YY1 and a unique DNA repeat element regulates the transcription of mouse CS1 (CD319, SLAMF7) gene

University of North Texas, Denton, Texas, United States
Molecular Immunology (Impact Factor: 2.97). 01/2013; 54(3-4):254-263. DOI: 10.1016/j.molimm.2012.12.017
Source: PubMed


CS1 (CD319, CRACC, SLAMF7, novel Ly9) activates NK cell-mediated cytotoxicity and proliferation of B lymphocytes during immune responses. The expression of CS1 is up regulated on B cells in multiple myeloma and systemic lupus erythematosus. In this study we describe the transcriptional regulation of mouse CS1 (mCS1) gene. We show that mCS1 gene transcription is regulated by YY1 (Ying Yang 1) and a unique (AG)(n=36) DNA repeat element. YY1 is known to play a significant role in B cell development by regulating the pro B cell to pre B cell transition. The consensus DNA binding site for YY1 was detected using TRANSFAQ on the mCS1 promoter region. Mutations in the YY1 site led to a significant increase in mCS1 promoter activity indicating that YY1 represses mCS1 transcription. YY1 binds to the mCS1 promoter at the expected site in vivo and in vitro as tested by chromatin immunoprecipitation assays and super-shift EMSA assays respectively. Unique (CT)(n=24) and (AG)(n=36) DNA repeat elements are present on mCS1 promoter that are sensitive to S1 nuclease and engage in DNA triplex structure as confirmed by AFM (atomic force microscopy) imaging. Interestingly, the (AG)(n=36) repeat element enhances mCS1 promoter activity.

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Available from: Porunelloor A Mathew, Jun 12, 2015
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    • "TYROBP, a transmembrane protein initially characterized in natural killer cells, is involved in a broad array of biological functions, including the innate response against viruses, and diverse inflammatory reactions mediated by neutrophils, monocytes and macrophages [43]. SLAMF7 is involved in the activation of natural killer cells and also in the proliferation of B lymphocytes during innate and adaptive immune responses [44]. LCP1, a leukocyte-specific F-actin bundling protein, is implicated in T lymphocyte polarity and migration in response to chemokines [45]. "
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