α-ENaC is a functional element of the hypertonicity-induced cation channel in HepG2 cells and it mediates proliferation

Pflugers Archiv European Journal of Physiology

Volumn 458, Issue 4, 2009, Pages 675-687

  Bondarava, Maryna ^a   Li, Tongju ^a,c   Endl, Elmar ^b   Wehner, Frank ^a  

^a MAX PLANCK INSTITUTE OF MOLECULAR PHYSIOLOGY   (Germany)

^b UNIVERSITY OF BONN   (Germany)

^c UNIVERSITY OF DUISBURG ESSEN   (Germany)

Author keywords

ENaC; Amiloride; Apoptosis; Flufenamate; HepG2; Proliferation; SiRNA; Volume regulation

Indexed keywords

AMILORIDE; CATION CHANNEL; EPITHELIAL SODIUM CHANNEL; FLUFENAMIC ACID; HYPERTONICITY INDUCED CATION CHANNEL; SMALL INTERFERING RNA; UNCLASSIFIED DRUG;

APOPTOSIS; ARTICLE; CELL CYCLE; CELL PROLIFERATION; CONCENTRATION RESPONSE; CONTROLLED STUDY; HEPATOMA CELL; HUMAN; HUMAN CELL; HYPEROSMOTIC STRESS; PRIORITY JOURNAL; SODIUM CONDUCTANCE;

CARCINOMA, HEPATOCELLULAR; CELL LINE, TUMOR; CELL PROLIFERATION; EPITHELIAL SODIUM CHANNEL; HUMANS; ION CHANNEL GATING; WATER-ELECTROLYTE BALANCE;

EID: 67649887788     PISSN: 00316768     EISSN: 14322013     Source Type: Journal    
DOI: 10.1007/s00424-009-0649-z     Document Type: Article

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