Key result
eNOS targeting to the membrane is labile and subject to receptor-regulated Ca2+-dependent reversible translocation, regulating NO-dependent signaling in the vascular endothelium.
The review elucidates the dynamic, Ca2+-dependent subcellular translocation of eNOS in endothelial cells, highlighting a key regulatory mechanism for NO signaling.
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May inform endothelial NO modulation strategies; extends mechanistic insights but leaves open clinical translation.
Thomas Michel (1999) reported a review. eNOS targeting to the membrane is labile and subject to receptor-regulated Ca2+-dependent reversible translocation, regulating NO-dependent signaling in the vascular endothelium.
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