کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9126958 | 1569967 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Regulation of the expression of the oncogene EVI1 through the use of alternative mRNA 5â²-ends
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کلمات کلیدی
SSCUTREVI15-AzacytidineAzaCActDPBSSDSFBSatRA - ATRADMSO - DMSOall-trans retinoic acid - آل – ترانس رتینوئیک اسیدstandard deviation - انحراف معیارOncogene - انکوژنGene expression - بیان ژنmRNA stability - ثبات mRNAbase pairs - جفت پایهDimethyl sulfoxide - دیمتیل سولفواکسیدsodium dodecyl sulfate - سدیم دودسیل سولفاتsodium chloride sodium citrate - سدیم سیترات کلرید سدیمfetal bovine serum - سرم جنین گاوPhosphate buffered saline - فسفات بافر شورuntranslated region - منطقه غیر ترجمه
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
ژنتیک
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The EVI1 gene plays important roles in development and leukemogenesis. Recently, human EVI1 has been shown to give rise to at least six different mRNA variants with alternative 5â²-ends, only some of which are conserved in mice. In order to gain a basic understanding of the regulation and potential biological importance of these alternative transcripts, we confirmed their expression by Northern blot, and, using real time quantitative RT-PCR, compared their abundance and stability under different conditions. The general expression patterns of the EVI1 5â²-end variants in a panel of 20 human tissues were similar, but particularly high or low levels of some of them were noted in certain tissues. Pronounced differences in the expression of the 5â²-end variants were noted in response to all-trans retinoic acid: in a human teratocarcinoma cell line, only the EVI1 transcript variants containing alternative exons 1a and 1b were upregulated in response to this agent. This induction required transcriptional activity of RNA polymerase, but was also associated with a substantial increase in the stability of these mRNA variants.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 356, 15 August 2005, Pages 160-168
Journal: Gene - Volume 356, 15 August 2005, Pages 160-168
نویسندگان
Metin Aytekin, Ursula Vinatzer, Monica Musteanu, Sophie Raynaud, Rotraud Wieser,