کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8472141 | 1550299 | 2009 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Translational repression of inducible NO synthase in macrophages by l-arginine depletion is not associated with an increased phosphorylation of eIF2α
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کلمات کلیدی
LPSiNOSISReIF2αATF-4GCN2eIF4l-arginine - آرژینین الTranslation - ترجمه (زیستشناسی)CHOP - تکه کردنinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییactivating transcription factor-4 - فعال کردن عامل رونویسی 4lipopolysaccharide - لیپوپلی ساکاریدMacrophages - ماکروفاژها،درشت خوارهاNitric oxide - نیتریک اکسیدIntegrated stress response - واکنش تنش مجدد
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
In mouse inflammatory macrophages the cytokine-mediated expression of inducible nitric oxide synthase (iNOS) is regulated by the availability of the substrate l-arginine. Following arginine starvation the levels of iNOS mRNA remain unimpaired, whereas the translation of iNOS protein is strikingly downregulated. In the present study we addressed the question, whether arginine-deficient macrophages follow the canonical integrated stress response (ISR) that in other cell types depleted of amino acids was characterized by the accumulation of phosphorylated (i.e. inactive) eukaryotic translation initiation factor-2α (eIF2α), the attenuation of global protein synthesis and the induction of certain stress response target genes. Unexpectedly, resting as well as stimulated inflammatory macrophages constitutively exhibited high levels of phosphorylated eIF2α, which was not further increased upon l-arginine starvation. At the same time, macrophages deprived of l-arginine showed a significant upregulation of the mRNA levels of ISR genes. From these data we conclude that l-arginine deficiency blocks the translation of iNOS and elicits a stress response in macrophages, both of which, however, do not result from an enhanced phosphorylation of eIF2α. Alternative modes of translational repression of iNOS need to be considered.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunobiology - Volume 214, Issues 9â10, September 2009, Pages 822-827
Journal: Immunobiology - Volume 214, Issues 9â10, September 2009, Pages 822-827
نویسندگان
Till König, Christian Bogdan, Ulrike Schleicher,