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العنوان
Long Noncoding Taurine Upregulated Gene and Its Possible Role in Vitiligo /
المؤلف
Ibrahim, Hanaa Mohamed Ibrahim.
هيئة الاعداد
باحث / هناء محمد إبراهيم إبراهيم
مشرف / عبد العزيز عبد السلام الرفاعي
مشرف / ليلي احمد راشد
مشرف / رحاب محمد نجيب
الموضوع
Vitiligo. Vitiligo etiology.
تاريخ النشر
2021.
عدد الصفحات
81 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الأمراض الجلدية
الناشر
تاريخ الإجازة
30/9/2021
مكان الإجازة
جامعة بني سويف - كلية الطب - الجلدية والتناسلية
الفهرس
Only 14 pages are availabe for public view

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from 104

Abstract

Summary
Vitiligo is a chronic, acquired depigmenting condition of the skin, strong evidence supporting an autoimmune pathogenesis of vitiligo.
Long noncoding RNAs (lncRNAs) are a family of endogenous noncoding RNAs with transcripts longer than 200 nucleotides and are involved in embryogenesis, angiogenesis, tumor progression.
Taurine upregulated gene 1 (TUG1) is considered an important member of the long noncoding RNA family. It promotes cell proliferation, invasion, and angiogenesis, but negatively regulated cell apoptosis, whereas its inhibition presents the opposite effects.
Our current study was done to to detect the expression of TUG1 in vitiligo skin of diseased patients.
The study includeded (30 ) patients suffering from vitiligo from the outpatient clinic of dermatology depatment of beniseuf University hospital and 30 apparently heaithy individuals of matched age and sex as a control group.
Assesment of TUG by quantitative real time PCR which include RNA extraction ,Reverse transcription and PCR amplification in patient and control groups was done .
We found that, our cases had a statistically significant Down-regulated in vitiligo cases as compared with healthy controls; the mean TUG gene levels (0.307 vs. 1.03) in skin tissue samples from vitiligo cases and healthy controls respectively with a statistically significant p-value< 0.001.
In conclusion, TUG might be a candidate biomarker for vitiligo. The results provide a new perspective for a better understanding of TUG mediated gene regulation in vitiligo, and provide a novel theoretical basis for further studies on the function of TUG in vitiligo.