Somatic Hypermutation and Class Switch Recombination in Msh6−/−Ung−/−Double-Knockout Mice

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Somatic hypermutation and class switch recombination in Msh6(-/-)Ung(-/-) double-knockout mice.

Somatic hypermutation (SHM) and class switch recombination (CSR) are initiated by activation-induced cytosine deaminase (AID). The uracil, and potentially neighboring bases, are processed by error-prone base excision repair and mismatch repair. Deficiencies in Ung, Msh2, or Msh6 affect SHM and CSR. To determine whether Msh2/Msh6 complexes which recognize single-base mismatches and loops were th...

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Related Mechanisms of Antibody Somatic Hypermutation and Class Switch Recombination.

The primary antibody repertoire is generated by mechanisms involving the assembly of the exons that encode the antigen-binding variable regions of immunoglobulin heavy (IgH) and light (IgL) chains during the early development of B lymphocytes. After antigen-dependent activation, mature B lymphocytes can further alter their IgH and IgL variable region exons by the process of somatic hypermutatio...

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Disparate roles of ATR and ATM in immunoglobulin class switch recombination and somatic hypermutation

Class switch recombination (CSR) and somatic hypermutation (SHM) are mechanistically related processes initiated by activation-induced cytidine deaminase. Here, we have studied the role of ataxia telangiectasia and Rad3-related protein (ATR) in CSR by analyzing the recombinational junctions, resulting from in vivo switching, in cells from patients with mutations in the ATR gene. The proportion ...

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A Role for Msh6 But Not Msh3 in Somatic Hypermutation and Class Switch Recombination

Somatic hypermutation is initiated by activation-induced cytidine deaminase (AID), and occurs in several kilobases of DNA around rearranged immunoglobulin variable (V) genes and switch (S) sites before constant genes. AID deaminates cytosine to uracil, which can produce mutations of C:G nucleotide pairs, and the mismatch repair protein Msh2 participates in generating substitutions of downstream...

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ژورنال

عنوان ژورنال: The Journal of Immunology

سال: 2006

ISSN: 0022-1767,1550-6606

DOI: 10.4049/jimmunol.177.8.5386