Ischemic conditioning prevents Na,K-ATPase dissociation from the cytoskeletal cellular fraction after repeat renal ischemia in rats

Pediatric Research

Volumn 51, Issue 6, 2002, Pages 722-727

  Aufricht, Christoph ^a   Bidmon, Bettina ^a   Ruffingshofer, Dagmar ^a   Regele, Heinz ^a   Herkner, Kurt ^a   Siegel, Norman J ^a   Kashgarian, Michael ^a   Van Why, Scott K ^a  

^a UNIVERSITY OF VIENNA   (Austria)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE TRIPHOSPHATASE (POTASSIUM SODIUM); TRITON X 100;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CELL FRACTIONATION; CHEMOLUMINESCENCE; CONDITIONING; CONTROLLED STUDY; CYTOSKELETON; DISSOCIATION; GENE DISRUPTION; GLOMERULUS FILTRATION RATE; IMMUNOHISTOCHEMISTRY; KIDNEY ISCHEMIA; KIDNEY PROXIMAL TUBULE; NONHUMAN; PRIORITY JOURNAL; PROTEIN LOCALIZATION; RAT;

EID: 0036105753     PISSN: 00313998     EISSN: None     Source Type: Journal    
DOI: 10.1203/00006450-200206000-00010     Document Type: Article

References (18)

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8. Induction and intracellular localization of HSP-72 after renal ischemia
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10. Expression and molecular regulation of Na+-K+-ATPase after renal ischemia
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13. Responses of the ischemic acute renal failure kidney to additional ischemic events
14. Induction of heat-shock proteins does not prevent renal tubular injury following ischemia
15. 2 deprivation, possibly by inducing uremia
16. Heat stress ameliorates ATP depletion-induced sublethal injury in mouse proximal tubule cells
17. Heat shock protein 70 overexpression protects LLC-PK1 tubular cells from heat shock but not hypoxia