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http://scihub22266oqcxt.onion/ C5883098!5883098 !29637003     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29637003 &cmd=llinks): Failed to open stream: HTTP request failed! 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TGF-?1 expression in regulatory NK1 1(-)CD4(+)NKG2D(+) T cells dependents on the PI3K-p85?/JNK, NF-?B and STAT3 pathways |pdf=|usr=}}{{29637003 }} gab.com Text TGF- 1 expression in regulatory NK1 1(-)CD4(+)NKG2D(+) T cells dependents on the PI3K-p85 /JNK, NF- B and STAT3 pathways JO: Am J Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=29637003 #FOAvip NK1.1(-)CD4(+)NKG2D(+) cells exert their immune-regulatory function in tumor as an unconventional regulatory T cell subset through the production of TGF-?1; however, the molecular mechanisms involving with the activation of nuclear factors for TGF-?1 transcription remain unclear. Here we determined that the PI3K-p85? subunit was specifically activated in NK1.1(-)CD4(+)NKG2D(+) cells following an 8-hour stimulation by sRAE-1 or ?-CD3/sRAE-1, subsequently leading to the activation of PI3K-p110, Akt, and JNK. On the contrary, ?-CD3/?-CD28 stimulation did not induce the activation of PI3K-p85 and JNK. Consequently, activation of the nuclear transcription factor AP-1 as a consequence of JNK activation regulated TGF-?1 expression in NK1.1(-)CD4(+)NKG2D(+) cells. Furthermore, activation of NF-?B in NK1.1(-)CD4(+)NKG2D(+) cells resulted from both protein kinase C activation downstream of TCR/CD3 signaling and PI3K activation induced by NKG2D engagement. The STAT3-Y705 phosphorylation, as activated by PI3K, under stimulations of the sRAE-1 or ?-CD3/sRAE-1 also contributed to the TGF-?1 expression in NK1.1(-)CD4(+)NKG2D(+) cells. Moreover, ChIP assay confirmed that STAT3 was capable of binding with the promoter regions of TGF-?1. In conclusion, our data showed that the TGF-?1 transcription in NK1.1(-)CD4(+)NKG2D(+) cells induced by sRAE-1 or ?-CD3/sRAE-1 was involved with the AP-1, NF-?B, and STAT3 signaling pathways; therefore, regulation of AP-1, NF-?B, and STAT3 activation may play important roles in the development and function of NK1.1(-)CD4(+)NKG2D(+) cells. Twit Text FOAVip TGF- 1 expression in regulatory NK1 1(-)CD4(+)NKG2D(+) T cells dependents on the PI3K-p85 /JNK, NF- B and STAT3 pathways ????Am J Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=29637003 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29637003 #FOAvip English Wikipedia <ref>{{Cite pmid|29637003 }}</ref> TGF-?1 expression in regulatory NK1 1(-)CD4(+)NKG2D(+) T cells dependents on the PI3K-p85?/JNK, NF-?B and STAT3 pathways #MMPMID29637003 Han S ; Ding S ; Miao X ; Lin Z ; Lu G ; Xiao W ; Ding Y ; Qian L ; Zhang Y ; Jia X ; Zhu G ; Gong W Am J Cancer Res 2018[]; 8 (3 ): 489-501 PMID29637003 show ga NK1.1(-)CD4(+)NKG2D(+) cells exert their immune-regulatory function in tumor as an unconventional regulatory T cell subset through the production of TGF-?1; however, the molecular mechanisms involving with the activation of nuclear factors for TGF-?1 transcription remain unclear. Here we determined that the PI3K-p85? subunit was specifically activated in NK1.1(-)CD4(+)NKG2D(+) cells following an 8-hour stimulation by sRAE-1 or ?-CD3/sRAE-1, subsequently leading to the activation of PI3K-p110, Akt, and JNK. On the contrary, ?-CD3/?-CD28 stimulation did not induce the activation of PI3K-p85 and JNK. Consequently, activation of the nuclear transcription factor AP-1 as a consequence of JNK activation regulated TGF-?1 expression in NK1.1(-)CD4(+)NKG2D(+) cells. Furthermore, activation of NF-?B in NK1.1(-)CD4(+)NKG2D(+) cells resulted from both protein kinase C activation downstream of TCR/CD3 signaling and PI3K activation induced by NKG2D engagement. The STAT3-Y705 phosphorylation, as activated by PI3K, under stimulations of the sRAE-1 or ?-CD3/sRAE-1 also contributed to the TGF-?1 expression in NK1.1(-)CD4(+)NKG2D(+) cells. Moreover, ChIP assay confirmed that STAT3 was capable of binding with the promoter regions of TGF-?1. In conclusion, our data showed that the TGF-?1 transcription in NK1.1(-)CD4(+)NKG2D(+) cells induced by sRAE-1 or ?-CD3/sRAE-1 was involved with the AP-1, NF-?B, and STAT3 signaling pathways; therefore, regulation of AP-1, NF-?B, and STAT3 activation may play important roles in the development and function of NK1.1(-)CD4(+)NKG2D(+) cells. äTGF-?1 expression in regulatory NK1 1(-)CD4(+)NKG2D(+) T cells depende(epmc).pdf DeepDyve Pubget Overpricing