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the inactivation of the annexin A7 gene did not interfere with the viability and development of knock out mice [10], their generation allowed us to address the role of Annexin A7 in specific cell types [8,9]. Indeed, when we analyzed primary astrocytes from an AnxA7-/- mouse for Ca2+-dependent signaling processes, we found that they exhibited a significantly increased velocity of mechanically induced astrocytic Ca2+-waves as compared to wild type [9]. This led us to propose, that Annexin A7 can act as a Ca2+-buffer and is involved in Ca2+-homeostasis. In neurons Ca2+ ions play major roles in various physiological and pathophysiological processes [20-25]. One can speculate about an involvement of Annexin A7 in the regulation of these Ca2+-dependent processes, propositions that need further investigation. However, such roles are confirmed for heart function by studies of Schrickel et al. [submitted], who described an involvement of Annexin A7 in the maintenance of a regular cardiac electrophysiology and Ca2+-homeostasis."}

    craft-ca-core-ex-dev

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    craft-ca-core-dev

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