کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10751204 | 1050307 | 2015 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Caenorhabditis elegans ATAD-3 modulates mitochondrial iron and heme homeostasis
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کلمات کلیدی
FACATAD3C. elegans - C. elegansRNAi - RNA سرکوبگر،RNA مداخلهگر، RNA خاموش کنندهIron - آهنFerric Ammonium Citrate - آهن آمونیوم سیتراتOxidative phosphorylation - فسفوریلاسیون اکسیداتیوMetabolism - متابولیسم RNA-mediated interference - مداخله RNAMitochondria - میتوکندریاHeme - هم Caenorhabditis elegans - کرم الگانس
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
ATAD3 (ATPase family AAA domain-containing protein 3) is a mitochondrial protein, which is essential for cell viability and organismal development. ATAD3 has been implicated in several important cellular processes such as apoptosis regulation, respiratory chain function and steroid hormone biosynthesis. Moreover, altered expression of ATAD3 has been associated with several types of cancer. However, the exact mechanisms underlying ATAD3 effects on cellular metabolism remain largely unclear. Here, we demonstrate that Caenorhabditis elegans ATAD-3 is involved in mitochondrial iron and heme homeostasis. Knockdown of atad-3 caused mitochondrial iron- and heme accumulation. This was paralleled by changes in the expression levels of several iron- and heme-regulatory genes as well as an increased heme uptake. In conclusion, our data indicate a regulatory role of C. elegans ATAD-3 in mitochondrial iron and heme metabolism.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 467, Issue 2, 13 November 2015, Pages 389-394
Journal: Biochemical and Biophysical Research Communications - Volume 467, Issue 2, 13 November 2015, Pages 389-394
نویسندگان
Daniela van den Ecker, Michael Hoffmann, Gesine Müting, Silvia Maglioni, Diran Herebian, Ertan Mayatepek, Natascia Ventura, Felix Distelmaier,