We saw that GPCRs have a basal level of constitutive activity. Not all receptors do. Why might having this constitutive activity be a benefit to the cells?

Which of the following statements is true?   Question 2 options:   a)  All cells will respond to the hormonal signal because hormones are broadcast throughout the body.   b)  The regulation of inflammatory responses at the site of an infection is an example of paracrine signaling.   c)  Paracrine signaling involves the secretion of stimuli into the bloodstream for distribution throughout the organism.   d)  The axons of neurons typically signal target cells using membrane-bound signaling molecules that act on receptors in the target cells.

Which of the following statements most accurately describes what happens when an antagonist binds to a receptor?     The antagonist binds non-covalently to the receptor and promotes internalisation of the receptor.     Antagonist binding alters the structure of the receptor making it unable to function normally.     At sufficiently high concentrations the antagonist can prevent the receptor from binding to its natural (endogenous) ligand.     The antagonist-receptor complex binds to a heterotrimeric G protein forming a stable and inactive ternary complex.

A GRK inhibitor would have what effect on GPCR inactivation in the presence of a GPCR agonist? (a) it would decrease it; (b) it would maintain the same rate of inactivation; (c) it would increase it.

Usually LTP requires repeated learning trials to occur but single trial LTP is possible. Explain. What is some of the evidence to support single trial LTP?

How could we promote rapid or slow signaling for medical purposes? So there are many examples of slow and rapid signaling via coupled receptors. For an example, salivary gland secretion is rapid signaling and cell growth is slow signaling. These pathways could be twisted and used to resolve medical issues in a more natural and less damaging way. Are there any experiments that have or could be done to test out promoting rapid signaling to speed up slow processes such as cell growth in a severe wound? What experiments have or could be done to test out slowing down signaling that is fast like cells responding to their environment negatively (over-active allergies)? Thank you.

You are studying a pathogenic bacterium which secretes a toxin that affects G protein receptor signaling. You perform a preliminary experiment in which you examine intracellular CAMP levels in untreated and toxin treated cells. The data is in the figure below. How does the toxin affect CAMP levels due to G protein receptor signaling? Select all that apply CAMP levels 250 200 150 100 50 0 no Toxin with Toxin The toxin stimulates GTP binding to the Gas subunit The toxin stimulates GTP binding to the Gai subunit The toxin inhibits GAP or GTPase activating proteins The toxin stimulates adenylyl cyclase activity

1. Researchers incubated J3’s in the absence of Unknown Factor X. Upon the addition of a membrane-permeant cGMP agonist (a cGMP agonist able to penetrate into the J3’s) you would expect to see STIMULATION/INHIBITION (highlight one) of the J3 activation pathway.2. Researchers incubated J3’s in the presence of Unknown Factor X, but with the addition of a membrane-permeant CYP antagonist. In this case, you would expect to see STIMULATION/INHIBITION (highlight one) of the J3 activation pathway.

Which of the following is most likely an example of signaling through a transmembrane receptor? The influenza virus recognizes specific proteins on the surface of host cells, causing the entrance of genetic materials into the cytoplasm of the host cells.  Low-density lipoproteins (LDL) bind to receptor proteins found on the membrane of receiving cells, triggering its internalization into the receiving cells. The binding of interleukin-6 (IL-6) to the interleukin-6 receptor causes the activation of protein kinases in the cytoplasm, activating the transcription factor NF-κB. The binding of aldosterone to the aldosterone receptor activates its transcription activity, leading to the transcription of genes that promote the uptake of ions and water.

You are designing neurotransmitters and hormones that activate G protein-coupled receptors. Based on the characteristics of these family of receptors,  Which should have a higher affinity for their receptors? Which should act more rapidly?