6c) In the cell in which the Iron Response Factor (IRF) protein is mutated so that it binds to its inding site, the Iron Response Element (IRE), at all times, whether the intracellular iron concentration is low or high, what effect, if any, would this mutation have on production of the iron storage protein ferritin? Briefly explain what would happen/why the mutant IRF protein would have the effect you predict.

6c) In the cell in which the Iron Response Factor (IRF) protein is mutated so that it binds to its inding site, the Iron Response Element (IRE), at all times, whether the intracellular iron concentration is low or high, what effect, if any, would this mutation have on production of the iron storage protein ferritin? Briefly explain what would happen/why the mutant IRF protein would have the effect you predict.

Name: 16c 16c) In the cell in which the Iron Response Factor (IRF) protein i
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Description: 16c 16c) In the cell in which the Iron Response Factor (IRF) protein is mutated so that it binds to itspinding site, the Iron Response Element (IRE), at all times, whether the intracellular ironconcentration is low or high, what effect, if any, would

Biology (MindTap Course List)

11th Edition

ISBN:9781337392938

Author:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg

Publisher:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg

Chapter6: Cell Communication

Section: Chapter Questions

Problem 10TYU

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1. The Iron Response Factor (IRF) regulates production of both the iron transport protein transferrin and the iron storage protein ferritin in response to intracellular iron conditions, but its effect on the production of these two proteins is not the same. Describe or explain how the IRF can simultaneously lead to decreased production of the iron transport protein transferrin and increased production of the iron storage protein ferritin in response to high intracellular iron concentrations.
33. Expression of the muscle specific protein dystrophin is important in the functional formation of muscle tissue by A. integrating the internal cytoskeleton through a transmembrane complex with the extracellular matrix. B. aiding transcription factors in entry into the muscle cells nucleus C.degrading non-muscle cell proteins. D. none of these
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. An interesting mutation in lacI results in repressorswith 110-fold increased binding to both operator andnonoperator DNA. These repressors display a “reverse”induction curve, allowing β-galactosidase synthesis inthe absence of an inducer (IPTG) but partly repressingβ-galactosidase expression in the presence of IPTG. Howcan you explain this? (Note that, when IPTG binds a repressor, it does not completely destroy operator affinity,but rather it reduces affinity 110-fold. Additionally, ascells divide and new operators are generated by thesynthesis of daughter strands, the repressor must findthe new operators by searching along the DNA, rapidlybinding to nonoperator sequences and dissociating fromthem.)
What effect does binding of the IRF protein to the IRE in the mRNA encoding ferritin have on the production of ferritin? Briefly explain why this effect is observed.
Describe the role of pH in regulating the interaction between mannose 6-phosphate and the M6P receptor. Why does a rise in endosomal pH lead to the secretion of newly synthesized lysosomal enzymes into the extracellular medium?
a. Panels G, H, and I show pattters wher fluorescence is detected in the cytosol or internal cellular membranes. Do these results support the hypothesis that the identity of the beta subunit also plays a role in subcellular localization? b.If co-expression of a given alpha subunit caused the pairs in panels G, H, and I to migrate to the plasma membrane, what would that tell you about the process of plasma membrane localization with heterotrimeric G-proteins containing the beta-5 subunit? (This is all the information that is provided!)
1. Researchers incubated J3’s in the absence of Unknown Factor X. Upon the addition of a membrane-permeant cGMP agonist (a cGMP agonist able to penetrate into the J3’s) you would expect to see STIMULATION/INHIBITION (highlight one) of the J3 activation pathway.2. Researchers incubated J3’s in the presence of Unknown Factor X, but with the addition of a membrane-permeant CYP antagonist. In this case, you would expect to see STIMULATION/INHIBITION (highlight one) of the J3 activation pathway.
Cell lines divide normally in a defined medium containing growth factors, but fail to divide in the absence AGF (a growth factor). However, a mutant cell line continues to divide even in the absence of AGF. Elevated levels of Rb phosphorylation and the effects of receptor and Mek inhibitors suggest a mutation activating an oncogene. Inhibitors of Mek inhibit cell division of the mutant cell line, but inhibitors to the ADGF receptor, a receptor tyrosine kinase (RTK) with homology to EGFR, do not. Outline the RTK pathway leading to the phosphorylation of Rb to form p-Rb.
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I just read an abstract of the paper “Disulfide bond-disrupting agents activate the tumor necrosis family-related apoptosis-inducing ligand/death receptor 5 pathway” and noted that “DDAs and TRAIL synergize to kill cancer cells and are cytotoxic to HER2+ cancer cells with acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib.” For the last sentence, I am not sure the meaning of the “acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib”. Is the “acquired resistance ... to inhibitor” a good thing or bad thing, as far as the synergize effect of DDAs and TRAIL”? Hope that expert can help.