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@article{1410132, author = {Zápražná, Kristína and Basu, A. and Tom, Nikola and Jha, V. and Hodawadekar, S. and Radová, Lenka and Malčíková, Jitka and Tichý, Boris and Pospíšilová, Šárka and Atchison, M.L.}, article_location = {HOBOKEN}, article_number = {2}, doi = {http://dx.doi.org/10.1002/eji.201747065}, keywords = {AID; class switch recombination; somatic hypermutation; YY1}, language = {eng}, issn = {0014-2980}, journal = {EUROPEAN JOURNAL OF IMMUNOLOGY}, title = {Transcription factor YY1 can control AID-mediated mutagenesis in mice}, url = {http://onlinelibrary.wiley.com/doi/10.1002/eji.201747065/full}, volume = {48}, year = {2018} }
TY - JOUR ID - 1410132 AU - Zápražná, Kristína - Basu, A. - Tom, Nikola - Jha, V. - Hodawadekar, S. - Radová, Lenka - Malčíková, Jitka - Tichý, Boris - Pospíšilová, Šárka - Atchison, M.L. PY - 2018 TI - Transcription factor YY1 can control AID-mediated mutagenesis in mice JF - EUROPEAN JOURNAL OF IMMUNOLOGY VL - 48 IS - 2 SP - 273-282 EP - 273-282 PB - WILEY SN - 00142980 KW - AID KW - class switch recombination KW - somatic hypermutation KW - YY1 UR - http://onlinelibrary.wiley.com/doi/10.1002/eji.201747065/full L2 - http://onlinelibrary.wiley.com/doi/10.1002/eji.201747065/full N2 - Activation-induced cytidine deminase (AID) is crucial for controlling the immunoglobulin (Ig) diversification processes of somatic hypermutation (SHM) and class switch recombination (CSR). AID initiates these processes by deamination of cytosine, ultimately resulting in mutations or double strand DNA breaks needed for SHM and CSR. Levels of AID control mutation rates, and off-target non-Ig gene mutations can contribute to lymphomagenesis. Therefore, factors that control AID levels in the nucleus can regulate SHM and CSR, and may contribute to disease. We previously showed that transcription factor YY1 can regulate the level of AID in the nucleus and Ig CSR. Therefore, we hypothesized that conditional knock-out of YY1 would lead to reduction in AID localization at the Ig locus, and reduced AID-mediated mutations. Using mice that overexpress AID (IgAID yy1(f/f)) or that express normal AID levels (yy1(f/f)), we found that conditional knock-out of YY1 results in reduced AID nuclear levels, reduced localization of AID to the S switch region, and reduced AID-mediated mutations. We find that the mechanism of YY1 control of AID nuclear accumulation is likely due to YY1-AID physical interaction which blocks AID ubiquitination. ER -
ZÁPRAŽNÁ, Kristína, A. BASU, Nikola TOM, V. JHA, S. HODAWADEKAR, Lenka RADOVÁ, Jitka MALČÍKOVÁ, Boris TICHÝ, Šárka POSPÍŠILOVÁ and M.L. ATCHISON. Transcription factor YY1 can control AID-mediated mutagenesis in mice. \textit{EUROPEAN JOURNAL OF IMMUNOLOGY}. HOBOKEN: WILEY, 2018, vol.~48, No~2, p.~273-282. ISSN~0014-2980. Available from: https://dx.doi.org/10.1002/eji.201747065.
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