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| G<sub>s</sub> is a stimulatory[[G-proteins| G-protein]] which regulates activity of [[Adenylyl cyclase|adenylyl cyclase]]. G-protiens are [[Heterotrimeric G-proteins|heterotrimers]] which are composed of [[G protein alpha subunit|alpha]], [[G protein beta subunit|beta]] and [[G protein gamma subunit|gamma]] subunits. The G<sub>s</sub>-alpha is the stimulatory subunit and causes increase in adenylyl cyclase activity which then increases the level of [[CAMP|cAMP]]<ref>(Genomics. 1991 May;10(1):257-61.)</ref>. | ||
cAMP stimulates an [[enzyme|enzyme]] or activates other [[molecules|molecules]] to affect an effector [[proteins|protein]] in the [[cell lysis|cell]]. | |||
| To this G<sub>s</sub> protein family also belongs the G<sub>olf</sub> olfactory protein responsible for the smell signalling pathway<ref>Marks. F, Klingmuller. U, Muller-Decker. K.Cellular Signal Processing,2009,German cancer Research centre</ref>.The G<sub>s</sub> protein can be affected negatively by cholera toxin that catalyses the synthesis of [[ADP-ribosyltransferase|ADP-ribosyltransferase]] enzyme in a cell that catalyses the [[ADP-ribosylation|ADP-ribosylation]] of an [[Arginine|Arg]] residue in the alpha-subunit of the G<sub>s</sub> Protein. That leads to inactivation of its [[GTPase|GTPase]] activity and so the G protein is contisously activated, activating adenylyl cyclase and increasing the [[cAMP|cAMP]] concentration in [[cytosol|cytosol]] of the cell that results in fluid release out of the extracellular membrane.<br> | ||
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Latest revision as of 20:36, 1 December 2016
Gs is a stimulatory G-protein which regulates activity of adenylyl cyclase. G-protiens are heterotrimers which are composed of alpha, beta and gamma subunits. The Gs-alpha is the stimulatory subunit and causes increase in adenylyl cyclase activity which then increases the level of cAMP[1].
cAMP stimulates an enzyme or activates other molecules to affect an effector protein in the cell.
To this Gs protein family also belongs the Golf olfactory protein responsible for the smell signalling pathway[2].The Gs protein can be affected negatively by cholera toxin that catalyses the synthesis of ADP-ribosyltransferase enzyme in a cell that catalyses the ADP-ribosylation of an Arg residue in the alpha-subunit of the Gs Protein. That leads to inactivation of its GTPase activity and so the G protein is contisously activated, activating adenylyl cyclase and increasing the cAMP concentration in cytosol of the cell that results in fluid release out of the extracellular membrane.