GTPase inhibiting mutations activate the alpha chain of Gs and stimulate adenylyl cyclase in human pituitary tumours
Article Abstract:
Mutations can cause autostimulation of cells, that normally would depend on outside signals, such as hormones, for growth. Abnormal cell growth and tumor development can occur. In patients with acromegaly, enlargement of bones of the face and extremities, mutations have been found in a subset of four human growth hormone-secreting pituitary tumors. These mutations cause autonomous stimulation of cyclic adenosine monophosphate (cAMP, which mediates many signals for cell growth), and result in abnormal secretion of growth hormone and increased cell growth. The mutations occur in a protein which normally binds and breakdowns guanosine triphosphate (GTP, which regulates the stimulation of cAMP). The binding of GTP is inhibited, and cAMP is constantly stimulated. These studies further the understanding of factors that control cell growth the relationship of mutation to abnormal growth or cancer.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1989
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The target sets the tempo
Article Abstract:
New details have been learned about how the G proteins effect cell signalling. Researchers V.Y. Arshavsky and M.D. Bownds followed by G. Berstein and colleagues found that the effector molecule targeted by alpha-GTP greatly hastens the process by speeding up the GTP hydrolysis by alpha-GTP. Hence effectors are now known to function as GTP-ase-activating proteins. These findings explain why the turn-off of alpha-GTP requires 10 to 60 seconds whereas the binding of GTP or GDP by G protein occurs in milliseconds.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1992
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G-protein diseases furnish a model for the turn-on switch
Article Abstract:
Trimeric (alphaBetagamma) G proteins mediate vision, taste, smell and the actions of several hormones and neurotransmitters. The 'turn-on- switch of the GTPase cycle has been much elucidated, and a speculative model is proposed, whereby the activating message is relayed to the GDP-binding pocket of Galpha, through two complementary routes. The model suggests a molecular activation mechanism, relaying hormonal and sensory signals transmitted by certain transmembrane receptors.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1998
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