLS Online TPP Program

#Question id: 13163

#Unit 4. Cell Communication and Cell Signaling

Following statements are regarding to the interaction between β2-adrenergic receptor and G- protein.

TLS Online TPP Program

#Question id: 13164

#Unit 4. Cell Communication and Cell Signaling

Match the following.

Column I	Column II	Column III
A. G Protein–Coupled Receptors That Activate PDE	i. cAMP	a. Increase in conversion of glycogen to glucose
B. G Protein–Coupled Receptors That Activate Adenylyl Cyclase	ii. cGMP	b. Hyperpolarization or depolarization of photoreceptor membrane
C. G Protein–Coupled Receptors That inhibit Adenylyl Cyclase	iii. DAG	c. activates genes necessary for cell division
D. G Protein–Coupled Receptors That Trigger Elevations in Cytosolic and Mitochondrial Calcium		d. increase in K+ permeability hyperpolarizes the membrane

Which one of the following is correct?

TLS Online TPP Program

#Question id: 14685

#Unit 4. Cell Communication and Cell Signaling

In dark-adapted rod cells, a high level of cGMP keeps cGMP-gated nonselective cation channels open, leading to hyperpolarization of the plasma membrane and neurotransmitter release. 

B - Light absorption generates activated rhodopsin, R*, which binds inactive, GDP-bound Gαt protein and mediates the exchange of GDP for GTP . 

C- The free Gαt∙GTP activates PDE by binding to its inhibitory γ subunits and dissociating them from the catalytic α and β subunits . Relieved of their inhibition, the α and β subunits of PDE hydrolyze GMP to cGMP . 

D- The resulting decrease in cytosolic cGMP leads to dissociation of cGMP from the cation channels in the plasma membrane and the closing of those channels . 

E- The membrane then becomes transiently hyperpolarized, and neurotransmitter release is reduced. 

TLS Online TPP Program

#Question id: 14686

#Unit 4. Cell Communication and Cell Signaling

This member of the AKAP family, designated mAKAP, anchors both PDE and the regulatory subunit  of PKA to the nuclear membrane, maintaining them in a negative feedback loop that provides close local control of the ATP level and PKA activity.

B- The basal level of PDE activity in the presence of hormone (resting state) keeps cAMP levels below those necessary for PKA activation. 

C- Activation of β-adrenergic receptors causes an increase in cAMP to a level in excess of that which can be degraded by PDE. 

D- The resulting binding of cAMP to the R subunits of PKA releases the active catalytic (C) subunits into the cytosol. Some C subunits enter the nucleus, where they phosphorylate and thus activate certain transcription factors . Other C subunits phosphorylate PDE, stimulating its catalytic activity.

E-  Active PDE hydrolyzes cAMP, thereby driving cAMP levels back to basal levels and causing re-formation of the inactive PKA C-R complex. Subsequent de-phosphorylation of PDE returns the complex to the resting state.

TLS Online TPP Program

#Question id: 14738

#Unit 4. Cell Communication and Cell Signaling

Choose correct statements about Muscarinic receptors;

a. An acetylcholine analog, In activated condition, these receptors slow the rate of heart muscle contraction.

b .This type of receptor is coupled to a Gαi protein, and ligand binding leads to the opening of an associated K+ channel.

c .The subsequent influx of K+ ions from the cytosol causes an increase in the magnitude of the usual inside-negative potential across the plasma membrane that lasts for several seconds. 

TLS Online TPP Program

#Question id: 14739

#Unit 4. Cell Communication and Cell Signaling

In heart muscle, activation series of the muscarinic acetylcholine receptor its effector K+ channel via the Gβγ subunit of a Gi protein.

a. Binding of acetylcholine triggers activation of the Gαi subunit and its dissociation from the Gβγ subunit in the usual way. 

b. The released Gβγ subunit (rather than Gαi∙GTP) binds to and opens the associated effector protein, a K+ channel. 

b. The increase in K+ permeability hyperpolarizes the membrane, which reduces the frequency of heart muscle contraction. 

d. Activation is terminated when the GTP bound to Gαi is hydrolyzed (by a GAP enzyme that is an intrinsic part of the Gαi subunit) to GDP and Gαi∙GDP recombines with Gβγ.