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10.1016/j.ceca.2020.102251 http://scihub22266oqcxt.onion/10.1016/j.ceca.2020.102251 32683175!ä!32683175 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Calcium 2020 ; 90 (ä): 102251 Nephropedia Template TP {{tp|p=32683175|t=2020. Insights and perspectives on calcium channel functions in the cockpit of cancerous space invaders |pdf=|usr=}}{{32683175}} gab.com Text Insights and perspectives on calcium channel functions in the cockpit of cancerous space invaders JO: Cell Calcium http://www.kidney.de/pget.php?&tw=1&pmid=32683175 #FOAvip Development of metastasis causes the most serious clinical consequences of cancer and is responsible for over 90 % of cancer-related deaths. Hence, a better understanding of the mechanisms that drive metastasis formation appears critical for drug development designed to prevent the spread of cancer and related mortality. Metastasis dissemination is a multistep process supported by the increased motility and invasiveness capacities of tumor cells. To succeed in overcoming the mechanical constraints imposed by the basement membrane and surrounding tissues, cancer cells reorganize their focal adhesions or extend acto-adhesive cellular protrusions, called invadosomes, that can both contact the extracellular matrix and tune its degradation through metalloprotease activity. Over the last decade, accumulating evidence has demonstrated that altered Ca(2+) channel activities and/or expression promote tumor cell-specific phenotypic changes, such as exacerbated migration and invasion capacities, leading to metastasis formation. While several studies have addressed the molecular basis of Ca(2+) channel-dependent cancer cell migration, we are still far from having a comprehensive vision of the Ca(2+) channel-regulated mechanisms of migration/invasion. This is especially true regarding the specific context of invadosome-driven invasion. This review aims to provide an overview of the current evidence supporting a central role for Ca(2+) channel-dependent signaling in the regulation of these dynamic degradative structures. It will present available data on the few Ca(2+) channels that have been studied in that specific context and discuss some potential interesting actors that have not been fully explored yet. Twit Text FOAVip Insights and perspectives on calcium channel functions in the cockpit of cancerous space invaders ????Cell Calcium http://www.kidney.de/pget.php?&tw=1&pmid=32683175 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32683175 #FOAvip English Wikipedia <ref>{{Cite pmid|32683175}}</ref> Insights and perspectives on calcium channel functions in the cockpit of cancerous space invaders #MMPMID32683175 Leverrier-Penna S; Destaing O; Penna A Cell Calcium 2020[Sep]; 90 (ä): 102251 PMID32683175show ga Development of metastasis causes the most serious clinical consequences of cancer and is responsible for over 90 % of cancer-related deaths. Hence, a better understanding of the mechanisms that drive metastasis formation appears critical for drug development designed to prevent the spread of cancer and related mortality. Metastasis dissemination is a multistep process supported by the increased motility and invasiveness capacities of tumor cells. To succeed in overcoming the mechanical constraints imposed by the basement membrane and surrounding tissues, cancer cells reorganize their focal adhesions or extend acto-adhesive cellular protrusions, called invadosomes, that can both contact the extracellular matrix and tune its degradation through metalloprotease activity. Over the last decade, accumulating evidence has demonstrated that altered Ca(2+) channel activities and/or expression promote tumor cell-specific phenotypic changes, such as exacerbated migration and invasion capacities, leading to metastasis formation. While several studies have addressed the molecular basis of Ca(2+) channel-dependent cancer cell migration, we are still far from having a comprehensive vision of the Ca(2+) channel-regulated mechanisms of migration/invasion. This is especially true regarding the specific context of invadosome-driven invasion. This review aims to provide an overview of the current evidence supporting a central role for Ca(2+) channel-dependent signaling in the regulation of these dynamic degradative structures. It will present available data on the few Ca(2+) channels that have been studied in that specific context and discuss some potential interesting actors that have not been fully explored yet. |Animals[MESH] |Calcium Channels/*metabolism[MESH] |Calcium/metabolism[MESH] |Cell Surface Extensions/metabolism[MESH] |Extracellular Matrix/metabolism[MESH] |Humans[MESH] |Neoplasm Invasiveness[MESH]Insights and perspectives on calcium channel functions in the cockpit (epmc).pdf DeepDyve Pubget Overpricing