Hot spot focusing of somatic hypermutation in MSH2-deficient mice suggests two stages of mutational targeting
about
AID-GFP chimeric protein increases hypermutation of Ig genes with no evidence of nuclear localization.Altered nucleotide misinsertion fidelity associated with poliota-dependent replication at the end of a DNA template.Somatic hypermutation of the AID transgene in B and non-B cellsThe translesion DNA polymerase theta plays a dominant role in immunoglobulin gene somatic hypermutationMemory in the B-cell compartment: antibody affinity maturationSecret sharers in the immune system: a novel RNA editing activity links switch recombination and somatic hypermutationDNA glycosylases: in DNA repair and beyondMSH2/MSH6 complex promotes error-free repair of AID-induced dU:G mispairs as well as error-prone hypermutation of A:T sitesRNA Exosome Regulates AID DNA Mutator Activity in the B Cell GenomeDifferential expression of APE1 and APE2 in germinal centers promotes error-prone repair and A:T mutations during somatic hypermutationDNA polymerase theta contributes to the generation of C/G mutations during somatic hypermutation of Ig genes.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 patternRole for mismatch repair proteins Msh2, Mlh1, and Pms2 in immunoglobulin class switching shown by sequence analysis of recombination junctionsAltered somatic hypermutation and reduced class-switch recombination in exonuclease 1-mutant miceSimultaneous in vitro characterisation of DNA deaminase function and associated DNA repair pathwaysSevere attenuation of the B cell immune response in Msh2-deficient miceReduced isotype switching in splenic B cells from mice deficient in mismatch repair enzymesMsh2 ATPase activity is essential for somatic hypermutation at a-T basepairs and for efficient class switch recombinationDifferent mismatch repair deficiencies all have the same effects on somatic hypermutation: intact primary mechanism accompanied by secondary modifications129-derived strains of mice are deficient in DNA polymerase iota and have normal immunoglobulin hypermutationMlh1 can function in antibody class switch recombination independently of Msh2Mice reconstituted with DNA polymerase beta-deficient fetal liver cells are able to mount a T cell-dependent immune response and mutate their Ig genes normallyIn vitro antibody evolution targeting germline hot spots to increase activity of an anti-CD22 immunotoxin.Isolation of anti-CD22 Fv with high affinity by Fv display on human cells.DNA-dependent protein kinase inhibits AID-induced antibody gene conversion.Activation-induced deaminase, AID, is catalytically active as a monomer on single-stranded DNA.Proximity to AGCT sequences dictates MMR-independent versus MMR-dependent mechanisms for AID-induced mutation via UNG2.Immunoglobulin class switch recombination: will genetics provide new clues to mechanism?The protein-protein interface evolution acts in a similar way to antibody affinity maturation.Generation and repair of AID-initiated DNA lesions in B lymphocytes.The liaison of isotype class switch and mismatch repair: an illegitimate affair.Altered spectra of hypermutation in DNA repair-deficient mice.Somatic hypermutation of immunoglobulin and non-immunoglobulin genes.Lysine residue 185 of Rad1 is a topological but not a functional counterpart of lysine residue 164 of PCNA.DNA cleavage in immunoglobulin somatic hypermutation depends on de novo protein synthesis but not on uracil DNA glycosylaseDifferent mutation signatures in DNA polymerase eta- and MSH6-deficient mice suggest separate roles in antibody diversificationVariable deletion and duplication at recombination junction ends: implication for staggered double-strand cleavage in class-switch recombinationSwitch junction sequences in PMS2-deficient mice reveal a microhomology-mediated mechanism of Ig class switch recombination.Correlation of somatic hypermutation specificity and A-T base pair substitution errors by DNA polymerase eta during copying of a mouse immunoglobulin kappa light chain transgene.Somatic immunoglobulin hypermutation.
P2860
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P2860
Hot spot focusing of somatic hypermutation in MSH2-deficient mice suggests two stages of mutational targeting
description
1998 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
1998 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 1998
@ast
im Juli 1998 veröffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedecký článok (publikovaný 1998/07/01)
@sk
vědecký článek publikovaný v roce 1998
@cs
wetenschappelijk artikel (gepubliceerd op 1998/07/01)
@nl
наукова стаття, опублікована в липні 1998
@uk
مقالة علمية (نشرت في يوليو 1998)
@ar
name
Hot spot focusing of somatic h ...... stages of mutational targeting
@ast
Hot spot focusing of somatic h ...... stages of mutational targeting
@en
Hot spot focusing of somatic h ...... stages of mutational targeting
@nl
type
label
Hot spot focusing of somatic h ...... stages of mutational targeting
@ast
Hot spot focusing of somatic h ...... stages of mutational targeting
@en
Hot spot focusing of somatic h ...... stages of mutational targeting
@nl
prefLabel
Hot spot focusing of somatic h ...... stages of mutational targeting
@ast
Hot spot focusing of somatic h ...... stages of mutational targeting
@en
Hot spot focusing of somatic h ...... stages of mutational targeting
@nl
P2093
P3181
P1433
P1476
Hot spot focusing of somatic h ...... stages of mutational targeting
@en
P2093
C. Milstein
M. R. Ehrenstein
M. S. Neuberger
P304
P3181
P356
10.1016/S1074-7613(00)80595-6
P407
P577
1998-07-01T00:00:00Z