کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9001592 | 1118537 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
HDAC inhibition prevents NF-κB activation by suppressing proteasome activity: Down-regulation of proteasome subunit expression stabilizes IκBα
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کلمات کلیدی
IKKSuc-LLVY-AMCInhibitor-κBPGPHβ1β2T-LIκBαCT-LEMSAIκBIL-1βSCFAHDACCaco-2TSANF-κBIκB kinase - IkB kinaseElectrophoretic mobility shift assay - آزمون تحرک تحرک الکتروفورزInterleukin-1β - اینترلوکین-1βButyrate - بوتیراتTrichostatin A - تریکوستاتین Atumor necrosis factor-α - تومور نکروز عامل αShort chain fatty acid - زنجیره کوتاه اسید چربTNF-α - فاکتور نکروز توموری آلفاnuclear factor-κB - فاکتور هسته ای κBChymotrypsin-like - مانند چیوتریپسینhistone deacetylase - هیستون داستیلازProteasome - پروتئازوم
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: HDAC inhibition prevents NF-κB activation by suppressing proteasome activity: Down-regulation of proteasome subunit expression stabilizes IκBα HDAC inhibition prevents NF-κB activation by suppressing proteasome activity: Down-regulation of proteasome subunit expression stabilizes IκBα](/preview/png/9001592.png)
چکیده انگلیسی
The short chain fatty acid (SCFA) butyrate (BA) and other histone deacetylase (HDAC) inhibitors can rapidly induce cell cycle arrest and differentation of colon cancer cell lines. We found that butyrate and the specific HDAC inhibitor trichostatin A (TSA) can reprogram the NF-κB response in colon cancer cells. Specifically, TNF-α activation is suppressed in butyrate-differentiated cells, whereas IL-1β activation is largely unaffected. To gain insight into the relationship between butyrate-induced differentiation and NF-κB regulation, we determined the impact of butyrate on proteasome activity and subunit expression. Interestingly, butyrate and TSA reduced the cellular proteasome activity in colon cancer cell lines. The drop in proteasome activity results from the reduced expression of the catalytic β-type subunits of the proteasome at both the protein and mRNA level. The selective impact of HDAC inhibitors on TNF-α-induced NF-κB activation appears to relate to the fact that the TNF-α-induced activation of NF-κB is mediated by the proteasome, whereas NF-κB activation by IL-1β is largely proteasome-independent. These findings indicate that cellular differentation status and/or proliferative capacity can significantly impact proteasome activity and selectively alter NF-κB responses in colon cancer cells. This information may be useful for the further development and targeting of HDAC inhibitors as anti-neoplastic and anti-inflammatory agents.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical Pharmacology - Volume 70, Issue 3, 1 August 2005, Pages 394-406
Journal: Biochemical Pharmacology - Volume 70, Issue 3, 1 August 2005, Pages 394-406
نویسندگان
Robert F. Place, Emily J. Noonan, Charles Giardina,