One can reduce fa Significantly ABCG2 mRNA and protein JNK Signaling Pathway and its function in the human brain endothelial cell line. Slightly reduced IL-6 mRNA levels P gp, w While TNF-mRNA increased Ht fa Is significant and P gp protein expression in these cells. Despite the reduction in the H Height of ABCG2 mRNA, HeLa cells with IL 1b, IL-6 or TNF for 72 h no Ver Modification of the protein ABCG2 and function were treated, showed. Important post-translational effects on protein expression k Nnte explained Ren, the differences between the mRNA and protein expression and function of ABCG2 regulation observed in these cells. Although no Change ABCG2 function was a gr Ere accumulation of MX in HeLa cells with IL 1b, IL-6 or TNF, the potential down-regulation of ABCG2 MX Tr offers hunters other than in the treated HeLa cells including normal MDR1, MRP1 or MRP2. IL-6 and TNF has not imposed its effects on mRNA and protein expression, and function of ABCG2 in EPG85 257 cells. Although IL 1b not touched ABCG2 mRNA or protein in cells EPG85 257, increases to Kinesin Spindle Protein hte ABCG2 function in these cells, F Promotion m Possible post-translational effects of IL 1b in the line of stomach cancer.
MX accumulation was larger It in IL 1bexposed EPG85 257-cells to be expected in the expression of ABCG2 transporter au He MX. The results of this study and HeLa cell lines JAK Signaling Pathway EPG85 257 were inconsistent with our observations on the cell line MCF-7 breast cancer. These differences in response to entzündungsf Facilitative cytokines are h Highest likely due to differences in cell types in this study, the previously reported MDR1 response to cytokines in different cell lines. In fact, significant differences between different cell types on the spectrum and the interaction of receptors and transcription factors in cytokine-mediated response submitted involved. Irresponsiveness cytokine k in some cell lines nnte To the lack of necessary receptors or transcription factors that bind regulatory elements in the MDR gene promoter. Since the content of transcription factors between different cell lines can be different k Which lead to the activation of different S UPRIGHTS of transcription factors, although the cells again Oivent the same signal by the same receptor. Moreover, k We can not rule S that regulatory elements may be mutated in a terbinex cell line, w While the other in the other, which leads to different responses to the same cytokine non-mutated.
Interesting Change, although resistant cell line, a lower accumulation of MX was HeLaRDB compared to its parental HeLa was the FTC in mediation HeLaRDB MFI of cells is much lower than that of HeLa cells. This may indicate that a functional ABCG2 plays Very low in the transport of MX by the plasma membrane of cells HeLaRDB. Most likely, cause the activity T and very high overexpression of P-glycoprotein, another carrier hunter MX shown that in cells HeLaRDB, the Ausflu MX is very effective, completely self-mediation with the FTC Requests reference requests getting blockade of ABCG2 pump in the plasma membrane of cells LaRDB it. This underlines the importance of considering the r The other airlines involved in the transport of MX and regulated by cytokines. The pleiotropic properties of multi-drug resistance were detected.