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Journal: BioMed Research International
Article Title: SEA Antagonizes the Imatinib-Meditated Inhibitory Effects on T Cell Activation via the TCR Signaling Pathway
doi: 10.1155/2014/682010
Figure Lengend Snippet: The cell proliferation and IL-2 production of Jurkat cells and PBMCs following TCR stimulation. (Control) Untreated Jurkat cells or PBMCs. (SEA) Cells were pretreated with SEA (20 ng/mL). (IM) Cells were pretreated with 40 nM imatinib. (SEA + IM) Cells were pretreated with SEA (20 ng/mL) for 24 h followed by 40 nM imatinib treatment for 15 min. Each group was stimulated with anti-CD3/CD28 coated beads at a cell : bead ratio of 5 : 1 for 24 h. Cell proliferation was assayed with the CCK-8 kit (a) and (b). The IL-2 level was assayed using a human IL-2 ELISA kit (c) and (d). The mean value and standard deviation of 3 independent experiments are shown.
Article Snippet:
Techniques: Control, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Standard Deviation
Journal: BioMed Research International
Article Title: SEA Antagonizes the Imatinib-Meditated Inhibitory Effects on T Cell Activation via the TCR Signaling Pathway
doi: 10.1155/2014/682010
Figure Lengend Snippet: SEA pretreatment inhibited the reduction in imatinib-induced phosphorylation of Lck, ZAP70, and PLC γ 1 in Jurkat cells (a) and PBMCs (b). Densitometry (target protein : GAPDH ratio normalized to control) was conducted on three independent experiments in Jurkat cells (c) and PBMCs (d). Jurkat cells or PBMCs were pretreated in the absence or presence of SEA (20 ng/mL) followed by treatment with or without imatinib (40 nM), and cells were then stimulated with anti-CD3/CD28 coated beads for 15 min. Total cell extracts were resolved by SDS-PAGE and subjected to immunoblot analysis using phosphospecific antibodies as indicated.
Article Snippet:
Techniques: Phospho-proteomics, Control, SDS Page, Western Blot