At puberty, the adolescent human body undergoes changes in both structure and function of several organ systems, primarily under the influence of estrogen and testosterone steroid hormones. Which of the following best explains how two molecules can trigger many different types of systemic changes that occur during adolescence? A Estrogen and testosterone are both produced in very large concentrations by nearly ev- ery cell in the body. B с D Estrogen and testosterone bind to specific receptors inside many types of cells, each with different signal transduction pathways. Estrogen and testosterone bind to different membrane-bound receptors on different cells, initiating different transduction pathways. Estrogen and testosterone are able to cross the membrane of some cells but not others.

A loss of function mutation in a gene encoding a SNARE protein would result in which of the following effects? оа. The anterior pituitary would be unable to release its hormones o b. Skeletal muscle cells, but not cardiac or smooth muscle, would lose their ability to contract O c. Neural cells would be unable to generate action potentials d. Neural cells would be unable to transmit action potentials via electrical synapses Neural cells would be unable to transmit action potentials via chemical synapses O e.

Thyroid hormone is produced within spherical shape structures in the thyroid gland known as 3. 1_ _ _This structure consists of an outer layer of 3.2 epithelial cells and an inner section known-as 3.3___ . This inner section is filled with 3.4 ____ that is synthesised and secreted by-the cells and contains many tyrosine residues. Within this inner section, organification occurs when 3. 5 ____ molecules attach to these tyrosine residues forming either 3. 6____  (with one molecule attacl1ed) or 3. 7____(with two molecules attached). Through coupling, T3 and T4 are also formed. Of these two hormones;- 3. 8 ____is less potent but forms approximately 93% of the metabolically active hormones secreted the thyroid gland.

—Hemophilia B, an X-linked genetic disorder which highly affects males, is a condition in which levels of Factor VIII are significantly decreased. Please describe the physiologic pathway which utilizes Factor VIII and describe the consequences of missing this factor from a physiologic perspective.

HDL-R: HDLs carry cholesterol to the liver for elimination. Liver cells respond to estrogen to express a protein receptor for HDLs coded by the HDL-R gene (HDL-R gene contains an estrogen response element.) PFK: codes for an enzyme called phosphofructokinase that is used in the first steps of breaking down glucose for energy in all cells. (Gene has no estrogen response element.) CD3: codes for a cell surface protein produced by immune B cells (Gene has no estrogen response element)mRNA transcripts can be collected from cells, made to glow with a fluorescent dye, and added to a microarray chip containing spots with DNA sequences from each of these genes. (In the depiction of the microarrays below ○ indicates no binding of the mRNA, and ● indicates binding.)Which of the gene expression patterns would you expect to see if you used mRNA from immune B cells to add to the microarray?

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?

A 67-year old man has been treated for prostate cancer. He is receiving a drug that blocks testosterone from binding to its intracellular receptor. Which of the following has this mechanism of action: Tamoxifen Flutamide Leuprolide Fulvestrant Interleukin-2

Provide annotated structure image/diagram of the EPH RECEPTOR B2 (EPHB2). Giving the ligand bidning sites.

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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 if