About: CPT-cGMP Is A New Ligand of Epithelial Sodium Channels

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About: CPT-cGMP Is A New Ligand of Epithelial Sodium Channels Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	CPT-cGMP Is A New Ligand of Epithelial Sodium Channels
Creator	Liu, Shan-Lu Chang, Yongchang Ji, Hong-Long Nie, Hong-Guang Lian, Qizhou
Source	PMC
abstract	Epithelial sodium channels (ENaC) are localized at the apical membrane of the epithelium, and are responsible for salt and fluid reabsorption. Renal ENaC takes up salt, thereby controlling salt content in serum. Loss-of-function ENaC mutations lead to low blood pressure due to salt-wasting, while gain-of-function mutations cause impaired sodium excretion and subsequent hypertension as well as hypokalemia. ENaC activity is regulated by intracellular and extracellular signals, including hormones, neurotransmitters, protein kinases, and small compounds. Cyclic nucleotides are broadly involved in stimulating protein kinase A and protein kinase G signaling pathways, and, surprisingly, also appear to have a role in regulating ENaC. Increasing evidence suggests that the cGMP analog, CPT-cGMP, activates αβγ-ENaC activity reversibly through an extracellular pathway in a dose-dependent manner. Furthermore, the parachlorophenylthio moiety and ribose 2'-hydroxy group of CPT-cGMP are essential for facilitating the opening of ENaC channels by this compound. Serving as an extracellular ligand, CPT-cGMP eliminates sodium self-inhibition, which is a novel mechanism for stimulating salt reabsorption in parallel to the traditional NO/cGMP/PKG signal pathway. In conclusion, ENaC may be a druggable target for CPT-cGMP, leading to treatments for kidney malfunctions in salt reabsorption.
has issue date	2016-01-28(xsd:dateTime)
bibo:doi	10.7150/ijbs.13764
bibo:pmid	27019621
has license	no-cc
sha1sum (hex)	c1a03657b225afb8628f4806530db7f57645ad54
schema:url	https://doi.org/10.7150/ijbs.13764
resource representing a document's title	CPT-cGMP Is A New Ligand of Epithelial Sodium Channels
has PubMed Central identifier	PMC4807156
has PubMed identifier	27019621
schema:publication	Int J Biol Sci
resource representing a document's body	covid:c1a03657b225afb8628f4806530db7f57645ad54#body_text
is schema:about of	covid:arg/c1a03657b225afb8628f4806530db7f57645ad54 named entity 'ENaC' named entity 'salt content' named entity 'hormones' named entity 'apical membrane' named entity 'Cyclic nucleotides' named entity 'salt' named entity 'protein kinase' named entity 'extracellular' named entity 'serum' named entity 'hydroxy group' named entity 'signaling pathways' named entity 'salt-wasting' named entity 'ENaC' named entity 'ENaC' named entity 'gain-of-function mutations' named entity 'cGMP' named entity 'Ligand' named entity 'hypertension' named entity 'cytosolic' named entity 'protein' named entity 'cGMP' named entity 'binding site' named entity 'sodium ion' named entity 'cGMP' named entity 'ENaC' named entity 'ENaC' named entity 'lung' named entity 'cAMP' named entity 'edematous' named entity 'PKG' named entity 'ENaC' named entity 'gain-of-function' named entity 'ENaC' named entity 'sodium' named entity 'heterologously expressed' named entity 'epithelial cell' named entity 'kidney diseases' named entity 'kidney' named entity 'salt-wasting' named entity 'signal molecule' named entity 'micromolar' named entity 'isoforms' named entity 'binding site' named entity 'cGMP' named entity 'ENaC' named entity 'signaling cascades' named entity 'binding sites' named entity 'epithelial sodium channels' named entity 'ENaC' named entity 'cGMP' named entity 'Ussing chamber' named entity 'distal convoluted tubule' named entity 'hydroxy groups' named entity 'permeability' named entity 'cGMP' named entity 'monogenic disorder' named entity 'cardiovascular' named entity 'ALI' named entity 'PKG' named entity 'cGMP' named entity 'kidney' named entity 'p-chloromercuribenzoate' named entity 'nitric oxide' named entity 'interacting proteins' named entity 'type 1' named entity 'kidney' named entity 'cloned' named entity 'hormones' named entity 'sodium transport' named entity 'proteases' named entity 'PKA' named entity 'ENaC' named entity 'lung' named entity 'signal transduction' named entity 'ALI' named entity 'colon'

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