Associated Papers
Nonamer dependent RAG cleavage at CpGs can explain mechanism of chromosomal translocations associated to lymphoid cancers.
Paranjape AM et al.
Plos Genetics, 2022
A Hyper-IgM Syndrome Mutation in Activation-Induced Cytidine Deaminase Disrupts G-Quadruplex Binding and Genome-wide Chromatin Localization.
Yewdell WT et al.
Immunity, 2020
TET enzymes augment activation-induced deaminase (AID) expression via 5-hydroxymethylcytosine modifications at the Aicda superenhancer.
Lio CJ et al.
Science Immunology, 2019
PARP activation promotes nuclear AID accumulation in lymphoma cells.
Tepper S et al.
Oncotarget, 2016
Cell Cycle Regulates Nuclear Stability of AID and Determines the Cellular Response to AID.
Le Q et al.
Plos Genetics, 2015
Mismatch repair proteins and AID activity are required for the dominant negative function of C-terminally deleted AID in class switching.
Ucher AJ et al.
Journal of Immunology (baltimore, Md. : 1950), 2014
Checkpoint kinase 1 negatively regulates somatic hypermutation.
Frankenberger S et al.
Nucleic Acids Research, 2014
AID recruits UNG and Msh2 to Ig switch regions dependent upon the AID C terminus [corrected].
Ranjit S et al.
Journal of Immunology (baltimore, Md. : 1950), 2011
Type two hyper-IgM syndrome caused by mutation in activation-induced cytidine deaminase.
Zhu Y et al.
Journal of Medical and Dental Sciences, 2003
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