دورية أكاديمية
أعرض في EDS

CPT-cGMP Is A New Ligand of Epithelial Sodium Channels.

التفاصيل البيبلوغرافية
العنوان: CPT-cGMP Is A New Ligand of Epithelial Sodium Channels.
المؤلفون: Ji HL; 1. Department of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, Texas 75708, USA., Nie HG; 2. Institute of Metabolic Disease Research and Drug Development, China Medical University, Shenyang 110001, China., Chang Y; 3. Barrow Neurological Institute, St Joseph's Hospital and Medical Center, Phoenix, Arizona, 85013, USA., Lian Q; 4. Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China., Liu SL; 5. Department of Molecular Microbiology and Immunology, Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USA.
المصدر: International journal of biological sciences [Int J Biol Sci] 2016 Jan 28; Vol. 12 (4), pp. 359-66. Date of Electronic Publication: 2016 Jan 28 (Print Publication: 2016).
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
اللغة: English
بيانات الدورية: Publisher: Ivyspring International Country of Publication: Australia NLM ID: 101235568 Publication Model: eCollection Cited Medium: Internet ISSN: 1449-2288 (Electronic) Linking ISSN: 14492288 NLM ISO Abbreviation: Int J Biol Sci Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Lake Haven, N.S.W., Australia : Ivyspring International, c2004-
مواضيع طبية MeSH: Cyclic GMP/*analogs & derivatives , Epithelial Sodium Channels/*metabolism, Animals ; Cyclic GMP/metabolism ; Humans ; Signal Transduction/physiology
مستخلص: 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.
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معلومات مُعتمدة: HL87017 United States HL NHLBI NIH HHS; R03 HL095435 United States HL NHLBI NIH HHS; 14GRNT20130034 United States AHA American Heart Association-American Stroke Association; R01 HL087017 United States HL NHLBI NIH HHS; HL095435 United States HL NHLBI NIH HHS
فهرسة مساهمة: Keywords: amiloride-sensitive sodium channel; cyclic guanosine nucleotides; lung edema.; molecular docking
المشرفين على المادة: 0 (CPT-cGMP)
0 (Epithelial Sodium Channels)
H2D2X058MU (Cyclic GMP)
تواريخ الأحداث: Date Created: 20160329 Date Completed: 20161219 Latest Revision: 20220129
رمز التحديث: 20240829
مُعرف محوري في PubMed: PMC4807156
DOI: 10.7150/ijbs.13764
PMID: 27019621
قاعدة البيانات: MEDLINE
الوصف
تدمد:1449-2288
DOI:10.7150/ijbs.13764