Activation-induced cytidine deaminase turns on somatic hypermutation in hybridomas (Q28217205)

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scientific article (publication date: 14 February 2002)

Language	Label	Description	Also known as
English	Activation-induced cytidine deaminase turns on somatic hypermutation in hybridomas	scientific article (publication date: 14 February 2002)

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scholarly article

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Activation-induced cytidine deaminase turns on somatic hypermutation in hybridomas (English)

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Matthew D Scharff

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object named as

Matthew D Scharff

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author name string

Alberto Martin

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Philip D Bardwell

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Caroline J Woo

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Manxia Fan

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Marc J Shulman

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language of work or name

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publication date

14 February 2002

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415

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802-6

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6873

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Specific expression of activation-induced cytidine deaminase (AID), a novel member of the RNA-editing deaminase family in germinal center B cells

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Linking class-switch recombination with somatic hypermutation

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TdT-accessible breaks are scattered over the immunoglobulin V domain in a constitutively hypermutating B cell line

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Induction of somatic mutation in a human B cell line in vitro

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Clonal instability of V region hypermutation in the Ramos Burkitt's lymphoma cell line

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Codon bias targets mutation.

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Somatic hypermutagenesis in immunoglobulin genes. II. Influence of neighbouring base sequences on mutagenesis

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Sequence dependent hypermutation of the immunoglobulin heavy chain in cultured B cells.

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The intrinsic hypermutability of antibody heavy and light chain genes decays exponentially

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The 5' hypermutation boundary of kappa chains is independent of local and neighbouring sequences and related to the distance from the initiation of transcription.

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Hot spot focusing of somatic hypermutation in MSH2-deficient mice suggests two stages of mutational targeting

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Increased transcription levels induce higher mutation rates in a hypermutating cell line

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Increased hypermutation at G and C nucleotides in immunoglobulin variable genes from mice deficient in the MSH2 mismatch repair protein

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Mismatch repair and immunoglobulin gene hypermutation: did we learn something?

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Severe attenuation of the B cell immune response in Msh2-deficient mice

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Somatic hypermutation in MutS homologue (MSH)3-, MSH6-, and MSH3/MSH6-deficient mice reveals a role for the MSH2-MSH6 heterodimer in modulating the base substitution pattern

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The translesion DNA polymerase zeta plays a major role in Ig and bcl-6 somatic hypermutation.

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DNA polymerase eta is an A-T mutator in somatic hypermutation of immunoglobulin variable genes

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Somatic mutation hotspots correlate with DNA polymerase eta error spectrum.

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Continuous cultures of fused cells secreting antibody of predefined specificity

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Testing the reverse transcriptase model of somatic mutation

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10.1038/NATURE714

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Springer Nature article ID

10.1038/nature714

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