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Titolo:
Loss of annexin A7 leads to alterations in frequency-induced shortening ofisolated murine cardiomyocytes
Autore:
Herr, C; Smyth, N; Ullrich, S; Yun, F; Sasse, P; Hescheler, J; Fleischmann, B; Lasek, K; Brixius, K; Schwinger, RHC; Fassler, R; Schroder, R; Noegel, AA;
Indirizzi:
Univ Cologne, Inst Biochem 1, D-50931 Cologne, Germany Univ Cologne Cologne Germany D-50931 Biochem 1, D-50931 Cologne, Germany Univ Cologne, Inst Biochem 2, D-50931 Cologne, Germany Univ Cologne Cologne Germany D-50931 Biochem 2, D-50931 Cologne, Germany Univ Cologne, Dept Neurophysiol, D-50931 Cologne, Germany Univ Cologne Cologne Germany D-50931 rophysiol, D-50931 Cologne, Germany Univ Cologne, Lab Muscle Res & Mol Cardiol, Clin Internal Med 3, D-50931 Cologne, Germany Univ Cologne Cologne Germany D-50931 nal Med 3, D-50931 Cologne, Germany Univ Hosp Bonn, Dept Neurol, Bonn, Germany Univ Hosp Bonn Bonn GermanyUniv Hosp Bonn, Dept Neurol, Bonn, Germany Univ Lund, Dept Expt Pathol, Lund, Sweden Univ Lund Lund SwedenUniv Lund, Dept Expt Pathol, Lund, Sweden
Titolo Testata:
MOLECULAR AND CELLULAR BIOLOGY
fascicolo: 13, volume: 21, anno: 2001,
pagine: 4119 - 4128
SICI:
0270-7306(200107)21:13<4119:LOAALT>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
GREEN FLUORESCENT PROTEIN; INDUCED INSULIN-SECRETION; ADRENAL CHROMAFFIN CELLS; RAT PANCREATIC-ISLETS; N-TERMINAL DOMAIN; 2-DIMENSIONAL ELECTROPHORESIS; VENTRICULAR MYOCYTES; CARDIAC MYOCYTES; VII SYNEXIN; CALCIUM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Noegel, AA Univ Cologne, Inst Biochem 1, Joseph Stelzmann Str 52, D-50931 Cologne, Germany Univ Cologne Joseph Stelzmann Str 52 Cologne Germany D-50931 y
Citazione:
C. Herr et al., "Loss of annexin A7 leads to alterations in frequency-induced shortening ofisolated murine cardiomyocytes", MOL CELL B, 21(13), 2001, pp. 4119-4128

Abstract

Annexin A7 has been proposed to function in the fusion of vesicles, actingas a Ca2+ channel and as Ca2+-activated GTPase, thus inducing Ca2+/GTP-dependent secretory events. To understand the function of annexin A7, we have performed targeted disruption of the Anxa7 gene in mice. Matings between heterozygous mice produced offspring showing a normal Mendelian pattern of inheritance, indicating that the loss of annexin A7 did not interfere with viability in utero. Mice lacking annexin A7 showed no obvious phenotype and were fertile. To assay for exocytosis, insulin secretion from isolated islets of Langerhans was examined. Ca2+-induced and cyclic AMP-mediated potentiation of insulin secretion was unchanged in the absence of annexin A7, suggesting that it is not directly implicated in vesicle fusion. Ca2+ regulationstudied in isolated cardiomyocytes, showed that while cells from early embryos displayed intact Ca2+ homeostasis and expressed all of the components required for excitation-contraction coupling, cardiomyocytes from adult Anra7(-/-) mice exhibited an altered cell shortening-frequency relationship when stimulated with high frequencies. This suggests a function for annexin A7 in electromechanical coupling, probably through Ca2+ homoeostasis.

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Documento generato il 02/04/20 alle ore 02:56:01