(Q28235340)

2

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Sariah Allen

3

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Phuong Pham

4

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Myron F Goodman

Journal of Biological Chemistry

5

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language of work or name

English

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publication date

23 June 2006

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published in

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volume

281

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issue

25

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page(s)

16833-6

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cites work

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Somatic hypermutation in the heavy chain locus correlates with transcription

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Both DNA strands of antibody genes are hypermutation targets

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The role of activation-induced cytidine deaminase in antibody diversification, immunodeficiency, and B-cell malignancies

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AID mutates E. coli suggesting a DNA deamination mechanism for antibody diversification

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Reward versus risk: DNA cytidine deaminases triggering immunity and disease

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Replication protein A interacts with AID to promote deamination of somatic hypermutation targets

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Biochemical analysis of hypermutational targeting by wild type and mutant activation-induced cytidine deaminase

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The TATA binding protein, c-Myc and survivin genes are not somatically hypermutated, while Ig and BCL6 genes are hypermutated in human memory B cells.

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The RNA polymerase II elongation complex

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Complex regulation of somatic hypermutation by cis-acting sequences in the endogenous IgH gene in hybridoma cells

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AID enzyme-induced hypermutation in an actively transcribed gene in fibroblasts

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Elucidation of IgH intronic enhancer functions via germ-line deletion

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Activation-induced cytidine deaminase (AID) can target both DNA strands when the DNA is supercoiled

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The balance between Pax5 and Id2 activities is the key to AID gene expression

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E-proteins directly regulate expression of activation-induced deaminase in mature B cells

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Somatic hypermutation is limited by CRM1-dependent nuclear export of activation-induced deaminase

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Activation-induced cytosine deaminase (AID) is actively exported out of the nucleus but retained by the induction of DNA breaks

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Activation-induced cytidine deaminase shuttles between nucleus and cytoplasm like apolipoprotein B mRNA editing catalytic polypeptide 1

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C-terminal deletion of AID uncouples class switch recombination from somatic hypermutation and gene conversion.

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Negative regulation of activation-induced cytidine deaminase in B cells

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PKA-mediated phosphorylation regulates the function of activation-induced deaminase (AID) in B cells

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The AID antibody diversification enzyme is regulated by protein kinase A phosphorylation

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AID mutant analyses indicate requirement for class-switch-specific cofactors

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Activation-induced cytidine deaminase deaminates deoxycytidine on single-stranded DNA but requires the action of RNase

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Cellular APOBEC3G restricts HIV-1 infection in resting CD4+ T cells

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Error-prone candidates vie for somatic mutation

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Immunity through DNA deamination

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DNA polymerases and somatic hypermutation of immunoglobulin genes

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The translesion DNA polymerase theta plays a dominant role in immunoglobulin gene somatic hypermutation

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DNA polymerase theta contributes to the generation of C/G mutations during somatic hypermutation of Ig genes

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Strand-biased defect in C/G transversions in hypermutating immunoglobulin genes in Rev1-deficient mice

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Error-prone repair DNA polymerases in prokaryotes and eukaryotes

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Ubiquitinated proliferating cell nuclear antigen activates translesion DNA polymerases eta and REV1

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Somatic hypermutation of immunoglobulin genes is linked to transcription initiation

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A pivotal role for DNase I-sensitive regions 3b and/or 4 in the induction of somatic hypermutation of IgH genes

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The immunoglobulin heavy-chain locus hs3b and hs4 3' enhancers are dispensable for VDJ assembly and somatic hypermutation

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Analysis of interactions between mismatch repair initiation factors and the replication processivity factor PCNA

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Ten commandments of enzymology, amended

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