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Annexin A7 has been proposed to function in the fusion of vesicles, acting as a Ca 2+ channel and as Ca 2+-activated GTPase, thus inducing Ca 2+/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. Ca 2+-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. Ca 2+ regulation studied in isolated cardiomyocytes, showed that while cells from early embryos …