کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1927567 | 1536530 | 2006 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
c-Jun N-terminal kinase regulates CTP:phosphocholine cytidylyltransferase
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
CTP:phosphocholine cytidylyltransferase (CCTα) is a rate-regulatory enzyme required for phosphatidylcholine (PtdCho) synthesis. CCTα is also a phosphoenzyme, but the physiologic role of kinases on enzyme function remains unclear. We report high-level expression of two major isoforms of the c-Jun N-terminal kinase family (JNK1 and JNK2) in murine lung epithelia. Further, JNK1 and JNK2 phosphorylated purified CCTα in vitro, and this was associated with a dose-dependent decrease (â¼40%) in CCT activity. To evaluate JNK in vivo, lung epithelial cells were infected with a replication defective adenoviral vector encoding murine JNK2 (Adv-JNK2) or an empty vector. Adv-JNK2 infection, unlike the empty vector, markedly increased JNK2 expression concomitant with increased incorporation of [32P]orthophosphate into endogenous CCTα. Although Adv-JNK2 infection only modestly reduced CCT activity, it reduced PtdCho synthesis by â¼30% in cells. These observations suggest a role for JNK kinases as negative regulators of phospholipid synthesis in murine lung epithelia.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Archives of Biochemistry and Biophysics - Volume 447, Issue 1, 1 March 2006, Pages 23-33
Journal: Archives of Biochemistry and Biophysics - Volume 447, Issue 1, 1 March 2006, Pages 23-33
نویسندگان
Alan J. Ryan, Matthew Andrews, Jiming Zhou, Rama K. Mallampalli,