کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5859174 | 1562327 | 2015 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Key role of phosphodiesterase 4A (PDE4A) in autophagy triggered by yessotoxin
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کلمات کلیدی
PFAPDE4AA-kinase anchoring proteinsAKAPDISCLC3CREBpKaRPMIBcl-2mTORSDSNCIBSA - BSAcAMP - cAMPMAPK - MAPKadenosine 3′,5′-cyclic monophosphate - آدنوزین 3 '، 5'-سیکلیک منوفسفرهbovine serum albumin - آلبومین سرم گاوcAMP response element binding - الگوریتم پاسخ cAMPlight chain 3 - زنجیره سبک 3sodium dodecyl sulphate - سدیم دودسیل سولفاتRoswell Park Memorial Institute - مؤسسه یادبود پارک RoswellNational Cancer Institute - موسسه ملی سرطانMechanistic target of rapamycin - هدف مکانیکی رپامایسینparaformaldehyde - پارافرمالدهیدprotein kinase A - پروتئین کیناز Adeath-inducing signaling complex - پیچیدگی سیگنالینگ ناشی از مرگcaveolin-1 - کائولین-1Cav-1 - کاو-1mitogen-activated protein kinases - کیناز پروتئین فعال Mitogen
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Understanding the mechanism of action of the yessotoxin (YTX) is crucial since this drug has potential pharmacological effects in allergic processes, tumor proliferation and neurodegenerative diseases. It has been described that YTX activates apoptosis after 24Â h of treatment, while after 48Â h of incubation with the toxin a decrease in cell viability corresponding to cellular differentiation or non-apoptotic cell death was observed. In this paper, these processes were extensively studied by using the erythroleukemia K-562 cell line. On one hand, events of K-562 cell differentiation into erythrocytes after YTX treatment were studied using hemin as positive control of cell differentiation. Cell differentiation was studied through the cyclic nucleotide response element binding (phospho-CREB) and the transferrin receptor (TfR) expression. On the other hand, using rapamycin as positive control, autophagic hallmarks, as non-apoptotic cell death, were studied after toxin exposure. In this case, the mechanistic target of rapamycin (mTOR) and light chain 3B (LC3B) levels were measured to check autophagy activation. The results showed that cell differentiation was not occurring after 48Â h of toxin incubation while at this time the autophagy was triggered. Furthermore after 24Â h of toxin treatment none of these processes were activated. In addition, the role of the type 4A phosphodiesterase (PDE4A), the intracellular target of YTX, was checked. PDE4A-silencing experiments showed different regulation steps of PDE4A in the autophagic processes triggered either by traditional compounds or YTX. In summary, after 48Â h YTX treatment PDE4A-dependent autophagy, as non-apoptotic programmed cell death, is activated.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology - Volume 329, 2 March 2015, Pages 60-72
Journal: Toxicology - Volume 329, 2 March 2015, Pages 60-72
نویسندگان
A. Fernández-Araujo, A. Alfonso, M.R. Vieytes, L.M. Botana,