Reyl-Desmars F, Zeytin F, Lewin M J
Peptides. 1986;7 Suppl 1:165-7. doi: 10.1016/0196-9781(86)90180-4.
We used a GH3 cell-line to compare the effects of rat GRF (rGRF) and VIP on the adenylate cyclase activity and to determine on what subunit the site of action of these two peptides is. In the GH3 cell-line, VIP was more potent than rGRF to stimulate adenylate cyclase activity. The stimulatory effects of rGRF and forskolin were additive. Cholera toxin decreased the apparent potency of these peptides and pertussis toxin reversed the inhibition by somatostatin of their adenylate cyclase stimulation. We conclude that rGRF acts on the regulatory subunit Ns, different from the regulatory subunit Ni on which somatostatin is suggested to be acting and that, in the GH3 cells, rGRF stimulates adenylate cyclase through VIP-preferring sites.
我们使用GH3细胞系来比较大鼠生长激素释放因子（rGRF）和血管活性肠肽（VIP）对腺苷酸环化酶活性的影响，并确定这两种肽的作用位点位于哪个亚基上。在GH3细胞系中，VIP刺激腺苷酸环化酶活性的效力比rGRF更强。rGRF和福斯可林的刺激作用是相加的。霍乱毒素降低了这些肽的表观效力，百日咳毒素则逆转了生长抑素对其腺苷酸环化酶刺激作用的抑制。我们得出结论，rGRF作用于调节亚基Ns，这与生长抑素被认为作用的调节亚基Ni不同，并且在GH3细胞中，rGRF通过优先结合VIP的位点刺激腺苷酸环化酶。
