Creutzfeldt‐Jakob infection increases adenylate cyclase activity in specific regions of guinea pig brain

FEBS Letters

Manuelidis, Laura²  Manuelidis, Elias E.²  Valley, Susan²  Rasenick, Mark M.¹ 

[1] Deparment of Physiology and Biophysics, University of Illinois College of Medicine, Chicago, IL 60680 USA;Section of Neuropathology, Department of Surgery, Yale University School of Medicine, New Haven, CT 06510, USA

关键词: GTP-binding protein;    Receptor-effector coupling;    Oncogene product;    Dementia;    Signal transduction;   

DOI  :  10.1016/0014-5793(86)81205-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Creutzfeldt-Jakob disease is a slow, infectious, progressive neurological disorder which results in human dementia. Synaptic membranes from various brain regions of guinea pigs infected with Creutzfeldt-Jakob disease show increased guanyl nucleotide- or 5-hydroxytryptamine-mediated activation of adenylate cyclase. This increased enzyme activity appears due, primarily, to facilitated ‘coupling’ between the GTP-binding protein which stimulates adenylate cyclase (GN_s) and the catalytic moiety of that enzyme rather than increased sensitivity to 5-hydroxytryptamine. It is possible that this phenomenon is due to direct effects of the Creutzfeldt-Jakob infectious agent, or a pathological product resulting from that agent, upon synaptic membrane adenylate cyclase.

【 授权许可】

Unknown