Enac

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EnaC is inhibited by [[Amiloride|amiloride]], which is a K<sup>+</sup> sparing [[Diuretic|diuretic]], this means that the movement of Na<sup>+</sup> is inhibited without disrupting the movement of K<sup>+</sup> which is beneficial for [[Liddle Syndrome|Liddle's Syndrome]] as they are [[Hypokalemic|hypokalemic]]. Amiloride is positively charged which allows it to plug the ENaC channel.  
 
EnaC is inhibited by [[Amiloride|amiloride]], which is a K<sup>+</sup> sparing [[Diuretic|diuretic]], this means that the movement of Na<sup>+</sup> is inhibited without disrupting the movement of K<sup>+</sup> which is beneficial for [[Liddle Syndrome|Liddle's Syndrome]] as they are [[Hypokalemic|hypokalemic]]. Amiloride is positively charged which allows it to plug the ENaC channel.  
  
[[Renin-Angiotensin System|Aldosterone]] ,whose release is triggered by [[Renin-Angiotensin System|Angiotensin II]], causes more ENaC channels to be open. <br>
+
[[Renin-Angiotensin System|Aldosterone]] ,whose release is triggered by [[Renin-Angiotensin System|Angiotensin II]], causes more ENaC channels to be open. <br>  
  
[[Nedd4-2|Nedd4-2]], a [[Ubiquitin ligase|ubiquitin ligase]],&nbsp;binds to the [[Proline|proline]] rich C-terminus to promote degradation of ENaC.
+
[[Nedd4-2|Nedd4-2]], a [[Ubiquitin ligase|ubiquitin ligase]],&nbsp;binds to the [[Proline|proline]] rich [[C-terminus|C-terminus]] to promote degradation of ENaC.

Revision as of 16:33, 11 November 2010

Enac is an epithelial Na+channel that can be mutated and cause Liddle Syndrome.

ENac is important in Cystic Fibrosis , usually it is inhibited by the CFTR channel but when the patient has CF ENac loses it's inhibition and lets many Na+ ions into the cell - this leads to a higher open state probability for the Na+ channels in the cell.

EnaC is inhibited by amiloride, which is a K+ sparing diuretic, this means that the movement of Na+ is inhibited without disrupting the movement of K+ which is beneficial for Liddle's Syndrome as they are hypokalemic. Amiloride is positively charged which allows it to plug the ENaC channel.

Aldosterone ,whose release is triggered by Angiotensin II, causes more ENaC channels to be open.

Nedd4-2, a ubiquitin ligase, binds to the proline rich C-terminus to promote degradation of ENaC.

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