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Biological Significance of Evi1 Mediated Transcriptional Regulation of Carbonic III Anhydrase Gene Expression

المؤلف الرئيسي: Al Ghamdi, Nehal Mashhour (Author)
مؤلفين آخرين: Pierotti, Adrian (Advisor)
التاريخ الميلادي: 2012
موقع: غلاسكو
الصفحات: 1 - 47
رقم MD: 604533
نوع المحتوى: رسائل جامعية
اللغة: الإنجليزية
الدرجة العلمية: رسالة ماجستير
الجامعة: Glasgow Caledonian University
الكلية: School of Biological and Life Sciences
الدولة: بريطانيا
قواعد المعلومات: +Dissertations
مواضيع:
رابط المحتوى:

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041 |a eng 
100 |9 11739  |a Al Ghamdi, Nehal Mashhour  |e Author 
245 |a Biological Significance of Evi1 Mediated Transcriptional Regulation of Carbonic III Anhydrase Gene Expression 
260 |a غلاسكو  |c 2012 
300 |a 1 - 47 
336 |a رسائل جامعية 
502 |b رسالة ماجستير  |c Glasgow Caledonian University  |f School of Biological and Life Sciences  |g بريطانيا  |o 0002 
520 |a The ecotropic viral integration site-1 (EVI-1) gene is localised in chromosome 3 and encodes a nuclear zinc finger protein, which acts as a transcription factor. This gene is associated with the progression of different types of leukaemia. In this study, the presence of EVI-1, Glyceraldehyde 3-phosphate dehydrogenase (GAPDH), and carbonic anhydrase III (CA III) proteins in Rat15.6 and Rat1neo cells was detected by western blot analyses, there is no band for EVI-1 protein has appeared in western blot whereas there are bands have appeared in both Rat1neo and Rat15.6 samples for GAPDH. However, for CA III the band has appeared in Rat1neo sample. The expression of CA III in Rat1neo and Rat15.6 cells was also detected by Real time quantitative PCR (qPCR), The expression of CA III in Rat1neo was higher than in Rat15.6 indicating that EVI-1 has an effect on CAIII expression. Furthermore, the promoter activities of CA III in Rat1neo and Rat15.6 cells were investigated, and that shows that EVI-1 can repress the transcription activity of CA III. Finally, the ability of CA III to protect the cells from oxidation was studied, showing that CA III can protect the cells from oxidation. EVI-1 showed that it can repress CA III activity. Moreover, EVI-1 overexpression can cause H2O2-induced cell death as a result of repressing CA III activity. This result is confirmed by the increase in caspase 3 catalytic activity, indicating the function of CA III in protecting cells from oxidation.  
653 |a الجينات  |a الجزيئات الحيوية  |a الفيروسات 
700 |9 44069  |a Pierotti, Adrian  |e Advisor 
856 |u 9823-057-004-0002-T.pdf  |y صفحة العنوان 
856 |u 9823-057-004-0002-A.pdf  |y المستخلص 
856 |u 9823-057-004-0002-C.pdf  |y قائمة المحتويات 
856 |u 9823-057-004-0002-F.pdf  |y 24 صفحة الأولى 
856 |u 9823-057-004-0002-1.pdf  |y 1 الفصل 
856 |u 9823-057-004-0002-2.pdf  |y 2 الفصل 
856 |u 9823-057-004-0002-3.pdf  |y 3 الفصل 
856 |u 9823-057-004-0002-4.pdf  |y 4 الفصل 
856 |u 9823-057-004-0002-R.pdf  |y المصادر والمراجع 
930 |d n 
995 |a +Dissertations 
999 |c 604533  |d 604533 

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