Gaudreau R, Le Gouill C, Métaoui S, Lemire S, Stankovà J, Rola-Pleszczynski M
Immunology Division, Department of Pediatrics, Faculty of Medicine, Université de Sherbrooke, Sherbrooke, QC J1H 5N4 Canada.
Biochem J. 1998 Oct 1;335 ( Pt 1)(Pt 1):15-8. doi: 10.1042/bj3350015.
COS-7 cells transfected with the leukotriene (LT) B4 receptor (BLTR) cDNA were unable to produce LTB4-induced inositol phosphates (IPs) in spite of the presence of endogenous Galphai, Galphaq and Galpha11 proteins. Co-transfection of BLTR with Galpha16, however, resulted in high levels of IP production, which were 17-, 10- and 6-fold higher than with co-transfected Galpha11, Galphaq and Galpha14, respectively. Co-transfection of BLTR with phospholipase C (PLC) beta2, on the other hand, resulted in efficient IP production and co-transfection of BLTR with both Galpha16 and PLCbeta2 resulted in a greater than additive response.
用白三烯（LT）B4受体（BLTR）cDNA转染的COS-7细胞，尽管存在内源性Gαi、Gαq和Gα11蛋白，但仍无法产生LTB4诱导的肌醇磷酸（IPs）。然而，将BLTR与Gα16共转染可导致高水平的IP产生，分别比与共转染的Gα11、Gαq和Gα14高17倍、10倍和6倍。另一方面，将BLTR与磷脂酶C（PLC）β2共转染可导致高效的IP产生，而将BLTR与Gα16和PLCβ2两者共转染则产生大于相加的反应。
