Which of the following is NOT an example of allosteric regulation? Select an answer and submit. For keyboard navigation, use the up/down arrow keys to select an answer. a Phosphorylation of the CTD of RNA polymerase II. b с d Lactose binding to the Repressor protein. GTP binding to elF2. CAMP binding to cAMP protein-dependent kinase

Which of the following is NOT an example of allosteric regulation? Select an answer and submit. For keyboard navigation, use the up/down arrow keys to select an answer. a Phosphorylation of the CTD of RNA polymerase II. b с d Lactose binding to the Repressor protein. GTP binding to elF2. CAMP binding to cAMP protein-dependent kinase

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 1VCQ: Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is...

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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
If a mutation is introduced into I-KBα that inhibits its phosphorylation by the IKK complex, this would prevent: dimerization of the p50 and p65 subunits. translocation of NF-kB into the nucleus. OTAK1 phosphorylation of IKKB. recruitment of Nemo to the IKK complex.
which of the following correctly describes how protein kinase A can activate genes? A: nuclear protein kinase A is activated by cAMP to phosphorylate general transcription factors B: cytosolic protein kinase A is activated by cAMP to release the catalytic subunits, which move into the nucleus and phosphorylate CREB C: cytosolic protein kinase A is activated by cAMP to release the catalytic subunits, which move into the nucleus and phosphorylate general transcription factors D: G protein-coupled receptors may be desensitized by serine phosphorylation
An SH2-containing protein contains a mutation that changes its binding pocket such that tyrosine and phosphotyrosine bind with equal afﬁnity. As a result, MEK activity: does not change with receptor dimerization and transautophosphorylation decreases due to changes in Raf activation increases with ligand binding-induced dimerization decreases due to allosteric inhibition of SH2-domain binding
A growth factor Fsh3 stimulates the proliferation of culture fish cells. The receptor that binds Fsh3 is a receptor tyrosine kinase (RTK) and there are numerous fish tumor cell lines that have a mutation for the gen for this receptor. Which of the following mutations would be expected to promote uncontrolled cell proliferation. a mutation that inactivates the protein tyrosine phosphatase that acts on the receptor a mutation that prevents the binding of the normal extracellular signal to the receptor a mutation that inhibits the Ras GEF a mutation that destroys the kinase activity of the receptor a mutation that prevents dimerization of the receptor
The figure below shows how normal signaling works with a Ras protein acting downstream of a receptor tyrosine kinase. CYTOSOL active receptor tyrosine kinase Taratas THERI signal molecule 00 active signaling Q Search active Ras protein GTP 99+ Į SIGNALING Il app.honorlock.com is sharing your screen. ✡ active signaling protein Y a
Which of the following would be expected to inhibit PKC activation by a GPCR ligand? phospholipase C inhibitor cAMP phosphodiesterase inhibitor Ras inhibitor MAP kinase inhibitor
Now read this abstract from a 2013 journal article What is the authors' explanation of how Gal80p works? Note UASG from the question above is the same as UASGAL The DNA-binding transcriptional activator Gal4 and its regulators Gal80 and Gal3 constitute a galactose-responsive switch for the GAL genes of Saccharomyces cerevisiae. Gal4 binds to GAL gene UASGAL. (upstream activation sequence in GAL gene pro- moter) sites as a dimer via its N-terminal domain and activates transcription via a C-terminal transcription activation domain (AD). In the absence of galactose, a Gal80 dimer binds to a dimer of Gal4, masking the Gal4AD. Galactose triggers Gal3-Gal80 interaction to rapidly initiate Gal4-mediated transcription activation. Just how Gal3 alters Gal80 to relieve Gals0 inhibition of Gal4 has been unknown, but previous analyses of Gal80 mutants suggested a possible competition between Gal3-Gal80 and Gal80 self-association interactions. Here we assayed Gal80-Gal80 interactions and tested for…
The progressive loss of cardiac myocytes due to cell death has been associated with cardiac dysfunction and heart failure. Which of the following would lead to a significant loss of cardiac myocytes? Select all that apply Treatment of rapamycin which results in inhibition of mTOR activity Prolonged or severe ER stress with increased accumulation of unfolded proteins Activation of AMPK and phosphorylation of the TSC1 complex mTOR activation and phosphorylation of Ulk1
See figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. Cyclin Serine Lysine Aspartic "Acid Lysine -OH NH3t -Coo NH3+ NH3 + -OH Aspartic Aad Aspartic Acid /Lysine Serine сок
See figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. A Explain what a kinase does and how the cyclin controls the activity of the Cdk.
Metabolic syndrome is a clustering of various conditions including high blood pressure, high blood sugar, excess body fat, high serum triglycerides, and low high-density lipoproteins. Scientists studying metabolic syndrome cultured fibroblast cells from a metabolic syndrome patient and a healthy volunteer and challenged the cells to 100 nM insulin. Ten minutes after the stimulus was applied, they used a protein immunoblot to measure the amount of phosphorylated insulin receptor in the cultures. Use the passage to answer the question. Insulin, in addition to regulating blood glucose, also promotes satiety. Ghrelin, on the other hand, is a peptide hormone that promotes hunger. Which statement BEST predicts the effect of ghrelin release on the insulin receptor? A. It increases insulin receptor expression. B. It decreases insulin receptor expression. C. It increases insulin receptor phosphorylation. D. It decreases insulin receptor phosphorylation.