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Deletion of Erk1/2 in either aortic or lung EC in vitro led to marked morphological changes, including larger and flattened cells.
Remarkably, incubation of TRPM7 with ATP in vitro led to the incorporation of 32±4 mol of phosphate per mol of kinase which was accompanied by a dramatic shift in electrophoretic mobility on SDS-PAGE gels (Fig. 2A).
Stimulation of rat aortic and human coronary VSMCs with recombinant profilin-1 (10−6 M) in vitro led to activation of intracellular signaling cascades such as phosphorylation of Erk1/2, p70S6 kinase and PI3K/Akt within 10 minutes.
Supplementation with as little as 1 U of oxidoreductase protein in vitro led to relatively large (up to 151-fold) increases in bioluminescent output levels, while supplementation with 0.002% n-decanal produced less substantial (up to 58-fold) increases in light production.
Blocking this interaction in vitro led to increased apoptosis and failed erythropoiesis [ 36].
Engagement of TCR on peripheral blood T cells in vitro led to down-regulation of TCR-ζ.
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We report that incubation of recombinant Kvβ2 with PKCα in vitro leads to rapid phosphorylation of the protein.
Fig. 2 Induction of autophagy in vitro leads to decreased osteoclast formation in critically ill patient PBMCs.
Over-expression of Zic2 in vitro leads to increased neurite growth and ejection at the optic chiasm.
Inhibition of PLK-1 in vitro leads to cell cycle arrest at G2/M and apoptosis in human cancer cell lines [39, 41].
Indeed, exposure of pDC to infectious or noninfectious HIV-1 particles in vitro leads to upregulation of functional CCR7 [52].
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