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To further verify that Notch signaling regulated macrophage infiltration through CCL2-CCR2 chemotaxis, we co-cultured RBP-J deficient or control macrophages with HEK293 cells overexpressing CCL2 using a transwell system.
BMSCs and AECs were co-cultured using a Transwell system under the following conditions: (1) separated co-culture AECs seeded on the insert and BMSco-culture AECsof the well; and (2) mixed co-culture—AECseededon of the monolayer of BMSCs on the culture insert and no cells in the BMSCsof the well.
The capacity of BMDC sup to induce IFN-γ-secretion by NK cells was further evaluated using a transwell system (Fig. 7A,B).
Migration of the lymphoblastoid cell line A3.01 or human primary CD4+ cells in response to CXCL12 was evaluated using a transwell system as described [52].
In this study, we examined how hUCB-MSCs can induce NEP in microglia by using a Transwell system.
Using a Transwell system, we demonstrated that the inhibition of IFN- γ and IL-4 production by cMSCs was cell cell contact dependent.
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To directly address this possibility, we used a transwell system to co-culture NAFs with breast cancer cells to test how NAFs respond to cancer cells.
When we used a Transwell system, cMSCs did not inhibit cytokine productions.
We further used a Transwell system to examine the effects of AuNPs on VEGF165-induced endothelial cell migration.
When we used a Transwell system, cMSCs did not suppress IgE production; this would be the case if the IL-4 receptors expressed on cMSCs interfered with IgE expression.
Seppen et al. have previously reported higher rates of transduction in Caco-2 cells but used a transwell system with GFP expressing first and third generation lentiviral vectors [ 41].
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