Sentence examples for stores induced by from inspiring English sources
Observations on Ca2+ release from intracellular stores induced by Mt-II, indicate a possible involvement of GPCRs in toxin-induced ATP release, via activation of PLC and IP3 production; moreover, various animal toxins, and among them also some PLA2s, have been found to bind GPCRs.
These data indicate that reliance on endogenous lipid stores induced by caloric restriction or endurance exercise has different effects on the fat depots in liver and muscle and suggest that the hepatic TG pool is under a quite flexible and dynamic control.
Since the trough in hepatic glycogen stores coincides in time with the reduced hyperglycemic response to BIC (i.e. at ZT15) [31]–[33], we investigated whether a (almost) complete absence of hepatic glycogen stores (induced by 2 nights of food deprivation) would result in a decreased hyperglycemic effect of BIC.
Thus the elevated glycogen stores induced by Rab25 appear to maintain ATP levels during the early phase of metabolic stress.
This suggests that nephrin is partially responsible for the release of Ca2+ from intracellular stores induced by FFA (seen in ciPod), even when expressed in endothelial cells.
In recent years a similar mechanism of Ca2+ release from stores induced by FFA as the one we describe in ciPod has been described for TRPM8, a temperature sensitive branch of the TRP family.
In these cells, both entry and the mobilization of the internal calcium store were induced by the addition of CCN3.
To understand whether the [Ca2+]i store release induced by FFA stimulation in ciPod is dependent on nephrin specifically or whether it is dependent on other podocyte proteins we carried out similar experiments in GEnC.
Replenisment of Ca2+ stores induces STIM1 dephosphorylation by as yet to be described phosphatases, leading to the reassociation of STIM1 with EB1, and the microtubule localization pattern of STIM1 (Fig. 1).
Whereafter, fine recrystallization grains were formed by the release of the stored fault energy induced by deformation at the elevated temperature.
The decreased mean arterial pressure and cardiac output as well as increased central venous pressure and body temperature were more severe for TRALI induced by "stored PRBC" than by "stored PLT".
