Role of Molecular Determinants of Store-operated Ca2+ Entry (Orai1, Phospholipase A2 Group 6, and STIM1) in Focal Adhesion Formation and Cell Migration

Abstract

Background: Store-operated Ca 2ϩ entry is important for cell migration. Results: This study presents characterization of localization and roles of Orai1, STIM1, and PLA2g6 in adhesion dynamics during cell migration. Conclusion: Orai1 and PLA2g6 are involved in adhesion formation at the front, whereas STIM1 participates in both adhesion formation and disassembly. Significance: Results uncovered new parameters of Orai1, STIM1, and PLA2g6 involvement in cell migration.

Differential Kras V12 protein levels control a switch regulating lung cancer cell morphology and motility

“…Migration velocity analysis was performed as described earlier (Schafer et al, 2012). Randomly selected cells that show motility were manually tracked.…”

Store-operated Ca2+-entry and adenylyl cyclase

“…The elements of SOCE, along with AKAP220, occur at focal adhesions [85,86]. Two recent reviews [87,88] summarize the consequences of AC knockout and over-expression studies which implicate ACs, many of them susceptible to regulation by SOCE, in a wide range of physiological processes.…”

Interplay between phosphoinositide lipids and calcium signals at the leading edge of chemotaxing ameboid cells

“…Contemporary leading edge models ignored Ca 2+ until local Ca 2+ signals at the leading edge were found to be essential for macrophage leading edge stability, dynamics and function (Evans and Falke, 2007), to play a role in directional control of migrating fibroblasts and endothelial cells (Wei et al, 2012; Tsai and Meyer, 2012; Wei et al, 2009), and to be involved in the guidance mechanism of neuronal growth (Zamburlin et al, 2013; Henle et al, 2011; Heckman and Plummer, 2013). Thus in recent years Ca 2+ has joined PI(3,4,5)P 3 as an essential second messenger in leading edge signaling (Collins and Meyer, 2009; Wei et al, 2012; Tsai and Meyer, 2012; Zamburlin et al, 2013; Henle et al, 2011; Tian et al, 2010; Wei et al, 2009; Evans and Falke, 2007; Heckman and Plummer, 2013; Schafer et al, 2012), with the possible exception of cells that lack constant external Ca 2+ levels such as Dictyostelium (Wessels et al, 2012; Traynor et al, 2000). Besides PI(3,4,5)P 3 and Ca 2+ , another second messenger – the signaling lipid diacylglycerol (DAG) and likely its phosphorylation product phosphatidic acid – is indirectly implicated at the leading edge (Tsai and Meyer, 2012; Abramovici et al, 2009).…”

“…The leading edge Ca 2+ signal has been linked to both influx through plasma membrane Ca 2+ channels and efflux from internal Ca 2+ stores, although certain cell types may employ only one of these mechanisms (Wei et al, 2012; Tsai and Meyer, 2012; Zamburlin et al, 2013; Henle et al, 2011; Tian et al, 2010; Wei et al, 2009; Evans and Falke, 2007; Heckman and Plummer, 2013; Schafer et al, 2012). Plasma membrane Ca 2+ channels including transient receptor potential (TRP) and Orai1 channels, and endoplasmic reticulum Ca 2+ channels including ryanodine and IP 3 receptors, are proposed to give rise to the leading edge Ca 2+ influxes and effluxes, respectively (Wei et al, 2012; Tsai and Meyer, 2012; Zamburlin et al, 2013; Henle et al, 2011; Tian et al, 2010; Wei et al, 2009; Heckman and Plummer, 2013; Schafer et al, 2012).…”

“…Plasma membrane Ca 2+ channels including transient receptor potential (TRP) and Orai1 channels, and endoplasmic reticulum Ca 2+ channels including ryanodine and IP 3 receptors, are proposed to give rise to the leading edge Ca 2+ influxes and effluxes, respectively (Wei et al, 2012; Tsai and Meyer, 2012; Zamburlin et al, 2013; Henle et al, 2011; Tian et al, 2010; Wei et al, 2009; Heckman and Plummer, 2013; Schafer et al, 2012). In neurite growth, plasma membrane L- and N-type voltage dependent Ca 2+ channels may also play a role (Zamburlin et al, 2013).…”