The promoter region of the CTLA4 gene is associated with type 1 diabetes mellitus

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Title:	The promoter region of the CTLA4 gene is associated with type 1 diabetes mellitus
Authors:	Lee, YJ;Lo, FS;Shu, SG;Wang, CH;Huang, CY;Liu, HF;Wu, CC;Yang, TY;Chang, JG
Contributors:	附設醫院醫研部;China Med Coll Hosp, Dept Med Res, Div Mol Med, Taichung, Taiwan;Mackay Mem Hosp, Dept Pediat, Taipei, Taiwan;Mackay Mem Hosp, Dept Endocrinol & Metab, Taipei, Taiwan;Mackay Mem Hosp, Dept Med Res, Taipei, Taiwan;Chang Gung Childrens Hosp, Dept Med, Div Endocrinol, Tao Yuan, Taiwan;Taichung Vet Gen Hosp, Dept Pediat, Taichung, Taiwan;Taipei Med Univ, Dept Pediat, Taipei, Taiwan
Date:	2001
Issue Date:	2010-09-24 14:56:08 (UTC+8)
Publisher:	FREUND PUBLISHING HOUSE LTD
Abstract:	Phosphorylation of extracellular signal-regulated kinase (ERK) in response to arachidonic acid (AA) was rapid and transient, peaking at 1 min and disappearing after 3 min, and it was accompanied by an increase in ERK activity in rat neutrophils, We examined the upstream regulation of AA-stimulated ERK activation using one of the following signaling pathway inhibitors to pretreat rat cells: the ERK kinase inhibitor U0126 or PD98059, the G(i/o) inhibitor pertussis toxin (PTX), the tyrosine kinase inhibitor genistein, the phosphatidylinositol 3-kinase (PI3K) inhibitor wort-mannin or LY294002, the Ca2+ chelator 1,2-bis(O-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid, or the phospholipase C (PLC) inhibitor U73122. All of these inhibitors attenuated AA-induced ERK activation. Activation of ERK was also effectively attenuated by the cyclooxygenase and lipoxygenase inhibitor BW755C and by the leukotriene biosynthesis inhibitor MK886, but the cyclooxygenase inhibitor indomethacin did not attenuate ERK activation. After exposing cells to three distinct protein kinase C (PKC) inhibitors, we found that Go6976 significantly attenuated ERK phosphorylation but potentiated ERK activity. Neither Go6983 nor GF109203X affected AA-induced responses. These data suggest that the li-poxygenase metabolite(s) produced mediates AA-stimulated ERK activation and that this effect is upstream regulated by PT-sensitive G protein, nonreceptor tyrosine kinase, PI3K, and PLC/Ca2+ signaling pathways in rat neutrophils.
Relation:	JOURNAL OF PEDIATRIC ENDOCRINOLOGY & METABOLISM 14(4):383-388
Appears in Collections:	[China Medical University Hospital] Jurnal articles

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