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Register a new userBcl-2-Overexpression Decreases Apoptosis Induced by Cystine Deprivation in Hepatocyes
التعبير المفرط لمورثة ال2-Bcl ينقص الموت الخلوي المبرمج المحرض في الخلايا الكبدية بحرمانها من السستين
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Damascus University ورقة بحثية
Publication date
2004
fields
Medicine
and research's language is
العربية
Authors
علي حسن( باحث )
Created by
Shamra Editor
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إن بروتينات زمرة 2-Bcl من العناصر الضرورية المعنية في الموت الخلوي الـذي تـسببه عوامل مختلفة و متعددة في أنماط خلوية واسعة، كما يعد السستين حمضاً أمينيـاً طليعيـاً و أساسياً في تركيب الثيول خصوصاً الغلوتاثيون (GSH) . تم الكشف عن الآلية التي بوساطتها يمكن لبروتينات الـ2-Bcl مقاومـة المـوت الخلـوي المبرمج الناتج عن انعدام السستين من وسط الزرع، في خلايا كبدية pEF/Hepz هجينـة و خلايا أخرى ذات تعبير مفرط لمورثة الـ2-Bcl تدعى 2-Bcl/Hepz.
The Bcl-2 family of proteins has been implicated as a necessary factor in the death caused by a large number of different agents of a wide variety of cell types. Cystine is a precursor for the biosynthesis of the intracellular Thiol, (glutathione) GSH. The mechanism by which Bcl-2 resist cystine deprivation induced apoptosis was investigated in hepatocyte Hepz/Bcl-2 and Hepz/pEF cell lines.
References used
Adriane- C, Florencia- GQ, Gregory- J, Nicholas- FL. Glutathion depletion is associated with decreased Bcl-2 expression and increased apoptosis in cholangiocytes. Am J physiol Gastrointest- Liver- Physiol. 1998; 275: G747-G757
Anderson- ME, Meister- A. Transport and direct utilization of gammaglutamylcyst(e)ine for glutathione synthesis. Proc- Natl- Acad- Sci- USA. 1983; 80:707-711
Bannai- S. Transport of cystine and cysteine in mammalian cells. Biochem- Biophys- Acta. 1984; 779: 289-306
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