Mechanism and regulation of class switch recombination.

By J. Stavnezer, J. Guikema, C. E. Schrader. Annual Review of Immunology, 2008

1,133 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/15de2ad84cf6a817fc8ccf120e339cf368ae22ea

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In Epidemiology

1. A. Cerutti
2. Christopher K. Glass
3. P. Calder
4. I. Tabas

In Immunology

1. A. Cerutti
2. Theam Soon Lim
3. F. Batista
4. Christopher K. Glass
5. Stephen J. Elledge
6. P. Calder
7. I. Tabas

Citations in the corpus

• Playing the end game: DNA double-strand break repair pathway choice. (2012, background): “…heavy-chain (IgH) locus that are separated by 60–200 kbp. Deletional repair between these DSBs occurs during G1 in amanner dependent on the classical and alternative NHEJ pathways (C/A-NHEJ), and is essential for the assembly of antibodies of different class and function (Stavnezer et al., 2008).”
• Management of Rheumatoid Arthritis: An Overview (2021, background): “At this level, B cells undergo somatic hypermutation or class-switch recombination and start to proliferate and differentiate intro plasma cells that produce autoantibodies depending on the receptors of the precursor cells [69].”
• Repair of strand breaks by homologous recombination. (2013, background): “Besides canonical NHEJ proteins like Ku and LIG4, the DNA damage response protein 53BP1 has a role in NHEJ (Nakamura et al. 2006; Stavnezer et al. 2008), and as with canonical NHEJ factors, 53BP1 disruption is associated with increased HR (Nakamura et al.”
• RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection (2013, background): “The assembly of antibodies of different class requires that AID-induced DSBs are subject to deletional repair through classical and alternative NHEJ pathways (Stavnezer et al., 2008; Yan et al., 2007).”
• Nuclear Receptor-Induced Chromosomal Proximity and DNA Breaks Underlie Specific Translocations in Cancer (2009, positive): “The presence of microhomology in multiple TMPRSS2:ERG and TMPRSS2:ETV1 fusion sites lends further support for the model that there are staggered sites of DNA breakage as might be expected from the sequential actions of AID and UNG, analogous to their predicted functions in CSR ( Stavnezer et al., 20”
• Naïve Human Antibody Libraries for Infectious Diseases (2018, background): “However, the V regions of antibodies will remain intact and unchanged [32, 49].”
• The DNA Damage Response: Making it safe to play with knives (2010, background): “Defects in AID and UNG have been shown to cause the Hyper-IgM Molecular Cell 40, October 22, 2010 ª2010 Elsevier Inc. 195 syndrome, which is characterized by normal IgM levels but few or no IgG, IgA, and IgE isotypes (Stavnezer et al., 2008).”
• The regulation of IgA class switching (2008, background): “In the presence of antigen, mature B cells diversify their antibody repertoire through somatic hypermutation (SHM) and class switchin”