Tkachuk V A, Hoffenberg S I, Starikova M G, Panchenko M P
Institute of Experimental Cardiology, Academy of Medical Sciences, Moscow, USSR.
J Mol Cell Cardiol. 1989 Feb;21 Suppl 1:91-5. doi: 10.1016/0022-2828(89)90842-0.
Signal-transducing GTP-binding Proteins of Mammalian Heart and Lungs. Journal of Molecular and Cellular Cardiology (1989) 21 (Suppl I) 91-95. Three distinct G-proteins have been found in mammalian heart sarcolemma: Gi (alpha i = 40 kDa, beta = 36 kDa, and lambda less than 14 kDa), Gp (alpha p = 23 kDa, beta = 36 kDa, and lambda less than 14 kDa), and Gs (alpha s = 42 kDa). ADP-ribosylation of sarcolemmal alpha i by pertussis toxin (PT) or preincubation of sarcolemma with protein kinase C and PMA resulted in increased adenylate cyclase activity and blockade of GTP-dependent inhibition by carbachol whereas the GTP-dependent activating effect of isoproterenol on the adenylate cyclase was preserved. ADP-ribosylation of alpha i in sarcolemma by endogenous NADP-sensitive ADP-ribosyltransferase abolished the PT-induced ADP-ribosylation of alpha i. Gpp (NH)p attenuated the PT-induced ADP-ribosylation of alpha i and promoted the cholera toxin (CT)-induced ADP-ribosylation of alpha s. The CT-induced alpha s ADP-ribosylation was enhanced in the presence of heart cytosol. Soluble Gi- and Gs-proteins were identified in lung cytosol. The 40 kDa alpha i in membrane and soluble fractions was ADP-ribosylated by PT, while the soluble 42 kDa alpha s was ADP-ribosylated by CT in lung tissue. The ADP-ribosylation of soluble alpha i by PT-suppressed guanyl nucleotide binding to Gi. The apparent molecular mass of partially purified soluble Gi was 75 kDa.
哺乳动物心脏和肺中的信号转导GTP结合蛋白。《分子与细胞心脏病学杂志》（1989年）21（增刊I）91 - 95页。在哺乳动物心脏肌膜中发现了三种不同的G蛋白：Gi（αi = 40 kDa，β = 36 kDa，λ小于14 kDa）、Gp（αp = 23 kDa，β = 36 kDa，λ小于14 kDa）和Gs（αs = 42 kDa）。百日咳毒素（PT）对肌膜αi进行ADP核糖基化，或肌膜与蛋白激酶C和佛波酯（PMA）预孵育，导致腺苷酸环化酶活性增加，并阻断卡巴胆碱对GTP的依赖性抑制作用，而异丙肾上腺素对腺苷酸环化酶的GTP依赖性激活作用得以保留。内源性NADP敏感的ADP核糖基转移酶对肌膜中αi进行ADP核糖基化，消除了PT诱导的αi的ADP核糖基化。鸟苷-5'-O-（3-硫代三磷酸）（Gpp（NH）p）减弱了PT诱导的αi的ADP核糖基化，并促进了霍乱毒素（CT）诱导的αs的ADP核糖基化。在心脏细胞溶质存在的情况下，CT诱导的αs ADP核糖基化增强。在肺细胞溶质中鉴定出了可溶性Gi和Gs蛋白。膜和可溶性部分中的40 kDaαi被PT进行ADP核糖基化，而肺组织中可溶性的42 kDaαs被CT进行ADP核糖基化。PT对可溶性αi进行ADP核糖基化抑制了鸟苷酸与Gi的结合。部分纯化的可溶性Gi的表观分子量为75 kDa。
