Biochemistry: Concepts and Connections (2nd Edition)
2nd Edition
ISBN: 9780134641621
Author: Dean R. Appling, Spencer J. Anthony-Cahill, Christopher K. Mathews
Publisher: PEARSON
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Chapter 20, Problem 11P
Suppose that a G protein undergoes a mutation that allows the exchange of bound GTP for GDP to occur in the absence of G protein binding to a receptor. How might this mutation affect signaling involving a GPCR? Which subunit of the G protein is most likely affected by the mutation?
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The G protein coupled receptor (GPCR) pathway elicits diverse intracellular responses in different cells. The basic steps of GPCR signaling are outlined in this diagram.
Which of the following statements correctly describes the process of GPCR signaling?
The GPCR activation is reversible after the signal of the ligand diminishes.
The membrane-embedded enzyme uses GTP as a secondary messenger to initiate gene expression.
The ligand attaches to both the GPCR and the membrane-embedded enzyme to activate the GPCR pathway.
The ligand-bound GPCR sends a GTP molecule to an enzyme in the membrane and switches it into an active state.
Upon activation by a receptor, a G protein exchanges bound GDP for
GTP, rather than phosphorylating GDP that is already bound. Similarly,
the a subunit-GTP complex has a slow GTPase activity that hydrolyzes
bound GTP, rather than exchanging it for GDP. Describe experimental
evidence that would be consistent with these conclusions.
In the case of GPCR (G protein coupled receptor) signaling pathways, which of the following statements is INCORRECT?
The gamma subunit of the trimeric G protein has a transmembrane domain whereas the alpha and beta subunits are peripheral proteins
If G alpha was locked in a GTP bound state, it would be bound to the effector enzyme rather than to the beta and gamma subunits.
In some but not all signaling pathways, when the beta and gamma subunits are separated from alpha - the beta/gamma pair can also stimulate the activation of effectors
Chapter 20 Solutions
Biochemistry: Concepts and Connections (2nd Edition)
Ch. 20 - Prob. 1PCh. 20 - Prob. 2PCh. 20 - Prob. 3PCh. 20 - Prob. 4PCh. 20 - Prob. 5PCh. 20 - Prob. 6PCh. 20 - Prob. 7PCh. 20 - Prob. 8PCh. 20 - Prob. 9PCh. 20 - Prob. 10P
Ch. 20 - Suppose that a G protein undergoes a mutation that...Ch. 20 - Prob. 12PCh. 20 - Prob. 13PCh. 20 - Prob. 14PCh. 20 - Prob. 15PCh. 20 - Prob. 16PCh. 20 - Prob. 17PCh. 20 - Prob. 18PCh. 20 - Prob. 19PCh. 20 - Explain the effectiveness of Gleevec in treating...Ch. 20 - Prob. 21PCh. 20 - Prob. 22P
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- A mutated form of the α subunit of the heterotrimeric G protein has been identified; this form readily exchanges nucleotides even in the absence of an activated receptor. What would be the effect on a signaling pathway containing the mutated α subunit?arrow_forwardNerve-growth factor (NGF) binds to a protein tyrosine kinase receptor. The amount of diacylglycerol in the plasma membrane increases in cells expressing this receptor when treated with NGF. Propose a simple signaling pathway and identify the isoform of any participating enzymes. Would you expect the concentrations of any other common second messengers to increase on NGF treatment?arrow_forwardwhen kidney cells secrete low levels of oxygen in the blood they secrete erythropoietin. in this particular signaling pathway (response to low oxygen) the secretion of erythropoietin represents which step of the signal transdution process?arrow_forward
- 1) the Ga subunit has a mutation resulting in increased GTPase activity? Why is the GPCR referred to as a GEF? What would occur in G protein signalling ifarrow_forwardList three ways in which a signal is amplified in a Gprotein-coupled receptor signaling pathway.arrow_forwardCholera toxins, produced by the pathogenic bacteria Vibrio cholerae, disrupt G Protein Coupled Receptor (GPCR) signaling pathways. They interfere with... the ability of the beta subunit of a G protein to bind to the GPCR the ability of the gamma subunit of a G protein to exchange GDP for GTP the ability of the beta subunit of a G protein to bind to an effector protein the ability of the alpha subunit of a G protein to hydrolyze GTP to GDParrow_forward
- Continuous exposure of a G protein-coupled receptor to its ligand leads to a phenomenon known as desensitization. Describe several molecule mechanisms for receptor desensitizationarrow_forwardIn the hypothetical signaling pathway shown below, the hormone 'square' binds to its high-affinity receptor, which activates a protein 'X,' which diffuses to and activates the enzyme 'Q synthase'. When active, Q synthase catalyzes the conversion of 'P' to 'Q.' 'Q' then diffuses to the enzyme 'C kinase', which catalyzes the phosphorylation of 'C'. Phosphorylated 'C' then diffuses to and binds to the Ca* channels in an organelle membrane, which causes them to open and release Ca, which then triggers the cellular response. The second messenger in this pathway is Square Q synthase C kinase AGBO +. ARP Ca2+arrow_forwardSignaling by soluble extracellular molecules can be classified as endocrine, paracrine, or autocrine. Describe how these three types of cellular signaling differ. Growth hormone is secreted from the pituitary, which is located at the base of the brain and acts through growth hormone receptors located on the liver. Is this an example of endocrine, paracrine, or autocrine signaling? Why?arrow_forward
- In vesicle based signaling, how is the regulated secretory pathway implicated in synaptic signaling ? Then, apply this information to describe in detail the pathway in which a neurotransmitter is received at the dendrites of one neuron and ultimately leads to the release of new transmitters that activate a second neuron .arrow_forwardCompare and contrast GPCR and RTK signaling. What role does GTP play in each? What role does phosphorylation play? How is each signal differently amplified? How do these two signaling types compare to steroid signaling with respect to gene activation?arrow_forwardYou 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.arrow_forward
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