Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity-Reference-Cited by-同舟云学术

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Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity

Published:2016-02-22 Issue:3 Volume:16 Page:164-176
ISSN:1474-1733
Container-title:Nature Reviews Immunology
language:en
Short-container-title:Nat Rev Immunol

Author:

Casellas Rafael,Basu Uttiya,Yewdell William T.,Chaudhuri Jayanta,Robbiani Davide F.,Di Noia Javier M.

Publisher

Springer Science and Business Media LLC

Subject

Energy Engineering and Power Technology,Fuel Technology

Link

http://www.nature.com/articles/nri.2016.2.pdf

Reference135 articles.

1. Pieper, K., Grimbacher, B. & Eibel, H. B-cell biology and development. J. Allergy Clin. Immunol. 131, 959–971 (2013).

2. Di Noia, J. M. & Neuberger, M. S. Molecular mechanisms of antibody somatic hypermutation. Annu. Rev. Biochem. 76, 1–22 (2007).

3. Revy, P. et al. Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the hyper-IgM syndrome (HIGM2). Cell 102, 565–575 (2000).

4. Muramatsu, M. et al. Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme. Cell 102, 553–563 (2000).

5. Shen, H. M., Peters, A., Baron, B., Zhu, X. & Storb, U. Mutation of BCL-6 gene in normal B cells by the process of somatic hypermutation of Ig genes. Science 280, 1750–1752 (1998).

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