16b) Suppose you have a cell in which the Iron Response Factor (IRF) protein is mutated so that it binds to its binding site, the Iron Response Element (IRE), at all times, whether the intracellular iron concentration is low or high. Describe the effect, if any, that this mutation would have on production of the iron transport protein transferrin. Briefly explain what would happen/why the mutant IRF protein would have the effect you predict.

16b) Suppose you have a cell in which the Iron Response Factor (IRF) protein is mutated so that it binds to its binding site, the Iron Response Element (IRE), at all times, whether the intracellular iron concentration is low or high. Describe the effect, if any, that this mutation would have on production of the iron transport protein transferrin. Briefly explain what would happen/why the mutant IRF protein would have the effect you predict.

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 33CTQ: A scientist notices that a cancer cell line shows high levels of phosphorylated ERK in the absence...

See similar textbooks

Similar questions

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?
Most mammalian cells have a single immobile cilium called the primary cilium, in which intraflagellar transport (IFT) motor proteins move elements of the Hedgehog (Hh) signaling pathway along microtubules. What parts of the Hh signaling pathway would mutations in the IFT motor proteins Kif3A, Kif7, and dynein disrupt?
Explain why in cells that are genetically NF1–/–, basal levels of GTP-bound activated Ras are higher than normal and respond to growth factor stimulation by increasing rapidly to far higher levels.
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!)
''In the cellular regulatory pathways that controlcell growth and proliferation, the products of oncogenesare stimulatory components and the products of tumorsuppressor genes are inhibitory components.'' 'Is this statement true? Explain why or why not.
explain the following prperties of G protein: structure of G- activation cycle and signaling pathway for Gaq
The Iron Response Factor (IRF) protein regulates production of both the iron transport protein transferrin, which imports iron into a cell, and the iron storage protein ferritin, which stores iron when the cell has more iron than in needs. IRF is an RNA binding protein, which binds to a specific RNA sequence, the Iron Response Element (IRE). When the IRF protein binds to the IRE sequence in the mRNA that codes for transferrin, what effect does this have on the expression of transferrin? Briefly explain why this effect is observed.
Thousands of caspase substrateshave been identified. Which onesare the critical proteins that mustbe cleaved to trigger the majorcell remodeling events underlyingapoptosis?
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.
A scientist notices that a cancer cell line shows high levels of phosphorylated ERK in the absence of EGF. What are two possible explanations for the increase in phosphorylated ERK? Be specific in which proteins are involved.
which of hthe following would result in a persisting proliferation response to growth factor receptor activation after the ligand is no longer binding to its rceptor kinase? 1. Both a mutation that blocks the GTPas activity of Ras and a mutation that blocks the exchange of GDP with GTP would cause the response to persist. 2. a mutation that blocks the GTPas activity of Ras 3. neither a mutation that blocks the GTPas activity of Ras nor a mutation that blocks the exchange of GDP with GTP would cause the response to persist 4. a mutatiaon that blocks the exchange of GDP with GTP