کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8302443 | 1537735 | 2013 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
3,5-Diiodo-l-thyronine induces SREBP-1 proteolytic cleavage block and apoptosis in human hepatoma (Hepg2) cells
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کلمات کلیدی
DAPIIRESp38MAPKSREBPPKCSREBP-13,5,3′-triiodo-l-thyroninePKC-δERKSRBPI3K3,5-diiodo-l-thyronine - 3،5-دیویدو-تریرونین3,5-Diiodothyronine - 3،5-دییدوتیرونین4,6-diamidino-2-phenylindole - 4،6-دیامیدین-2-فنیلینولMAPK - MAPKAkt - آکتfatty acid synthase - اسید چرب سنتازApoptosis - خزان یاختهایrenilla luciferase - رگیلا لوسیفرازinternal ribosome entry site - سایت ورودی ریبوزوم داخلیsulforhodamine B - سولفوردامین بFasn - فسادphosphoinositide 3-kinase - فسفینوزیتید 3-کینازFirefly luciferase - لوسیفراز فیرفیلیMammalian target of rapamycin complex 1 - هدف پستانداران مجتمع رپامایسین 1Thyroid hormone - هورمون تیروئیدsterol regulatory element binding protein - پروتئین اتصال دهنده عصاره استرولProtein kinase C - پروتئین کیناز سیmitogen activated protein kinase - پروتئین کیناز فعال Mitogen فعال استextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Thyroid hormone 3,5,3â²-triiodo-l-thyronine (T3) is known to affect cell metabolism through both the genomic and non-genomic actions. Recently, we demonstrated in HepG2 cells that T3 controls the expression of SREBP-1, a transcription factor involved in the regulation of lipogenic genes. This occurs by activation of a cap-independent translation mechanism of its mRNA. Such a process is dependent on non-genomic activation of both MAPK/ERK and PI3K/Akt pathways. The physiological role of 3,5-diiodo-l-thyronine (T2), previously considered only as a T3 catabolite, is of growing interest. Evidences have been reported that T2 rapidly affects some metabolic pathways through non-genomic mechanisms. Here, we show that T2, unlike T3, determines the block of proteolytic cleavage of SREBP-1 in HepG2 cells, without affecting its expression at the transcriptional or translational level. Consequently, Fatty Acid Synthase expression is reduced. T2 effects depend on the concurrent activation of MAPKs ERK and p38, of Akt and PKC-δ pathways. Upon the activation of these signals, apoptosis of HepG2 cells seems to occur, starting at 12 h of T2 treatment. PKC-δ appears to act as a switch between p38 activation and Akt suppression, suggesting that this PKC may function as a controller in the balance of pro-apoptotic (p38) and anti-apoptotic (Akt) signals in HepG2 cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1831, Issue 12, December 2013, Pages 1679-1689
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1831, Issue 12, December 2013, Pages 1679-1689
نویسندگان
Alessio Rochira, Fabrizio Damiano, Santo Marsigliante, Gabriele V. Gnoni, Luisa Siculella,