Title : TRPV4 calcium influx controls sclerostin protein loss independent of purinergic calcium oscillations.

Pub. Date : 2020 Jul

PMID : 32272228






4 Functional Relationships(s)
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1 TRPV4 calcium influx controls sclerostin protein loss independent of purinergic calcium oscillations. Calcium transient receptor potential cation channel subfamily V member 4 Homo sapiens
2 We have recently shown that the osteocyte responds to fluid shear stress via the microtubule network-dependent activation of NADPH oxidase 2 (NOX2)-generated reactive oxygen species and subsequent opening of TRPV4 cation channels, leading to calcium influx, activation of CaMKII, and rapid sclerostin protein downregulation. Calcium transient receptor potential cation channel subfamily V member 4 Homo sapiens
3 Here, we showed that NOX2 and TRPV4-dependent calcium influx is required for calcium oscillations, and that TRPV4 activation is both necessary and sufficient for sclerostin degradation. Calcium transient receptor potential cation channel subfamily V member 4 Homo sapiens
4 Here, we showed that NOX2 and TRPV4-dependent calcium influx is required for calcium oscillations, and that TRPV4 activation is both necessary and sufficient for sclerostin degradation. Calcium transient receptor potential cation channel subfamily V member 4 Homo sapiens