The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
AID and Somatic Hypermutation
Open accessAbstract
In response to an assault by foreign organisms, peripheral B cells can change their antibody affinity and isotype by somatically mutating their genomic DNA. The ability of a cell to modify its DNA is exceptional in light of the potential consequences of genetic alterations to cause human disease and cancer. Thus, as expected, this mechanism of antibody diversity is tightly regulated and coordinated through one protein, activation induced deaminase (AID). AID produces diversity by converting cytosine to uracil within the immunoglobulin loci. The deoxyuracil residue is mutagenic when paired with deoxyguanosine, since it mimics thymidine during DNA replication. Additionally, B cells can manipulate the DNA repair pathways so that deoxyuracils are not faithfully repaired. Therefore, an intricate balance exists which is regulated at multiple stages to promote mutation of immunoglobulin genes, while retaining integrity of the rest of the genome. Here we discuss and summarize the current understanding of how AID functions to cause somatic hypermutation.
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Cites
DNA polymerase η is an A-T mutator in somatic hypermutation of immunoglobulin variable genes
Zeng, X., Winter, D. B., Kasmer, C., Kraemer, K. H., Lehmann, A. R., & Gearhart, P. J. (2001) · Nature Immunology · doi:10.1038/88740 · Cited by 420 · cited 1×
“…mutation of Polη in humans with xeroderma pigmentosum variant disease or deletion of the gene in mice, resulted in a dramatic decrease in mutations at A:T residues with a modest decrease in overall mutation frequency (Delbos et al., 2005; Faili et al., 2004; Zeng et al., 2004; Zeng et al., 2001).”
BackgroundSelf-citationFrasca, D., Landin, A. M., Lechner, S. C., Ryan, J. G., Schwartz, R., Riley, R. L., & Blomberg, B. B. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.180.8.5283 · Cited by 333 · cited 1×
“This may be due in part to degradation of E47 mRNA, which encodes molecules that stimulate AID transcription (Frasca et al., 2008).”
BackgroundError rate and specificity of human and murine DNA polymerase η
Matsuda, T., Bebenek, K., Masutani, C., Rogozin, I. B., Hanaoka, F., & Kunkel, T. A. (2001) · Journal of Molecular Biology · doi:10.1006/jmbi.2001.4937 · Cited by 170
Cited by
Krokan, H. E., & Bjoras, M. (2013) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a012583 · Cited by 1,322
Different B Cell Populations Mediate Early and Late Memory During an Endogenous Immune Response
Pape, K. A., Taylor, J. J., Maul, R. W., Gearhart, P. J., & Jenkins, M. K. (2011) · Science · doi:10.1126/science.1201730 · Cited by 572
Self-citationRelated Mechanisms of Antibody Somatic Hypermutation and Class Switch Recombination
Hwang*, J. K., Alt*, F. W., & Yeap, L.-S. (2015) · Microbiology Spectrum · doi:10.1128/microbiolspec.mdna3-0037-2014 · Cited by 126
Antibody diversification caused by disrupted mismatch repair and promiscuous DNA polymerases
Zanotti, K. J., & Gearhart, P. J. (2016) · DNA Repair · doi:10.1016/j.dnarep.2015.11.011 · Cited by 57
Self-citationIn vitro affinity maturation of antibody against membrane-bound GPCR molecules
Wang, J., An, L., Zhao, Y., Zhang, C., Li, S., Ye, C., Jing, S., & Hang, H. (2019) · Applied Microbiology and Biotechnology · doi:10.1007/s00253-019-10030-x · Cited by 11
Metadata
- Authors
- Maul, R. W., & Gearhart, P. J.
- Venue
- Advances in Immunology
- Publisher
- Elsevier
- Published
- 2010
- Volume
- 105
- Pages
- 159-191
- ISSN
- 0065-2776 (ISSN-L)
- OpenAlex
- W1499793841
- Cited by
- 204
- References
- 3
- FWCI
- 23.68
- Type
- book chapter
- Language
- en
- Open access
- green
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