کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8477449 | 1550903 | 2013 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
HDAC3 interacts with sumoylated C/EBPα to negatively regulate the LXRα expression in rat hepatocytes
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کلمات کلیدی
CBSsilencing mediator for retinoid and thyroid receptorsCCAAT/enhancer binding proteinsSMRTSUMOylationLXRαHDAC3LPLPTMqRT-PCRHDACNCoRCYP7A1FASTSSSUMOC/EBPs - C / EBPC/EBPα - C / EBPαchromatin immunoprecipitation assay - آزمون ایمن زدایی کروماتینfatty acid synthase - اسید چرب سنتازPost translational modification - اصلاح پست ترجمهRoom temperature - دمای اتاقtranscription start site - رونویسی شروع سایتCo-IP - شرکت-IPLipoprotein lipase - لیپو پروتئین لیپازnuclear receptor corepressor - هسته گیرنده گیرنده اتمیCo-Immunoprecipitation - هم ایمن زداییhistone deacetylase - هیستون داستیلازquantitative real-time PCR - واکنش زنجیره ای پلیمراز واقعی در زمان واقعیCHiP - چیپliver X receptor alpha - کبد X گیرنده آلفاcholesterol 7α-hydroxylase - کلسترول 7α-هیدروکسیلازNuclear receptor - گیرنده هستهای، گیرندههای هستهای
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: HDAC3 interacts with sumoylated C/EBPα to negatively regulate the LXRα expression in rat hepatocytes HDAC3 interacts with sumoylated C/EBPα to negatively regulate the LXRα expression in rat hepatocytes](/preview/png/8477449.png)
چکیده انگلیسی
The expression changes of liver X receptor alpha (LXRα), histone deacetylase 3 (HDAC3) and CCAAT/enhancer binding protein alpha (C/EBPα) were detected in liver tissues of our high-fat-diet E3 rat model. The aim of this study is to pinpoint the molecular mechanism of HDAC3 and C/EBPα to orchestrate LXRα expression in hepatocytes. We confirmed that LXRα and its target genes were negatively regulated by HDAC3 in stable expressed clones with pEGFP-Hdac3 or shRNA-Hdac3 vector. However, transient pEGFP-C/EBPα plasmid transfection showed an upregulation of LXRα expression and C/EBPα enhanced LXRα promoter activity in a dose-dependent manner in CBRH-7919 cells. By using 5â²-serial deletion reporter analysis, we identified that fragment from â2881 to â1181 bp of LXRα promoter was responsible for C/EBPα binding to the promoter, especially CBS1 and CBS4 were identified essentially by using ChIP and luciferase reporter assay. Co-IP, qRT-PCR and ChIP revealed that HDAC3 interacted with C/EBPα co-regulated LXRα expression. Sumoylation of C/EBPα at lysine 159 was detected in CBRH-7919 cells with transient overexpressed C/EBPα, and Co-IP assay detected that sumoylated C/EBPα interacted with more HDAC3 than C/EBPα K159L mutant. Luciferase reporter assay demonstrated that C/EBPα participated in HDAC3-repressed LXRα transcription, and HDAC3 was involved in sumoylated C/EBPα-inactivated LXRα activity. Luciferase reporter assay demonstrated that sumoylation of C/EBPα by SUMO-1 directly reversed the activation of C/EBPα on LXRα promoter. The results suggested that HDAC3 interacts with sumoylated C/EBPα to negatively regulate the LXRα expression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 374, Issues 1â2, 15 July 2013, Pages 35-45
Journal: Molecular and Cellular Endocrinology - Volume 374, Issues 1â2, 15 July 2013, Pages 35-45
نویسندگان
Juan Ren, Dongmin Li, Yue Li, Xi Lan, Jianhuai Zheng, Xuan Wang, Jie Ma, Shemin Lu,