. What physiological effect would you predict from a mutation thatreplaced with serine the cysteine in the constant part of theimmunoglobulin light chain that is involved in disulfide-bond for-mation with the heavy chain? ,

Immunoglobulin (Ig), is considered as the protein, which is produced by the immune cells such as…

Answered: . What physiological effect would you…

Biochemistry

9th Edition

ISBN:9781319114671

Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Chapter1: Biochemistry: An Evolving Science

Section: Chapter Questions

Problem 1P

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The affinity of integrins for matrix components canbe modulated by changes to their cytoplasmic domains:a process known as inside-out signaling. You have iden-tified a key region in the cytoplasmic domains of αIIbβ3integrin that seems to be required for inside-out signaling(Figure Q19–3). Substitution of alanine for either D723in the β chain or R995 in the α chain leads to a high levelof spontaneous activation, under conditions where thewild-type chains are inactive. Your advisor suggests thatyou convert the aspartate in the β chain to an arginine(D723R) and the arginine in the α chain to an aspartate(R995D). You compare all three α chains (R995, R995A,and R995D) against all three β chains (D723, D723A, andD723R). You find that all pairs have a high level of sponta-neous activation, except D723 vs R995 (the wild type) andD723R vs R995D, which have low levels. Based on theseresults, how do you think the αIIbβ3 integrin is held in itsinactive state?
Nearly all immune deficiency diseases that result in impaired TH17 and ILC3 function lead to chronic mucocutaneous candidiasis (CMC), usually accompanied by increased susceptibility to pyogenic bacterial infections. However, a subset of these patients also show increased susceptibility to intracellular bacterial infections, such as those caused by Mycobacteria species. What is the explanation for why some, but not all, of these patients have increased susceptibility to intracellular bacteria and which patients fall into this category?
1. NSF is an enzyme that uses the energy of ATP hydrolysis to disassemble complexes between V-SNARES and t-SNARES. a) Why do you suppose such an enzyme is needed? b) If NSF were suddenly inactivated and then the cells were examined a short time later, what types of effects would you expect to see?
47. Define group transfer and its role in the cell (Hint: How are amino acids activated by aminoacyl t-RNA synthetase?).
What type of mutation might render the following proteins constitutively ac- tive: (a) Smad3, (b) MAP kinase, and (c) NF-κB?
Mice and humans with inactivating mutations in the gene encoding activation-induced cytidine deaminase (AID) have an immunodeficiency disease known as ‘hyper IgM type 2’. Since AID is the enzyme that catalyzes the conversion of cytosines in the DNA to uracils, thereby initiating the process of somatic hypermutation, why do individuals with this deficiency only produce IgM antibodies?
Explain the presence of the protein identified by peptide keratin, type I cytoskeletal ?
a.What would happen if IKKbeta did not phosphorylate IkappaB? b.Why is it so hard to make cytokine therapies? c.Why would you use the MyD88 independent pathway versus the MyD88 dependent pathway?
. In the experiments of Barrick, et al. ( observed that replacement of histidine by a noncovalently bonded imidazole not only reduced cooperativity but also increased the oxy- gen affinity of the hemoglobin. Suggest an explanation. it was
The MARCH-1 E3-ubiquitin ligase is expressed in B cells, dendritic cells, and macrophages. The pathway regulated by MARCH-1 is targeted by some pathogens in an immune evasion strategy. In this strategy, the pathogens encode: A protein that induces degradation of MARCH-1 A protein that mimics MARCH-1 and functions similarly A protein that binds to MARCH-1 and inhibits its function A protein that is induced by IL-10 in macrophages and dendritic cells A protein that induces degradation of CD86
Poliovirus is highly cytopathic both in cultured cells and in animals. Inoculation of mice with poliovirus leads to a robust antibody and cellular response. Explain why mice infected with a poliovirus mutant that cannot cause cell death have poor antibody and cellular responses. What would be one strategy to restore robust antibody and cellular responses in mice infected with this mutant virus?
You have synthesized an oligopeptide containing an RGD motif surrounded by other amino acids. What is the effect of this peptide when added to a fibroblast cell culture grown on a layer of fibronectin adsorbed to the tissue culture dish? Why does this happen?

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. What physiological effect would you predict from a mutation that replaced with serine the cysteine in the constant part of the immunoglobulin light chain that is involved in disulfide-bond for- mation with the heavy chain? ,