“…The main conclusions are: (1) stimulation of TECs with high eATP triggers [Ca(2+)]c signals which include Ca(2+) mobilization from intracellular stores (mainly ER) and Ca(2+) entry through the plasma membrane; (2) the long-lasting Ca(2+) influx phase requires both store-operated Ca(2+) entry (SOCE) and non-SOCE components; (3) SOCE is not significantly involved in the antimigratory effect of high ATP stimulation; (4) ER is the main source for intracellular Ca(2+) release by eATP: it is required for the constitutive migratory potential of TECs but is not the only determinant for the inhibitory effect of high eATP; (5) a complex interplay occurs among ER, mitochondria and lysosomes upon purinergic stimulation; (6) high eUTP is unable to inhibit TEC migration and evokes [Ca(2+)]c signals very similar to those described for eATP. …”
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“…In the future, targeting distinct heteromeric SOCE channel subtypes may be the key to tailored SOCE-based therapies.…”
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“…CASQ1 also regulates store-operated Ca(2+) entry (SOCE) by binding to stromal interaction molecule 1 (STIM1). …”
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“…Store-operated calcium entry (SOCE) is a major pathway for calcium ions influx into cells and has a critical role in various cell functions. …”
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“…In conclusion, Orai3 constitutes a native SOCE pathway in NSCLC that controls cell proliferation and cell cycle progression likely via Akt pathway.…”
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“…Growing evidence supports a role for STIM1 and SOCE in the preservation of dendritic spines required for long-term potentiation and the formation of memory. …”
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“…Deregulated store‐operated calcium entry (SOCE) mediated by aberrant STIM1‐ORAI1 signaling is closely implicated in cancer initiation and progression. …”
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“…We found reduced store-operated Ca(2+) entry (SOCE), but unaltered store release in GluN1-deficient platelets. …”
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“…Our results showed that knockdown of BMPRII: 1) attenuated BMP4 induced activation of P-Smad1/5/8, without altering BMP4 induced P-p38MAPK and P-ERK1/2 activation in PASMCs; 2) did not attenuate the BMP4-induced TRPC1, 4 and 6 expression; 3) did not affect BMP4-enhanced SOCE and basal [Ca(2+)](i). Thus, we concluded that BMP4 activated Smad1/5/8 pathway is BMPRII-dependent, while the BMP4 – ERK/p-P38 – TRPC – SOCE signaling axis are likely mediated through other receptor rather than BMPRII.…”
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“…We also show that pacemaker cells express TRPC3 and several other molecular components related to SOCE/ROCE signaling, including STIM1 and IP(3)R. …”
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“…It is interesting to note that the bradykinin‐induced cell cycle progression and migration were not observed in cells with siRNA‐silenced IP3R3 or the SOCE component TRPC1, Orai1 or STIM1. Also the bradykinin‐induced increase in pAkt and pERK1/2 as well as cyclin D1 was reduced in these cells. …”
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“…SOCE inhibitors reduced the IL-6 production induced by IL-17/TNFα. …”
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“…T cell proliferation is stimulated by store operated Ca(2+) entry (SOCE) resulting from stimulation of Orai1 by STIM1/STIM2. …”
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“…We found that CRC cells showed enhanced resting Ca(2+) and store-operated Ca(2+) entry (SOCE) but decreased Ca(2+) store content relative to normal cells. …”
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“…Lastly, confocal Ca(2+) fluorescence examination found that 8pCPT could inhibit SOCE in ASMCs at 100 μM, and ESI-09 promoted SOCE of ASMCs at 10 μM and 100 μM. …”
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“…Cav1 silencing in stable TRPC1‐transfected cells by transfection with siCav1 reduced SOCE without effect on the level of resting [Ca(2+)](cyt). …”
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“…Here, we find that SMase D inhibits store-operated Ca(2+) entry (SOCE) in human T cells and lowers the production of the SOCE-dependent cytokines interleukin-2, which is critical for T cell growth, proliferation, and differentiation, and tumor necrosis factor α, which is crucial for the formation and maintenance of granulomas in microbial infections. …”
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“…Core components of SOCE in salivary gland acinar cells are Orai1 and STIM1. …”
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“…In addition to blocking Orai1-dependent SOCE, we found a BTP2-dependent inhibition of resting extracellular Ca(2+) flux. …”
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“…Proper skeletal muscle function is controlled by intracellular Ca(2+) concentration and by efficient production of energy (ATP), which, in turn, depend on: (a) the release and re-uptake of Ca(2+) from sarcoplasmic-reticulum (SR) during excitation–contraction (EC) coupling, which controls the contraction and relaxation of sarcomeres; (b) the uptake of Ca(2+) into the mitochondrial matrix, which stimulates aerobic ATP production; and finally (c) the entry of Ca(2+) from the extracellular space via store-operated Ca(2+) entry (SOCE), a mechanism that is important to limit/delay muscle fatigue. …”
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