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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Potential mechanism for bradykinin-activated and inositol tetrakisphosphate-dependent Ca2+ influx by Ras and GAP1 in fibroblast cells.

Here we propose a molecular model for bradykinin receptor-operated and second messenger (inositol-1,3,4,5-tetrakisphosphate)-evoked Ca2+ influx and its potentiation by oncogenic Ras, which is not store-depletion-induced, so-called capacitative, Ca2+ influx. The principal idea for this hypothesis stems from observation that two bradykinin B2 receptor-activated signal pathways, protein tyrosine phosphorylation and formation of inositol tetrakisphosphate, merge during the Ca2+ influx process and that GTPase activating-protein 1 (GAP 1) is inositol tetrakisphosphate binding protein.[1]

References

  1. Potential mechanism for bradykinin-activated and inositol tetrakisphosphate-dependent Ca2+ influx by Ras and GAP1 in fibroblast cells. Higashida, H., Taketo, M., Takahashi, H., Yokoyama, S., Hashii, M. Immunopharmacology (1999) [Pubmed]
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