Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1016/j.ceca.2020.102187 http://scihub22266oqcxt.onion/10.1016/j.ceca.2020.102187 32146159!7202080!32146159     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Calcium 2020 ; 87 (ä): 102187 Nephropedia Template TP {{tp|p=32146159|t=2020. TRPM7 activation potentiates SOCE in enamel cells but requires ORAI |pdf=|usr=}}{{32146159}} gab.com Text TRPM7 activation potentiates SOCE in enamel cells but requires ORAI JO: Cell Calcium http://www.kidney.de/pget.php?&tw=1&pmid=32146159 #FOAvip Calcium (Ca(2+)) release-activated Ca(2+) (CRAC) channels mediated by STIM1/2 and ORAI (ORAI1-3) proteins form the dominant store-operated Ca(2+) entry (SOCE) pathway in a wide variety of cells. Among these, the enamel-forming cells known as ameloblasts rely on CRAC channel function to enable Ca(2+) influx, which is important for enamel mineralization. This key role of the CRAC channel is supported by human mutations and animal models lacking STIM1 and ORAI1, which results in enamel defects and hypomineralization. A number of recent reports have highlighted the role of the chanzyme TRPM7 (transient receptor potential melastanin 7), a transmembrane protein containing an ion channel permeable to divalent cations (Mg(2+), Ca(2+)), as a modulator of SOCE. This raises the question as to whether TRPM7 should be considered an alternative route for Ca(2+) influx, or if TRPM7 modifies CRAC channel activity in enamel cells. To address these questions, we monitored Ca(2+) influx mediated by SOCE using the pharmacological TRPM7 activator naltriben and the inhibitor NS8593 in rat primary enamel cells and in the murine ameloblast cell line LS8 cells stimulated with thapsigargin. We also measured Ca(2+) dynamics in ORAI1/2-deficient (shOrai1/2) LS8 cells and in cells with siRNA knock-down of Trpm7. We found that primary enamel cells stimulated with the TRPM7 activator potentiated Ca(2+) influx via SOCE compared to control cells. However, blockade of TRPM7 with NS8593 did not decrease the SOCE peak. Furthermore, activation of TRPM7 in shOrai1/2 LS8 cells lacking SOCE failed to elicit Ca(2+) influx, and Trpm7 knock-down had no effect on SOCE. Taken together, our data suggest that TRPM7 is a positive modulator of SOCE potentiating Ca(2+) influx in enamel cells, but its function is fully dependent on the prior activation of the ORAI channels. Twit Text FOAVip TRPM7 activation potentiates SOCE in enamel cells but requires ORAI ????Cell Calcium http://www.kidney.de/pget.php?&tw=1&pmid=32146159 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32146159 #FOAvip English Wikipedia <ref>{{Cite pmid|32146159}}</ref> TRPM7 activation potentiates SOCE in enamel cells but requires ORAI #MMPMID32146159 Souza Bomfim GH; Costiniti V; Li Y; Idaghdour Y; Lacruz RS Cell Calcium 2020[May]; 87 (ä): 102187 PMID32146159show ga Calcium (Ca(2+)) release-activated Ca(2+) (CRAC) channels mediated by STIM1/2 and ORAI (ORAI1-3) proteins form the dominant store-operated Ca(2+) entry (SOCE) pathway in a wide variety of cells. Among these, the enamel-forming cells known as ameloblasts rely on CRAC channel function to enable Ca(2+) influx, which is important for enamel mineralization. This key role of the CRAC channel is supported by human mutations and animal models lacking STIM1 and ORAI1, which results in enamel defects and hypomineralization. A number of recent reports have highlighted the role of the chanzyme TRPM7 (transient receptor potential melastanin 7), a transmembrane protein containing an ion channel permeable to divalent cations (Mg(2+), Ca(2+)), as a modulator of SOCE. This raises the question as to whether TRPM7 should be considered an alternative route for Ca(2+) influx, or if TRPM7 modifies CRAC channel activity in enamel cells. To address these questions, we monitored Ca(2+) influx mediated by SOCE using the pharmacological TRPM7 activator naltriben and the inhibitor NS8593 in rat primary enamel cells and in the murine ameloblast cell line LS8 cells stimulated with thapsigargin. We also measured Ca(2+) dynamics in ORAI1/2-deficient (shOrai1/2) LS8 cells and in cells with siRNA knock-down of Trpm7. We found that primary enamel cells stimulated with the TRPM7 activator potentiated Ca(2+) influx via SOCE compared to control cells. However, blockade of TRPM7 with NS8593 did not decrease the SOCE peak. Furthermore, activation of TRPM7 in shOrai1/2 LS8 cells lacking SOCE failed to elicit Ca(2+) influx, and Trpm7 knock-down had no effect on SOCE. Taken together, our data suggest that TRPM7 is a positive modulator of SOCE potentiating Ca(2+) influx in enamel cells, but its function is fully dependent on the prior activation of the ORAI channels. |Ameloblasts/drug effects/metabolism[MESH] |Animals[MESH] |Calcium/*metabolism[MESH] |Cell Line[MESH] |Dental Enamel/*cytology[MESH] |Female[MESH] |Male[MESH] |Mice[MESH] |Naltrexone/analogs & derivatives/pharmacology[MESH] |ORAI1 Protein/*metabolism[MESH] |RNA, Small Interfering/metabolism[MESH] |Rats, Sprague-Dawley[MESH]TRPM7 activation potentiates SOCE in enamel cells but requires ORAI (epmc).pdf DeepDyve Pubget Overpricing