Enac

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ENac is important in [[Cystic fibrosis|Cystic Fibrosis]] too, usually it is inhibited by the [[CFTR|CFTR]] channel but when the patient has [[Cystic Fibrosis|CF]] ENac loses it's inhibition and lets many Na<sup>+</sup> [[Ions|ions]] into the cell - this leads to a higher open state probability for the Na<sup>+</sup> channels in the cell.  
 
ENac is important in [[Cystic fibrosis|Cystic Fibrosis]] too, usually it is inhibited by the [[CFTR|CFTR]] channel but when the patient has [[Cystic Fibrosis|CF]] ENac loses it's inhibition and lets many Na<sup>+</sup> [[Ions|ions]] into the cell - this leads to a higher open state probability for the Na<sup>+</sup> channels in the cell.  
  
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]].
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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]].
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Nedd4-2, a ubiquitin ligase,&nbsp;binds to the proline rich C-terminus to promote degradation of ENaC.

Revision as of 10:51, 8 November 2010

Enac is a Na+channel, it can be mutated and cause Liddle Syndrome.

ENac is important in Cystic Fibrosis too, 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.


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

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