Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme.

By M. Muramatsu, K. Kinoshita, S. Fagarasan, S. Yamada, Y. Shinkai, Tasuku Honjo. Cell, 2000

3,602 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/94ec6c3a0a8f5a956a62d94953d30efdd4661da0

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Citations in the corpus

Hypermutation of multiple proto-oncogenes in B-cell diffuse large-cell lymphomas (2001, neutral): “, and seems not to involve the activation-induced deaminase (AID; a cytidine deaminase required for somatic hypermutatio”
Follicular B helper T cells in antibody responses and autoimmunity (2005, background): “; and AID is crucial for immunoglobulin class switching and somatic hypermutatio”
Cytokine-secreting follicular T cells shape the antibody repertoire (2009, methodology): “major 14 d before and used semiquantitative RT-PCR to assess the expression of activation-induced cytidine deaminase (AID), an enzyme required for somatic hypermutation and isotype class switching that is confined mainly to GC B cell”
DNA Methylation and Its Basic Function (2013, background): “Overexpression of AID/APOBEC promotes DNA demethylation in zebrafish (Rai et al, 2008), whereas knockdown or knockout inhibits the DNA demethylation of various genes necessary for cellular reprogramming and development (Bhutani et al, 2010; Muramatsu et al, 2000; Popp et al, 2010).”
DNA Demethylation Dynamics (2011, background): “Mice completely lacking AID (AID / ) (Muramatsu et al., 2000) exhibited an increase in genome-wide hypermethylation in their primordial germ cells (PGCs), suggesting that AID is involved in DNA demethylation.”
MicroRNA control in the immune system: basic principles. (2009, background): “AID is also, however, causally involved in oncogenic reciprocal translocations between IgH and c-myc (c-myc-IgH), an unwanted byproduct of CSR in the course of the germinal center reaction (Muramatsu et al., 2000; Ramiro et al., 2004).”
DNA methylation dynamics during epigenetic reprogramming in the germline and preimplantation embryos (2014, background): “Aside from its global function in the maternal genome, STELLA also protects at least two paternally methylated, imprinted gene loci (Rasgrf1 and H19, but not the IG-DMR) from aberrant demethylation (Nakamura et al. 2006).”
Induction of activation‐induced cytidine deaminase gene expression by IL‐4 and CD40 ligation is dependent on STAT6 and NFκB (2004, background): “The similarities between these two genes, the observation that recombinant AID has in vitro cytidine deaminase activity and the requirement for de novo protein synthesis for an event downstream to AID expression in CSR (14, 16 ), have suggested that AID might be an RNA editing enzyme which can give ”
Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2). (2000, background): “An identical picture was observed in 2 other patients. mice (Muramatsu et al., 2000 [this issue of Cell]) demon- machinery (Lorenz et al., 1995; Hein et al., 1998), and the formation of RNA:DNA complexes with R-loop struc-strates the causative role of AID gene mutations in the disease.”
The evolution of adaptive immune systems. (2006, neutral): “Presently, however, the activation-induced deaminase ( AID ) gene (Muramatsu et al., 2000), which is essential for the gene-conversion mechanism used for antibody diversiﬁcation, has been identiﬁed only in gnathostomes (Conticello et al., 2005).”
Multiple layers of B cell memory with different effector functions (2009, background): “, with both of these transactions being initiated by the GC-specific enzyme activation-induced cytidine deaminase (AID”