Sentence examples for migration assay of from inspiring English sources

(c) Migration assay of THP-1-derived macrophages, with scr or siKif4A pre-treated, towards Cal-27 was achieved.

(a) Transwell cell migration assay of A431 (including polyclonal and monoclonal cells) and SqCC/Y1 cells showed that overexpression of Dsg3 enhanced cell migration compared with Vect cells.

THP-1-derived macrophages (1 × 105 cells/well, for migration assay of macrophages) or Cal-27 cells (1 × 105 cells/well, for migration assay of cancer cells) in 600 μL RPMI 1640 medium containing 10% FBS were added into the lower chambers of the transwell plate correspondingly, 600 μL RPMI 1640 medium containing 10% FBS in lower chambers without cells as medium control.

(a) Migration assay of Cal-27 towards THP-1-derived macrophages and THP-1-derived macrophages towards Cal-27 was achieved as described in the Methods Medium in lower chambers without cells groups were use as control.

(D) Migration assay of ECs isolated from WT and CD146EC-KO mice without or with VEGF (50 ng/mL) treatment.

In addition, the transwell migration assay of our experiment also demonstrated that G-CSF could mobilize MDSC and this indicated that G-CSF may be one of various cytokines in recruiting MDSCs from bone marrow to peripheral blood.

Transendothelial migration assays of breast cancer cells were performed as described previously with a minor modification [53].

Migration assays of isolated monocytes provided no results, owing to the obviously high activation status of the cells.

We performed migration assays of LNCaP cells co-cultured with the macrophage cell lines, THP-1 scr and siAR cells (Fig 1 A).

(Additional file 1: Figure S1) Cell migration assays of MG-63 cells reveal that ZOL treatment decreased the number of cells that migrated into the scratch in a dose-dependent manner (Fig.  2a, b).

Through adhesion and migration assays of purified neutrophils from wild-type and Hcar2−/− mice, they attributed the protective effect of DMF in EAE to inhibition of neutrophil adhesion to brain endothelial cells, and thereby their extravasation into brain tissue, through activation of HCAR2, as reported for other Gi-coupled receptors [ 10].