Somatic mutation hotspots correlate with DNA polymerase η error spectrum

Rogozin, Igor B., Pavlov, Youri I., Bebenek, Katarzyna, Matsuda, Toshiro, Kunkel, Thomas A.·2001·Nature Immunology

Cited by (300)

Items 201–300 of 300

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  3. Characterization of Ig Gene Somatic Hypermutation in the Absence of Activation-Induced Cytidine Deaminase
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  4. A Regulatory Role for NBS1 in Strand-Specific Mutagenesis during Somatic Hypermutation
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  5. DNA polymerases in immunity: profiting from errors
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  6. Hypermutation at A/T Sites during G·U Mismatch Repair in Vitro by Human B-cell Lysates
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  7. DNA polymerases β and λ do not directly affect Ig variable region somatic hypermutation although their absence reduces the frequency of mutations
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  8. The mismatch repair pathway functions normally at a non-AID target in germinal center B cells
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  9. DNA polymerase η is a limiting factor for A:T mutations in Ig genes and contributes to antibody affinity maturation
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  10. Biased dA/dT somatic hypermutation as regulated by the heavy chain intronic iEμ enhancer and 3′Eα enhancers in human lymphoblastoid B cells
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  11. Bcl-2 Rescues the Germinal Center Response But Does Not Alter the V Gene Somatic Hypermutation Spectrum in MSH2-Deficient Mice
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  14. Somatic hypermutation does not require Rad54 and Rad54B‐mediated homologous recombination
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  16. Response 1 to 'Smaller role for pol η?'
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  17. Genetic analysis reveals an intrinsic property of the germinal center B cells to generate A:T mutations
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  44. Canonical and Non-Canonical Roles of Human DNA Polymerase η
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  45. Correlations in Somatic Hypermutation Between Sites in IGHV Genes Can Be Explained by Interactions Between AID and/or Polη Hotspots
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  46. Somatic Hypermutation of Ig Genes is Affected Differently by Failures in Apoptosis Caused by Disruption of Fas (lpr Mutation) or by Overexpression of Bcl‐2
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