Two kinds of graphene coatings are obtained by the graphene drop-coating drying method (DCDM) and the coating graphene conductive adhesive (CGCA). The effects of these two kinds of graphene coatings on the friction, wear, and voltage signals of the electrical contact interface are explored. The test results show that the presence of the graphene coating can effectively reduce the friction coefficient and friction force, and the graphene coating prepared by the DCDM possesses the best ability in reducing the friction coefficient. Although the presence of the graphene coating will lead to the increase in interface contact voltage at the initial stage, the voltage signal gradually becomes stable with the progress of friction and wear, suggesting that the graphene coating will not affect the stability of sliding electrical contact. Wear analysis results show that the graphene coating prepared by the DCDM has a good anti-wear effect, and the graphene particles in the abrasion area play the role of solid lubrication. Finite element analysis results show that the graphene coating will generate thermal expansion when electric current is applied, accordingly avoid the direct contact between the metal substrate, and, thus, reduce the interface friction and alleviate the wear degree of interface. However, the normal force fluctuation of the interface may increase.
Csk-binding protein/phosphoprotein associated with glycosphingolipid-enriched microdomains (CBP/PAG) is a membrane-bound adaptor protein that downregulates the activation of Src family kinases present in lipid rafts. To elucidate the role of CBP/PAG in human T cell activation, a cell line overexpressing CBP/PAG was constructed and the function of CBP/PAG in Jurkat cells was examined. The present study revealed that increased CBP/PAG expression in T cells significantly enhanced their apoptosis and reduced cellular activation and proliferation. Overexpression of CBP/PAG suppressed the growth of Jurkat cells by recruiting c-Src and its negative regulator, C-terminal Src kinase (CSK), to lipid rafts. The negative regulation of CBP/PAG was enhanced in the presence of anti-cluster of differentiation (CD)59 monoclonal antibodies. In addition, a significant association was revealed between the location of CBP/PAG and CD59, which were co-expressed in the same region of the cell membrane, implicating a potential overlap of the elicited signaling pathways. These results indicate that CBP/PAG functions as a negative regulator of cell signal transduction and suggest that CD59 may strengthen the role of negative feedback regulation.
Abstract:Objective: To study SP22 the closed short peptide of CD59 specific site on Jurkat cell signal transduction molecules (LAT, STAT3) genes, proliferation genes (Nf-κb3, Bcl-2) and apoptosis genes (caspase-3) effect, research CD59 specific site closed by short peptide concrete mechanism of Jurkat cells. Methods: Jurkat cells were divided into blank control group and SP22 peptide closed group, Training after 48h respectively with the method of CCK 8 to detect each cell proliferation rate; Flow cytometry --check each group cell apoptosis; Real time quantitative PCR --from gene level determination of two kinds of cells before and after the experiment the expression of stat3 and joint protein Lat, detection of cell proliferation and apoptosis protein before and after test the Nf-κb3, Bcl-2, the expression of Caspas-3; Enzyme-linked immunosorbent assay (ELISA) to detect the related cytokines. Results: add SP22 peptide group cell proliferation inhibition rate is greater than the blank control group (P < 0.01);Add SP22 group compared with blank control group Lat, Stat3, Nf-κb3, Bcl-2 gene expression decline, Caspas-3 gene expression rise; Add SP22 40 mg group cell death ratio increased, compared with the blank control group difference has statistically significant (P < 0.01). In short peptide SP22 group, cells secrete and promote tumor to growth of interleukin 2 (IL-2) and TGF-βhad been inhibited. Conclusion: CD59 specific site closed short peptide can inhibit Jurkat cell proliferation, reduce the expression of Lat, Stat3, Nf-κb and Bcl-2, activating caspase-3, promote the apoptosis of Jurkat cells.
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