get help please with this question? Two mutations have occurred to proteins within the glucagon signaling pathway: A) The glucagon receptor has a mutation. This mutation causes this GPCR to always have a conformation that will induce nucleotide exchange for any associated heterotrimeric G proteins, even without glucagon binding to the receptor. B) The alpha subunit of the heterotrimeric G protein has a mutation. This mutation causes the Gαarginine finger to always be in a position to properly order the catalytic residues within the Gαsubunit to promote catalysis. Question: What will the combined effect of both mutations be on the signaling pathway and what is the mechanistic reason for this effect

get help please with this question? Two mutations have occurred to proteins within the glucagon signaling pathway: A) The glucagon receptor has a mutation. This mutation causes this GPCR to always have a conformation that will induce nucleotide exchange for any associated heterotrimeric G proteins, even without glucagon binding to the receptor. B) The alpha subunit of the heterotrimeric G protein has a mutation. This mutation causes the Gαarginine finger to always be in a position to properly order the catalytic residues within the Gαsubunit to promote catalysis. Question: What will the combined effect of both mutations be on the signaling pathway and what is the mechanistic reason for this effect

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter4: Principles Of Neural And Hormonal Communication

Section: Chapter Questions

Problem 18RE

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Can I get help on how to do this question? Two mutations have occurred to proteins within the glucagon signaling pathway: A) The glucagon receptor has a mutation. This mutation causes this GPCR to always have a conformation that will induce nucleotide exchange for any associated heterotrimeric G proteins, even without glucagon binding to the receptor. B) The alpha subunit of the heterotrimeric G protein has a mutation. This mutation causes the Gαarginine finger to always be in a position to properly order the catalytic residues within the Gαsubunit to promote catalysis. Question: What will the effect of the glucagon receptor mutation be on the GPCRs function and what is the mechanistic reason for this effect?
Can I get help on how to do this question? Two mutations have occurred to proteins within the glucagon signaling pathway: A) The glucagon receptor has a mutation. This mutation causes this GPCR to always have a conformation that will induce nucleotide exchange for any associated heterotrimeric G proteins, even without glucagon binding to the receptor. B) The alpha subunit of the heterotrimeric G protein has a mutation. This mutation causes the Gα arginine finger to always be in a position to properly order the catalytic residues within the Gα subunit to promote catalysis. Question: What will the effect of the Gα mutation be on Gα's function and what is the mechanistic reason for this effect?
Why do signals indicating damage to cells result in increase in the expression of p21Cip1? I need new answer
Place the following events in the proper order to describe the production of a second messenger from a G-protein. 1. Dissociation of G alpha from the beta and gamma subunits in the G protein complex 2. Ligand interaction with the G protein-coupled receptor (GPCR) 3. Recruitment of a G protein to the GPCR and replacement of GDP with GTP on the G alpha subunit 4. Conformational change in the G alpha a subunit causing a decreased affinity for the beta and gamma subunits 5. Activation of an effector, such as adenylyl cyclase to make CAMP, by the active G alpha subunit OA. 4, 5, 1, 2, 3 OB. 4, 3, 2, 1, 5 OC-3, 2, 1, 5, 4 OD. 1, 2, 3, 4, 5 OE. 2, 3, 4, 1,5 QUESTION 17 Kinases are essential in the cell because they directly OA. destroy IP3, turning off that signaling pathway. OB. phosphorylate proteins to cause conformational changes that change their activity. OC. directly activate translation. O D bind hydrophobic hormones in the cytoplasm to activate them. O E. bind and release calcium…
I am stuck on a question about cell growth signaling and RTKs. If phosphatase is nonfunctional, could it lead to uncontrollable growth resulting in cancer?
The transforming growth factory beta (TGF-b) family of hormones / growth factors are dimers and they interact with specific receptors. Which of the following statements about these receptors is correct? a) A receptor complex is formed from a type 1 and a type 2 receptor b) A receptor complex is formed between the ligand and the receptor c) This family interacts with a single serine- threonine kinase receptor d) The major receptor is intracellular e) The receptor is a G-protein receptor
Put the following steps for the outline of the growth factor signaling pathway in order: Map Kinase Kinase is Phosphorylated Proteins involved in gene transcription are activated Growth factor binds to its receptor in the cytoplasmic membrane Receptor recruits adaptor protein and GEF Autophosphorylation of tyrosine residues on the receptor Structural change of the receptor activates Tyrosine Kinase Map Kinase Kinase Kinase is phosphorylated Ras, a small GTPase, is activated by the exchange of GTP for GDP Map Kinase is Phosphorylated Map Kinase enters the nucleus
G protein coupled receptors play an important role in signal transduction in many cells. Label the four essential components of the G protein coupled receptor signaling system (blanks a-d in the picture) by choosing from the menus below. a b b Each answer will be used at most once, while some will not be used at all (select one for each): Group of answer choices transcription factor с transcription factor Show Transcribed Text d transcription factor B C. transcription factor G protein second messenger G protein second messenger IE G protein second messenger G protein second messenger receptor receptor receptor receptor enzyme enzyme enzyme enzyme steroid hormone steroid hormone steroid hormone steroid hormone
Cholera 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 GDP
Use your knowledge of Cell & Molecular Biology to design solutions for treating COVID-19 based on your understanding of the signaling pathways discussed in class.
Answer both to get a like or don't attempt.Thanks Question 9 Listen Transphosphorylation, the bidirectional recpiprocal phosphorylation of growth factor dimers, results in the phosphorylation of an array of tyrosine residues present in cytoplasmic portions of the growth factor receptor outside the kinase domain. Question 9 options: TRUE FALSE Question 10 Listen For the EGF receptor: Question 10 options: Spontaneous receptor dimerization precedes receptor binding. The EGF ligand serves as a bridge to dimerize receptors. Are overexpressed in many human cancers making them hyper-responsive to low levels of ligand. A and C are both correct. B and C are both correct.
Current Attempt in Progress To answer this question, first click here to view the associated animation. The enzyme phospholipase is responsible for (select all that apply): O Cleaving inositol trisphosphate (IP3) into two different second messengers. O Cleaving phosphatidylinositol bisphosphate (PIP2) into two different second messengers. O Cleaving phosphatidylinositol bisphosphate (PIP2) into two different primary messengers. O Producing diacylglycerol (DAG) as a result of cleaving a phospholipid component of the cell membrane. Cleaving inositol trisphosphate (IP3) into two different primary messengers. Save for Later Attempts: 0 of 3