Associated Papers
Insights on SNPs of Human Activation-Induced Cytidine Deaminase AID.
Koveshnikova EA et al.
International Journal of Molecular Sciences, 2025
A single-center study points to diverse features and outcome in patients with Hyperimmunoglobulin M Syndrome and Class- Switch Recombination defects.
Akarsu A et al.
Scandinavian Journal of Immunology, 2022
Clinical implications of experimental analyses of AID function on predictive computational tools: Challenge of missense variants.
Abolhassani H et al.
Clinical Genetics, 2020
Activation-induced cytidine deaminase targets SUV4-20-mediated histone H4K20 trimethylation to class-switch recombination sites.
Rodríguez-Cortez VC et al.
Scientific Reports, 2017
AID Recognizes Structured DNA for Class Switch Recombination.
Qiao Q et al.
Molecular Cell, 2017
AID and Apobec3G haphazard deamination and mutational diversity.
Jaszczur M et al.
Cellular and Molecular Life Sciences : Cmls, 2013
Potential roles of activation-induced cytidine deaminase in promotion or prevention of autoimmunity in humans.
Durandy A et al.
Autoimmunity, 2013
A structural basis for the biochemical behavior of activation-induced deoxycytidine deaminase class-switch recombination-defective hyper-IgM-2 mutants.
Mu Y et al.
The Journal of Biological Chemistry, 2012
Novel mutation of the activation-induced cytidine deaminase gene in a Tajik family: special review on hyper-immunoglobulin M syndrome.
Mahdaviani SA et al.
Expert Review of Clinical Immunology, 2012
Activation-induced cytidine deaminase splice variants are defective because of the lack of structural support for the catalytic site.
van Maldegem F et al.
Journal of Immunology (baltimore, Md. : 1950), 2010
Inherited defects of immunoglobulin class switch recombination.
Kracker S et al.
Advances in Experimental Medicine and Biology, 2010
Activation-induced cytidine deaminase: structure-function relationship as based on the study of mutants.
Durandy A et al.
Human Mutation, 2006
Analysis of class switch recombination and somatic hypermutation in patients affected with autosomal dominant hyper-IgM syndrome type 2.
Imai K et al.
Clinical Immunology (orlando, Fla.), 2005
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