Human and mouse Ig genes are diversified in mature B-cells by distinct processes known as Ig heavy-chain CSR (class switch recombination) and Ig variable-region exon SHM (somatic hypermutation). These DNA-modification processes are initiated by AID (activation-induced cytidine deaminase), a DNA cytidine deaminase predominantly expressed in activated B-cells. AID is post-transcriptionally regulated via multiple mechanisms, including microRNA regulation, nucleocytoplasmic shuttling, ubiquitination and phosphorylation. Among these regulatory processes, AID phosphorylation at Ser38 has been a focus of particularly intense study and debate. In the present paper, we discuss recent biochemical and mouse genetic studies that begin to elucidate the functional significance of AID Ser38 phosphorylation in the context of the evolution of this mode of AID regulation and the potential roles that it may play in activated B-cells during a normal immune response.
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June 2009
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Conference Article|
May 20 2009
Regulation of activation-induced cytidine deaminase DNA deamination activity in B-cells by Ser38 phosphorylation
Uttiya Basu;
Uttiya Basu
*Howard Hughes Medical Institute, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, U.S.A.
†Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, NRB 0330, Boston, MA 02115, U.S.A.
‡Immune Disease Institute, 800 Huntington Avenue, Boston, MA 02115, U.S.A.
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Andrew Franklin;
Andrew Franklin
*Howard Hughes Medical Institute, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, U.S.A.
†Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, NRB 0330, Boston, MA 02115, U.S.A.
‡Immune Disease Institute, 800 Huntington Avenue, Boston, MA 02115, U.S.A.
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Bjoern Schwer;
Bjoern Schwer
*Howard Hughes Medical Institute, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, U.S.A.
†Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, NRB 0330, Boston, MA 02115, U.S.A.
‡Immune Disease Institute, 800 Huntington Avenue, Boston, MA 02115, U.S.A.
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Hwei-Ling Cheng;
Hwei-Ling Cheng
*Howard Hughes Medical Institute, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, U.S.A.
†Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, NRB 0330, Boston, MA 02115, U.S.A.
‡Immune Disease Institute, 800 Huntington Avenue, Boston, MA 02115, U.S.A.
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Jayanta Chaudhuri;
Jayanta Chaudhuri
§Memorial Sloan Kettering Cancer Center, Immunology Program, New York, NY 10021, U.S.A.
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Frederick W. Alt
Frederick W. Alt
1
*Howard Hughes Medical Institute, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, U.S.A.
†Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, NRB 0330, Boston, MA 02115, U.S.A.
‡Immune Disease Institute, 800 Huntington Avenue, Boston, MA 02115, U.S.A.
1To whom correspondence should be addressed (email alt@enders.tch.harvard.edu).
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Publisher: Portland Press Ltd
Received:
January 07 2009
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2009 Biochemical Society
2009
Biochem Soc Trans (2009) 37 (3): 561–568.
Article history
Received:
January 07 2009
Citation
Uttiya Basu, Andrew Franklin, Bjoern Schwer, Hwei-Ling Cheng, Jayanta Chaudhuri, Frederick W. Alt; Regulation of activation-induced cytidine deaminase DNA deamination activity in B-cells by Ser38 phosphorylation. Biochem Soc Trans 1 June 2009; 37 (3): 561–568. doi: https://doi.org/10.1042/BST0370561
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