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10.18632/oncotarget.25672 http://scihub22266oqcxt.onion/10.18632/oncotarget.25672 C6047677!6047677!30034631     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2018 ; 9 (50): 29468-83 Nephropedia Template TP {{tp|p=30034631|t=2018. The calcium channel proteins ORAI3 and STIM1 mediate TGF-? induced Snai1 expression |pdf=|usr=}}{{30034631}} gab.com Text The calcium channel proteins ORAI3 and STIM1 mediate TGF- induced Snai1 expression JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=30034631 #FOAvip Calcium influx into cells via plasma membrane protein channels is tightly regulated to maintain cellular homeostasis. Calcium channel proteins in the plasma membrane and endoplasmic reticulum have been linked to cancer, specifically during the epithelial-mesenchymal transition (EMT), a cell state transition process implicated in both cancer cell migration and drug resistance. The transcription factor SNAI1 (SNAIL) is upregulated during EMT and is responsible for gene expression changes associated with EMT, but the calcium channels required for Snai1 expression remain unknown. In this study, we show that blocking store-operated calcium entry (SOCE) with 2-aminoethoxydiphenylborane (2APB) reduces cell migration but, paradoxically, increases the level of TGF-? dependent Snai1 gene activation. We determined that this increased Snai1 transcription involves signaling through the AKT pathway and subsequent binding of NF-?B (p65) at the Snai1 promoter in response to TGF-?. We also demonstrated that the calcium channel protein ORAI3 and the stromal interaction molecule 1 (STIM1) are required for TGF-? dependent Snai1 transcription. These results suggest that calcium channels differentially regulate cell migration and Snai1 transcription, indicating that each of these steps could be targeted to ensure complete blockade of cancer progression. Twit Text FOAVip The calcium channel proteins ORAI3 and STIM1 mediate TGF- induced Snai1 expression ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=30034631 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30034631 #FOAvip English Wikipedia <ref>{{Cite pmid|30034631}}</ref> The calcium channel proteins ORAI3 and STIM1 mediate TGF-? induced Snai1 expression #MMPMID30034631 Bhattacharya A; Kumar J; Hermanson K; Sun Y; Qureshi H; Perley D; Scheidegger A; Singh BB; Dhasarathy A Oncotarget 2018[Jun]; 9 (50): 29468-83 PMID30034631show ga Calcium influx into cells via plasma membrane protein channels is tightly regulated to maintain cellular homeostasis. Calcium channel proteins in the plasma membrane and endoplasmic reticulum have been linked to cancer, specifically during the epithelial-mesenchymal transition (EMT), a cell state transition process implicated in both cancer cell migration and drug resistance. The transcription factor SNAI1 (SNAIL) is upregulated during EMT and is responsible for gene expression changes associated with EMT, but the calcium channels required for Snai1 expression remain unknown. In this study, we show that blocking store-operated calcium entry (SOCE) with 2-aminoethoxydiphenylborane (2APB) reduces cell migration but, paradoxically, increases the level of TGF-? dependent Snai1 gene activation. We determined that this increased Snai1 transcription involves signaling through the AKT pathway and subsequent binding of NF-?B (p65) at the Snai1 promoter in response to TGF-?. We also demonstrated that the calcium channel protein ORAI3 and the stromal interaction molecule 1 (STIM1) are required for TGF-? dependent Snai1 transcription. These results suggest that calcium channels differentially regulate cell migration and Snai1 transcription, indicating that each of these steps could be targeted to ensure complete blockade of cancer progression. äThe calcium channel proteins ORAI3 and STIM1 mediate TGF-? induced Sna(epmc).pdf DeepDyve Pubget Overpricing