A Structural Basis for the Biochemical Behavior of Activation-induced Deoxycytidine Deaminase Class-switch Recombination-defective Hyper-IgM-2 Mutants
Author:
Publisher
Elsevier BV
Subject
Cell Biology,Molecular Biology,Biochemistry
Reference40 articles.
1. Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the hyper-IgM syndrome (HIGM2);Revy;Cell,2000
2. Mutations in activation-induced cytidine deaminase in patients with hyper-IgM syndrome;Minegishi;Clin. Immunol.,2000
3. Analysis of class switch recombination and somatic hypermutation in patients affected with autosomal dominant hyper-IgM syndrome type 2;Imai;Clin. Immunol.,2005
4. Activation-induced cytidine deaminase deaminates deoxycytidine on single-stranded DNA but requires the action of RNase;Bransteitter;Proc. Natl. Acad. Sci. U.S.A.,2003
5. Processive AID-catalyzed cytosine deamination on single-stranded DNA simulates somatic hypermutation;Pham;Nature,2003
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2. C‐terminal deletion‐induced condensation sequesters AID from IgH targets in immunodeficiency;The EMBO Journal;2022-04-26
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