Somatic immunoglobulin hypermutation

Current Opinion in Immunology

Volumn 14, Issue 2, 2002, Pages 235-240

  Diaz, Marilyn ^a   Casali, Paolo ^b  

^a SCRIPPS RESEARCH INSTITUTE   (United States)

^b WEILL CORNELL MEDICAL COLLEGE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANTIGEN; DNA POLYMERASE; IMMUNOGLOBULIN; PROTEIN; PROTEIN BCL 6;

AMINO ACID SEQUENCE; ANTIBODY AFFINITY; ANTIBODY RESPONSE; CELL LINE; CELL MATURATION; DNA DAMAGE; DNA REPAIR; DNA STRAND BREAKAGE; DNA SYNTHESIS; GENE DELETION; GENE LOCATION; GENE SEQUENCE; GENETIC VARIABILITY; HUMAN; NONHUMAN; POINT MUTATION; PREVALENCE; PROMOTER REGION; REGULATORY MECHANISM; REVIEW; SOMATIC CELL;

EID: 0036533341     PISSN: 09527915     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0952-7915(02)00327-8     Document Type: Review

References (57)

1. Variability in the lambda light chain sequences of mouse antibody
2. Inter- and intraclonal diversity in the antibody response to influenza hemagglutinin
3. Evolution of somatic hypermutation and gene conversion in adaptive immunity
4. Cis-acting sequences that affect somatic hypermutation of Ig genes
5. TdT-accessible breaks are scattered over the immunoglobulin V domain in a constitutively hypermutating B cell line
6. Cell-cycle-regulated DNA double stranded breaks in somatic hypermutation of immunoglobulin genes
7. DNA double-strand breaks in immunoglobulin genes undergoing somatic hypermutation
8. DNA breaks in hypermutating immunoglobulin genes: Evidence for a break-and-repair pathway of somatic hypermutation
9. DNA polymerase eta is an A-T mutator in somatic hypermutation of immunoglobulin variable genes
10. The translesion DNA polymerase zeta plays a major role in Ig and BCL-6 somatic hypermutation
11. Decreased frequency of somatic hypermutation and impaired affinity maturation but intact germinal center formation in mice expressing antisense RNA to DNA polymerase zeta
12. Ablation of XRCC2/3 transforms immunoglobulin V gene conversion into somatic hypermutation
13. Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme
14. Boundaries of somatic mutation in rearranged immunoglobulin genes: 5′ Boundary is near the promoter, and 3′ boundary is approximately 1 kb from V(D)J gene
15. Mapping the upstream boundary of somatic mutations in rearranged immunoglobulin transgenes and endogenous genes
16. Characterization of the cis-acting elements required for somatic hypermutation of murine antibody V genes using conventional transgenic and transgene homologous recombination approaches
17. The transcriptional promoter regulates hypermutation of the antibody heavy chain locus
18. Mutations in Ig V(D)J genes are distributed asymmetrically and independently of the position of V(D)J
19. Monitoring and interpreting the intrinsic features of somatic hypermutation
20. Somatic hypermutation of immunoglobulin genes is linked to transcription initiation
21. Mutations of the chloramphenicol acetyl transferase transgene driven by the immunoglobulin promoter and intron enhancer
22. Elements regulating somatic hypermutation of an immunoglobulin kappa gene: Critical role for the intron enhancer/matrix attachment region
23. Multiple sequences from downstream of the J kappa cluster can combine to recruit somatic hypermutation to a heterologous, upstream mutation domain
24. Mutation of BCL-6 gene in normal B cells by the process of somatic hypermutation of Ig genes
25. Frequent somatic hypermutation of the 5′ noncoding region of the BCL-6 gene in B-cell lymphoma
26. B cell receptor engagement and T cell contact induce BCL-6 somatic hypermutation in human B cells: Identity with Ig hypermutation
27. Induction of Ig somatic hypermutation and class switching in a human monoclonal IgM+IgD+B cell line in vitro: Definition of the requirements and modalities of hypermutation
28. Somatic hypermutation in the absence of DNA-dependent protein kinase catalytic subunit (DNA-PK(cs)) or recombination-activating gene (RAG)1 activity
29. Hypermutation of immunoglobulin genes in memory B cells of DNA repair-deficient mice
30. Might gene conversion be the mechanism of somatic hypermutation of mammalian immunoglobulin genes
31. Rearrangement/hypermutation/gene conversion: When, where and why
32. Templated insertions in the rearranged chicken IgL V gene segment arise by intrachromosomal gene conversion
33. Point mutations cause the somatic diversification of IgM and IgG2a antiphosphorylcholine antibodies
34. Probing immunoglobulin gene mutation with microsatellites suggests a nonreplicative short patch DNA synthesis process
35. Mutational pattern of the nurse shark antigen receptor gene (NAR) is similar to that of mammalian Ig genes and to spontaneous mutations in evolution: The translesion synthesis model of somatic hypermutation
36. Evolution and somatic diversification of immunoglobulin light chains
37. Mutagenesis in eukaryotes dependent on DNA polymerase zeta and Rev1p
38. Error rate and specificity of human and murine DNA polymerase eta
39. DNA polymerase iota and related rad30-like enzymes
40. Eukaryotic polymerases iota and zeta act sequentially to bypass DNA lesions
41. Specificity of DNA lesion bypass by the yeast DNA polymerase eta
42. A role for REV3 in mutagenesis during double-strand break repair in Saccharomyces cerevisiae
43. Somatic mutation hotspots correlate with DNA polymerase eta error spectrum
44. Altered nucleotide misinsertion fidelity associated with poliota-dependent replication at the end of a DNA template
45. Mice reconstituted with DNA polymerase beta-deficient fetal liver cells are able to mount a T cell-dependent immune response and mutate their Ig genes normally
46. Human genetic defects in class-switch recombination (hyper-IgM syndromes)
47. Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2)
48. RNA editing meets DNA shuffling
49. Increased hypermutation at G and C nucleotides in immunoglobulin variable genes from mice deficient in the MSH2 mismatch repair protein
50. Hot spot focusing of somatic hypermutation in MSH2-deficient mice suggests two stages of mutational targeting
51. 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
52. Mismatch repair deficiency interferes with the accumulation of mutations in chronically stimulated B cells and not with the hypermutation process
53. Severe attenuation of the B cell immune response in Msh2-deficient mice
54. Smaller role for pol η?
55. Response 1
56. Response 2
57. Somatic hypermutation of immunoglobulin and non-immunoglobulin genes