Explain the difference between the actions of water-soluble and lipid-soluble hormones.  Your explanation should include a detailed description of how/where these two different classes of hormones bind to receptors and what each type of mechanism triggers.  Specifically, detail the events involving water-soluble hormones with G-protein coupled receptors and the events that occur when a lipid-soluble hormone binds to an intracellular receptor, triggering transcription and translation.  Include two simple, numbered, labeled diagrams to help in your explanation.

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…

In a hypothetical cAMP-mediated signal transduction cascade, the GTP-αs/adenylate cyclase interaction following a single hormone–receptor binding event lasts for 2.3 seconds. The catalytic rate (turnover number) for the adenylate cyclase in question is 350 cAMP molecules produced per second. How many cAMP molecules would be produced if five hormone-receptor binding events were to occur before the hormone molecule dissipates in the bloodstream? What is the amplification effect of this step in the signaling pathway?

Hormone 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.…

Progesterone is a steroid hormone that is produced by the placenta during pregnancy. Based on its structure (shown below), explain why progesterone’s effects are mediated by a receptor located inside the cell rather than on the cell membrane.

Ligand binding to proteins may occur with varying strengths; some ligands bind tightly to proteins while others bind less tightly. The strengths of reversible binding are determined experimentally by varying concentrations of ligands, and measuring the saturation of the protein in the various ligand concentrations. One such laboratory study investigated the binding of a hormone to three different receptor proteins in the cell membrane. The data collected are shown in the table below 1) Which of the proteins demonstrate the tightest/strongest binding of the hormone? Which demonstrates the least tight binding of the hormone? What is the basis for your answer?

Ligand binding to proteins may occur with varying strengths; some ligands bind tightly to proteins while others bind less tightly. The strengths of reversible binding are determined experimentally by varying concentrations of ligands, and measuring the saturation of the protein in the various ligand concentrations. One such laboratory study investigated the binding of a hormone to three different receptor proteins in the cell membrane. The data collected are shown in the table below: 1) Provide a brief explanation as to why ligand binding to proteins must be a reversible process.  2)  Calculate the dissociation constant (Kd) for the hormone binding to each of the three proteins.

Steroid 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?

What is the purpose of having a sex hormone binding protein within the blood stream? What is the purpose of having a specific receptor for estrogen within the cell? The estrogen receptor binding domain has many known mutations that effect estrogen binding and result in breast cancer. One particular mutation found at aspartic acid is changed to glycine in cancer patients. Draw a potential interaction with the side chain of this aspartic acid with estrogen (name and label it) and how a mutation to glycine could affect this ability to efficiently bind to estrogen. 6.

Describe a mechanism by which a steroid hormone might act to increase intracellular levels of cyclic AMP. Match the words in the left column to the appropriate blanks in the sentences on the right. activate decrease inhibit repressed induced increase Reset Help Since steroid hormone-receptor complexes specific genes, a steroid hormone could in principle transcription of the gene for adenylate cyclase and, hence, steady-state level of this enzyme. Other possibilities could include synthesis of a phosphodiesterase inhibitor or synthesis of cAMP phosphodiesterase. the transcription of the