Somatic hypermutation in the absence of DNA-dependent protein kinase catalytic subunit (DNA-PK(cs)) or recombination-activating gene (RAG)1 activity

Journal of Experimental Medicine

Volumn 192, Issue 10, 2000, Pages 1509-1514

  Bemark, Mats ^a   Sale, Julian E ^a   Kim, Hye Jung ^b   Berek, Claudia ^b   Cosgrove, Ruth A ^a   Neuberger, Michael S ^a  

^a MRC LABORATORY OF MOLECULAR BIOLOGY   (United Kingdom)

^b DEUTSCHES RHEUMA FORSCHUNGSZENTRUM   (Germany)

Author keywords

B lymphocyte; End joining; Immunoglobulin gene; Mutation; Switch recombination

Indexed keywords

DNA DEPENDENT PROTEIN KINASE; IMMUNOGLOBULIN; T LYMPHOCYTE RECEPTOR;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; B LYMPHOCYTE; ENZYME ACTIVE SITE; GENE ACTIVITY; GENE SWITCHING; GENETIC RECOMBINATION; GERMINAL CENTER; MOUSE; NONHUMAN; PRIORITY JOURNAL; SOMATIC MUTATION; TRANSGENE;

ANIMALS; BASE SEQUENCE; CATALYTIC DOMAIN; DNA-ACTIVATED PROTEIN KINASE; DNA-BINDING PROTEINS; GENE REARRANGEMENT; GENES, RAG-1; GERMINAL CENTER; HOMEODOMAIN PROTEINS; IMMUNOGLOBULINS; MICE; MICE, SCID; MOLECULAR SEQUENCE DATA; MURAMIDASE; MUTAGENESIS; PROTEIN SUBUNITS; PROTEIN-SERINE-THREONINE KINASES; RECEPTORS, ANTIGEN, B-CELL; RECEPTORS, ANTIGEN, T-CELL; RECOMBINATION, GENETIC; TRANSPOSASES;

EID: 0034694086     PISSN: 00221007     EISSN: None     Source Type: Journal    
DOI: 10.1084/jem.192.10.1509     Document Type: Article

References (20)

1. Increased hypermutation at G and C nucleotides in immunoglobulin variable genes from mice deficient in the MSH2 mismatch repair protein
2. Mismatch repair deficiency interferes with the accumulation of mutations in chronically stimulated B cells and not with the hypermutation process
3. Somatic hypermutation in MSH2 deficient mice is more focussed on intrinsic hotspots suggesting targeting to be a two stage process
4. Deficiency in Msh2 affects the efficiency and local sequence specificity of immunoglobulin class-switch recombination: Parallels with somatic hypermutation
5. Reduced isotype switching in splenic B cells from mice deficient in mismatch repair enzymes
6. The SCID but not the RAG-2 gene product is required for S mu-S epsilon heavy chain class switching
7. Ku80 is required for immunoglobulin isotype switching
8. Ku70 is required for late B cell development and immunoglobulin heavy chain class switching
9. TdT accessible breaks are scattered over the V domain in a constitutively hypermutating cell line
10. Frequent occurrence of deletions and duplications during somatic hypermutation: Implications for oncogenic translocations and heavy chain disease
11. Somatic hypermutation introduces insertions and deletions into immunoglobulin V genes
12. Association of terminal deoxynucleotidyl transferase with Ku
13. Modulation of terminal deoxynucleotidyltransferase activity by the DNA-dependent protein kinase
14. A severe combined immunodeficiency mutation in the mouse
15. The C-terminal conserved domain of DNA-PKcs, missing in the SCID mouse, is required for kinase activity
16. Altered immunoglobulin expression and functional silencing of self-reactive B lymphocytes in transgenic mice
17. +TCR(lo) thymocytes in vivo
18. Functional immunoglobulin transgenes guide ordered B-cell differentiation in Rag-1 deficient mice
19. Rapid induction of anti-idiotypic responses to unmodified monoclonal antibodies from syngeneic mice following primary immunization
20. Immunoglobulin gene hypermutation in germinal centres is independent of the RAG-1 V(D)J recombinase