How does a compound that inhibits the GTPase activity of G-alpha affect liver cell responses to epinephrine?     It would increase proliferation.     It would decrease glucose production.     It would decrease proliferation.     It would increase glucose production.

What do steroid hormone signaling and receptor tyrosine kinase (RTK) signaling have in common?     Their pathways involve G-proteins that are activated by GDP-GTP exchange.     They both result in gene transcription.     They both use the second messenger cAMP.     The receptors are both enzymes.

Digoxin, a toxin derived from the foxglove (shown), can be used to treat heart disorders such as atrial fibrillation. Digoxin’s mechanism of action is to inhibit the Na+/K+ ATPase. Which of the following is the most likely side effect of Digoxin treatment? Failure to transport glucose into cells during an extended fast     Failure to transport glucose into cells after after eating a large meal     Enhanced response of muscle cells to Acetylcholine     Failure to transport Cl- out of the cell using direct active transport

When insulin binds to its receptor, a conformational change occurs that results in auto phosphorylation of the receptor on a specific Tyr residues. In the next step of the signaling pathway, an adaptor protein called IRS-1(insulin receptor substrate-1) docks with the phosphorylated receptor. This step is essential for the downstream activation of several kinases including Alk, also known as protein B as well as protein C kinase and GSK-3. Protein kinase 3 is involved in mobilizing GLUT 4 glucose transporters to the plasma membrane and GSK-3 phosphorylates glycogen sunthase. What would be the effects of a mammalian organism over expressing IRS-1 were also deficient in muscle GAK-3? Would this deficiency be lethal ?

A certain type of tumor results in the overproduction of glucagon. Researchers claim that treatment with insulin can counteract the effects of the excess glucagon on the pathway shown in Figure 2. Provide reasoning to justify the researchers' claim.

The hormone, glucagon, is released in the body when glucose levels are low.  Briefly describe how each of the following participate in the response to glucagon: gluconeogenesis glycolysis F16BP F26BP PFK-1 PFK-2 FBPase-1 FBPase-2

You are studying a drug that affects a cAMP signalling pathway that is normally initiated when a signalling molecule binds to a G-protein coupled receptor. You determine that the drug prevents the hydrolysis of GTP bound to G-proteins in this pathway.  Describe the impact, if any, that this drug would have on the G-protein coupled receptor (GPCR), assuming that the pathway has been activated by the presence of the signalling molecule (first messenger).  Include an explanation for your response.

Considering the endocrine function of adipose tissue, why is it so hard for people to maintain weight loss? I was thinking from the adipose tissue there is: adiponectin → hormone synthesized by adipose cells → reduce cellular insulin resistance + protects blood vessels from inflammation + atherosclerosis. However, the levels of the hormone are lower in people who are obese. But I'm not sure if that is correct or not.

Old fashioned licorice candy is made from the root of the licorice plant. If you have never had it, this natural candy is delicious, far superior to the artificially flavored junk commonly sold. But don't eat too much, because licorice root extract contains glycyrrhizin, a plant steroid that is a powerful inhibitor of the adrenal 113-hydroxysteroid dehydrogenase, causing a mild increase in cortisol levels. What Is another potential side effect? A. Goiter B. Type 2 diabetes C.Osteoporosis D. Hypokalemia OE. Achondroplasia

If protein phosphatase 1 (PP1) is inhibited does Glycogen Synthase Kinase 3 become more active?