Sentence examples for externalization at from inspiring English sources

Exact(5)

PMN phosphatidylserine (PS) externalization at indicated time points was measured with annexin V-FITC (Annexin V-FITC Apoptosis Detection kit II; BD Biosciences, San Jose, CA) as described previously [32].

Our previous works have demonstrated that brief activation of D1-type receptor accelerates GluA1 externalization at extrasynaptic sites through a PKA-dependent pathway in hippocampal pyramidal neurons.

They induce hallmarks of the intrinsic pathway of apoptosis (mitochondrial membrane depolarization, cytochrome c release, caspase-3/7 activation and caspase-dependent phosphatidylserine externalization at the cell surface).

Significant numbers of cells showed increases in PI uptake and phosphatidylserine externalization at 24 kV/cm, indicating changes in permeability and phospholipid orientation in plasma membranes.

After incubation of SUVEC cells transiently expressing GFP pJAB1 or GFP with 10 1000 nM STS for 24 h, we co-incubated the cells with annexin V PE as an early marker for phosphatidylserine externalization at the cell membrane.

Similar(55)

A substantial drop in cells showing PS externalization is seen at the highest pulse numbers for Jurkat cells.

The striking difference in activity of Bcl2-cb5 and BclX-cb5 was also evident when TNFα induced apoptosis was assessed qualitatively by staining cells with Hoescht dye (to visualize chromatin condensation) and Annexin V (to visualize externalization of phosphatidylserine at the plasma membrane).

One characteristic event in apoptosis is the externalization of phosphatidylserines [PS] at the plasma membrane.

At the protein level, dexamethasone provoked a rapid externalization of annexin 1 (maximal at 2 h) followed by delayed time-dependent changes in the cell cytosol.

Phosphatidylserine externalization was assessed by observing at fluorescence microscopy the extent of streptavidin-fluorescein isothiocyanate (FITC) annexin-V binding.

As shown in Figure 3, the presence or absence of ABCA1 makes no detectable difference in the rate at which PS externalization occurs in cells in which the scramblase is activated by Ca2+.

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