Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN: 9780134580999
Author: Elaine N. Marieb, Katja N. Hoehn
Publisher: PEARSON
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- 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.arrow_forwardHormone H regulates these effects via its receptors which are found at both the cell surface (csRH) and within the cell (içRH). The signalling pathways that become activated in the presence of hormone H are depicted and described below. hormone H. H H extracellular fluid inactive GTP inactive RAS Lyn cell-surface receptor for H (csR») icR GDP RAS-GTP hexose metabolism cell survival H icR G, phase (resting) Raf HK GSK-3P MEK M G2 icR - hexose kinase ERK promoter HRE CDK1 Cyclin A nucleus cyclin A Fos A promoter Created in BioRender.com bio Signalling via the cell surface receptor Hormone H mediates its cell cycle stimulatory and pro-survival effects by binding to and activating the cell surface hormone H receptor (csRH). The activated CSRH activates Lyn, which activates RAS and ultimately the Raf/MEK/ERK kinase cascade. Active ERK: o phosphorylates and inactivates GSK-3B. Inhibition of GSK-3ß promotes cell survival. inhibits p27, preventing it from inhibiting cell cycle progression.…arrow_forwardGTP is an important high-energy molecule that facilitates the activation of many cellular sig- nal transduction pathways. Certain genetic dysfunctions can inhibit the ability of a cell to synthesize GTP. Which of the following describes the most direct result of GTP synthesis inhibition? A B с D The cell would be able to carry out reception and transduction but would not be able to produce the cellular response in the relevant signal transduction pathway. The G protein-coupled receptor will not be able to bind corresponding ligands, inhibiting the reception components of the relevant signal transduction pathway. The cell will use ATP instead of GTP to activate the G protein on the intracellular region of the G protein-coupled receptor. The cell would not be able to activate G proteins on the intracellular regions of G pro- tein-coupled receptors.arrow_forward
- Under what conditions does the CAP protein become a functional activating protein? Group of answer choices when cAMP is absent and CAP is bound to glucose when glucose is absent and CAP is bound to cAMP none of these when glucose is abundant and CAP is bound to cAMP when cAMP is abundant and CAP is bound to glucosearrow_forwardLabel the molecules in this figure showing how IP3 and DAG function as second messengers. Note: not all labels are used. IP3 and calcium activating protein kinase C Activated phospholipase C DAG triggering calcium release Activated G-protein with GTR bound Siy IP3 triggering calcium release Phosphatidyl inositol Ligand bound to receptor DAG and calcium activating protein kinase C Activated G-protein with GDP bound Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display. TH ,,arrow_forwardRGS proteins accelerate the GAP activity of Gα subunits. What is the direct result of this GAP activity? - hydrolysis of GTP, resulting in a GDP-bound Gα - phosphorylation of GDP to GTP, resulting in a GTP-bound Gα - an exchange of GTP for GDP bound to Gα - an exchange of GDP for GTP bound to Gαarrow_forward
- You decide to investigate cell signaling of a pair of newly identified GPCRs, GPCR-W and GPCR-Z. Each binds the same ligand, but activates different downstream heterotrimeric G-proteins that act on adenylyl cyclase. You discover that ligand binding has opposite effects on adenylyl cyclase activity for each receptor. GPCR-W causes an increase in adenylyl cyclase activity, while GPCR-Z causes a decrease in adenylyl cyclase activity. You obtain a cell line expressing GPCR-W, GPCR-Z, the relevant G-proteins, and adenylyl cyclase. There is baseline adenylyl cyclase activity producing a baseline amount of cAMP. You embark on a research project to characterize the following mutations in the components of the signaling pathway. 2. Will each of the following mutations increase or decrease the levels of cAMP inside the cell upon adding the ligand to the cell culture? A mutation in Gi that prevents release of bound GDP. A mutation in Gs that prevents GTP hydrolysis. A mutation in Gi that…arrow_forwardA signaling molecule M is active when it is phosphorylated (M-P). The M-P has downstream target molecules in nucleus. Provide a possible mechanism by which M does its jobarrow_forwardSteroid hormones are required by the body at puberty and into adolescence to regulate growth and cell division at more rapid pace than in later life. This regulation occurs via their interaction with cellular receptors and the signaling cascades/pathways that follow. Describe for me the difference between the two major classes of steroids, anabolic and catabolic steroids. What might you expect the result of signaling cascades to be in cells receiving either anabolic or catabolic “signals”? (B) At some point in late adolescence, steroid production decreases by almost 100 fold, as we transition into “adulthood”. Why might we wish to stop these signals from constantly being in our blood stream, (like, Say, between 17-24 years of age)? What result might these steroids have on cancer cells where abhorrent signaling is already causing an increased rate of cell division/growth? Could steroid use result in Cancer?arrow_forward
- Binding EGF to the EGF receptor causes phosphorylation of tyrosines on the cytoplasmic tail of the receptor. Which of the following best describes the mechanism by which this phosphorylation activates downstream signaling complexes? Select one A. Causes degradation of receptor by proteasome pathway B. Causes EGF receptor to be internalized so it can interact directly with downstream signaling molecules C. Tyrosine phosphorylation alters 3D structure of downstream signaling proteins causing them to change from an inactive to active conformation D. Causes release of EGF from receptor E. Alters the localization of downstream signaling partners in the cytoplasmarrow_forwardWould nitrosylation of cysteine or ubiquitination of lysine disrupt binding the most in a G protein coupled receptor?arrow_forwardExplain how an indirect neurotransmitter receptor mechanism (like A-G linked receptor) conduct cell signaling?arrow_forward
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