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please help answer this question
Explain how ACE2-like carboxypeptidase B38-CAP protects from SARS-CoV-2-induced lung injury in the paper by Yamaguchi et al.?
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- Discuss the potential of peptide and peptide-based inhibitors of SARS-CoV-2 entry. In your answer include the potential advantages of peptide drugs as well as challenges commonly encountered in developing peptide therapeutics.Compare and contrast the c4 pathway and the malate–aspartate shuttle in bullet format, meaning list the similarities and differences.Hydroxyurea has been shown to increase the expression of fetal hemoglobin in adult red blood cells, by a mechanism that remains unclear. Explain why hydroxyurea can be a useful therapy for patients with sickle-cell anemia.
- Would the following alterations to Src be oncogenic? Explain. (a) The mutation of Tyr 527 to Phe. (b) The replacement of Src residues 249 to 253 with the sequence APTMP.Can anyone suggest a way of increasing phosphorylation of IKK alpha (Ser176/180)? Any potent phosphatase inhibitor in combination with TNF alpha?explain the most likely steps of what might happen inside a MDA-MB-231 cell after it is exposed to UV light.
- Sigma-32 is probably an autoregulator. Why and how?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?When challenged with a low oxygen environment, knownas hypoxia, the body produces a hormone called erythropoietin(EPO), which then stimulates red blood cell production tocarry more oxygen. Transcription of the gene encoding EPO isdependent upon the hypoxia-inducible factor (HIF), which is atranscriptional activator. However, HIF alone is not sufficientto activate EPO. For example, Wang et al. (2010. PLOS ONE 5:e10002) showed that HIF recruits another protein called p300to an enhancer for the EPO gene. Furthermore, deletion of p300significantly impaired transcription of the EPO gene in responseto hypoxia. Given that p300 is a type of histone acetyl transferase,how might p300 influence transcription of the EPO gene?
