CCK and gastrin inhibit adenylate cyclase activity through a pertussis toxin‐sensitive mechanism in the tumoral rat pancreatic acinar cell line AR 4‐2J

FEBS Letters

Christophe, Jean¹  De Neef, Philippe¹  Waelbroeck, Magali¹  Pradayrol, Lucien²  Vaysse, Nicole²  Scemama, Jean Luc²  Robberecht, Patrick¹ 

[1] Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles, 115 Bd of Waterloo, B-1000 Brussels, Belgium;Unité INSERM U 151, CHU Rangueil, 31054 Toulouse Cédex, France

关键词: Cholecystokinin receptor;    Gastrin receptor;    Adenylate cyclase;    Guanine nucleotide-binding regulatory protein;    Pertussis toxin;    (Rat pacreas;    Tumoral rat pancreatic cell line AR 4-2J);   

DOI  :  10.1016/0014-5793(88)80985-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

(Thr²⁸,Nle³¹)CCK(23–33) (CCK-9) and gastrin(1–17)_I (gastrin) inhibited adenylate cyclase activity in membranes from the tumoral rat pancreatic acinar cell line AR 4-2J through a Bordetella pertussis toxin-sensitive mechanism. This contrasted with the stimulatory effect exerted by CCK-9 on adenylate cyclase activity in membranes from normal rat pancreas. The relative potency of CCK-9, gastrin, and related peptides in inhibiting adenylate cyclase, when confronted with previous evidence, suggests that ‘non-selective CCK-gastrin CCK-B receptors’ predominating over ‘selective CCK-A receptors’ in the AR 4-2J cell line, favored the coupling of the first receptors to adenylate cyclase through G_i, while CCK-A receptors capable of stimulating the enzyme through G_s were detected only after Bordetella pertussis toxin pretreatment.

【 授权许可】

Unknown