Associated Papers
A Novel AICDA Splice-Site Mutation in Two Siblings with HIGM2 Permits Somatic Hypermutation but Abrogates Mutational Targeting.
Dirks J et al.
Journal of Clinical Immunology, 2022
UnAIDed Class Switching in Activated B-Cells Reveals Intrinsic Features of a Self-Cleaving IgH Locus.
Dalloul I et al.
Frontiers in Immunology, 2021
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
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
Inherited defects of immunoglobulin class switch recombination.
Kracker S et al.
Advances in Experimental Medicine and Biology, 2010
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
AID mutant analyses indicate requirement for class-switch-specific cofactors.
Ta VT et al.
Nature Immunology, 2003
Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2).
Revy P et al.
Cell, 2000
Molecular basis of multiple exostoses: mutations in the EXT1 and EXT2 genes.
Wuyts W et al.
Human Mutation, 2000
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