AID for Immunoglobulin Diversity by Frederick W. Alt

By Frederick W. Alt

Advances in Immunology, an extended confirmed and hugely revered serial, provides present advancements in addition to entire reports in immunology. Articles handle the wide variety of subject matters that contain immunology, together with molecular and mobile activation mechanisms, phylogeny and molecular evolution, and medical modalities. Edited and authored by way of the major scientists within the box, every one quantity offers updated info and instructions for destiny examine.

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2003). The apolipoprotein B mRNA editing complex performs a multifunctional cycle and suppresses nonsense‐mediated decay. EMBO J. 22, 3971–3982. Conticello, S. , Thomas, C. , Petersen‐Mahrt, S. , and Neuberger, M. S. (2005). Evolution of the AID/APOBEC family of polynucleotide (deoxy)cytidine deaminases. Mol. Biol. Evol. 22, 367–377. , and Neuberger, M. S. (2002). Altering the pathway of immunoglobulin hypermutation by inhibiting uracil‐DNA glycosylase. Nature 419, 43–48. Di Noia, J. , and Neuberger, M.

Demonstration of M cells in the specialized follicle‐ associated epithelium overlying isolated lymphoid follicles in the gut. J. Leukoc. Biol. 35, 397–404. Rush, J. , Fugmann, S. , and Schatz, D. G. (2004). Staggered AID‐dependent DNA double strand breaks are the predominant DNA lesions targeted to Sm in Ig class switch recombination. Int. Immunol. 16, 549–557. , Schreier, M. , Eugster, H. , and Quesniaux, V. F. (1997). Lack of type 2 T cell‐independent B cell responses and defect in isotype switching in TNF‐lymphotoxin a‐deficient mice.

7 and 7% of wild‐ type binding, respectively) showed much weaker dominant negative effects on CSR. Another Vpr mutant (R90K) that can interact with UNG but does not affect the cell cycle regulation showed a dominant negative effect similar to that of wild‐type Vpr. Importantly, infectants expressing less Vpr showed weaker effects, indicating that Vpr is probably competing with an unknown host factor for binding to UNG. Analogous to Vpr‐mediated transport of the preintegration complex during the viral life cycle, a Vpr‐like host protein might exist that recruits UNG to the CSR machinery.

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