Article ; Online: NME proteins regulate class switch recombination.
2018 Volume 593, Issue 1, Page(s) 80–87
Abstract: Class switch recombination (CSR) in B cells involves deletion-recombination at switch (S) region DNA and is important for the diversification of antibody isotypes during an immune response. Here, we identify two NME [NM23/NDPK (nucleoside diphosphate ... ...
| Abstract | Class switch recombination (CSR) in B cells involves deletion-recombination at switch (S) region DNA and is important for the diversification of antibody isotypes during an immune response. Here, we identify two NME [NM23/NDPK (nucleoside diphosphate kinase)] isoforms, NME1 and NME2, as novel players in this process. Knockdown of NME2 leads to decreased CSR, while knockdown of the highly homologous NME1 results in increased CSR. Interestingly, these NME proteins also display differential occupancy at S regions during CSR despite their homology; NME1 binds to S regions prior to stimulation, while NME2 binds to S regions only after stimulation. To the best of our knowledge, this represents the first report of a role for these proteins in the regulation of CSR. |
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| MeSH term(s) | Animals ; B-Lymphocytes/metabolism ; Cell Proliferation ; Cells, Cultured ; Gene Knockdown Techniques ; Immunoglobulin Class Switching ; Immunoglobulin Heavy Chains/chemistry ; Immunoglobulin Heavy Chains/metabolism ; Immunoglobulin Switch Region ; Mice ; NM23 Nucleoside Diphosphate Kinases/genetics ; NM23 Nucleoside Diphosphate Kinases/metabolism ; Protein Binding |
| Chemical Substances | Immunoglobulin Heavy Chains ; NM23 Nucleoside Diphosphate Kinases ; Nme1 protein, mouse (EC 2.7.4.6) ; Nme2 protein, mouse (EC 2.7.4.6) |
| Language | English |
| Publishing date | 2018-11-23 |
| Publishing country | England |
| Document type | Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't |
| ZDB-ID | 212746-5 |
| ISSN | 1873-3468 ; 0014-5793 |
| ISSN (online) | 1873-3468 |
| ISSN | 0014-5793 |
| DOI | 10.1002/1873-3468.13290 |
| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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