کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2833048 | 1163856 | 2006 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Differential regulation of chromatin structure of the murine 3â² IgH enhancer and IgG2b germline promoter in response to lipopolysaccharide and CD40 signaling
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کلمات کلیدی
LPSCSRBAFbRGHDAC1IgHBrahma-related geneSWI/SNF - SWI / SNFHistone acetylation - استیلیت هیستونchromatin immunoprecipitation - ایمن سازی کروماتینChromatin remodeling - بازسازی کروماتینclass switch recombination - بازوی سوئیچ کلاسImmunoglobulin heavy chain - زنجیره سنگین ایمونوگلوبولینlipopolysaccharide - لیپوپلی ساکاریدhistone deacetylase 1 - هیستون دیازتیلاز 1CHiP - چیپ
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
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چکیده انگلیسی
Class switch recombination (CSR) of murine immunoglobulin heavy chain (IgH) is controlled by germline transcription-coupled modification of the accessibility of the highly repetitive switch regions (S) located upstream of the constant region genes. Activation of the 3â² IgH enhancer (3â²E) is believed to regulate CSR during B cell terminal differentiation, although the detailed molecular mechanism remains unclear. Here, we show that BAF57 and BRG1, two essential subunits of murine SWI/SNF complex, differentially associate with the DNase I hypersensitive region HS1/2 of 3â²E and the IgG2b germline promoter in response to LPS activation or CD40 engagement. Both LPS and CD40 signaling cause SWI/SNF complex to dissociate from HS1/2 and associate with their responsive IgG2b germline promoter, suggesting the potential fluidity of chromatin structure and specific regulatory mode for the ATP-dependent chromatin remodeler during CSR. More interesting, increase in histone acetylation is either inverse or parallel with the action of SWI/SNF complex at HS1/2 enhancer or IgG2b germline promoter, respectively. Chromatin immunoprecipitation experiments show that alteration of histone H3 and H4 acetylation has overall similarities in response to LPS and CD40 signaling, with H3 hyperacetylated and H4 hypoacetylated at the HS1/2 enhancer and reversed modification patterns at the IgG2b germline promoter. Finally, the specificity of LPS and CD40 signaling in control of CSR could be partially coded by the specific acetylation marking of H3 and H4. Our results further strengthen the notion that chromatin remodeling plays a critical role in CSR.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 43, Issue 8, March 2006, Pages 1211-1220
Journal: Molecular Immunology - Volume 43, Issue 8, March 2006, Pages 1211-1220
نویسندگان
Xincheng Qin, Hong Tang,