in opossum kidney cells that show endogenous Gsα expression [70] and in mouse embryonic fibroblasts that endogenously lack Gsα and XLαs due to homozygous disruption of Gnas exon 2 [71]. Finally, mutations that impair Gsα activity have similar effects on XLαs activity when introduced into the backbone of the latter [70]. Interestingly, however, beta-adrenergic stimulation seemingly fails to elicit cAMP generation in XLαs transfected S49 lymphoma cells that are also Gsα deficient (cyc- clone) [69]. Furthermore, attempts to show coupling of XLαs to receptors have failed, using PC12 cells transfected with XLαs cDNA and pituitary membranes [69]. Taken together, these findings suggest that the Gsα-like activity of XLαs may be cell specific.
