Gs: Difference between revisions

From The School of Biomedical Sciences Wiki
Jump to navigation Jump to search
added more information about Gs Protein
added more information about GsPprotein
Line 1: Line 1:
Gs is a stimulatory[[G-proteins|&nbsp;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.&nbsp;The Gs-alpha is the stimulatory subunit and causes increase in adenylyl cyclase activity which then increases the level of [[CAMP|cAMP]]&nbsp;<ref>(Genomics. 1991 May;10(1):257-61.)</ref>.
Gs is a stimulatory[[G-proteins|&nbsp;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.&nbsp;The Gs-alpha is the stimulatory subunit and causes increase in adenylyl cyclase activity which then increases the level of [[CAMP|cAMP]]&nbsp;<ref>(Genomics. 1991 May;10(1):257-61.)</ref>.  


cAMP stimulates an enzyme or activates other molecules to affect an effector protein in the cell.
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&nbsp; for&nbsp;the smell signalling pathway<sup>2</sup>.&nbsp;The Gs&nbsp;protein can be&nbsp;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 a- subunit of the Gs Protein. That leads to inactivation of its GTP-ase activity and so the G protein is contisously activated&nbsp;,activating Adenylyl syclase and increasing the cAMP concentration in cytosol of the cell that results in fluid release out of the exracellular membrane<sup>2</sup>.<br>
To this Gs Protein family also belongs the Golf olfactory Protein responsible&nbsp; for&nbsp;the smell signalling pathway<references /><sup>2]</sup>.&nbsp;The Gs&nbsp;protein can be&nbsp;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 a- subunit of the Gs Protein. That leads to inactivation of its GTP-ase activity and so the G protein is contisously activated&nbsp;,activating Adenylyl syclase and increasing the cAMP concentration in cytosol of the cell that results in fluid release out of the exracellular membrane<sup>2</sup>.<br>


=== References  ===
=== References  ===


Marks. F, Klingmuller. U, Muller-Decker. K.Cellular Signal Processing,2009,German cancer Research centre
Marks. F, Klingmuller. U, Muller-Decker. K.Cellular Signal Processing,2009,German cancer Research centre

Revision as of 14:49, 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

  1. (Genomics. 1991 May;10(1):257-61.)

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 a- subunit of the Gs Protein. That leads to inactivation of its GTP-ase activity and so the G protein is contisously activated ,activating Adenylyl syclase and increasing the cAMP concentration in cytosol of the cell that results in fluid release out of the exracellular membrane2.

References

Marks. F, Klingmuller. U, Muller-Decker. K.Cellular Signal Processing,2009,German cancer Research centre