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Figure 2 | Journal of Biomedical Science

Figure 2

From: Remodeling of calcium signaling in tumor progression

Figure 2

STIM1-dependent SOCE activation. STIM1 exists as the dimer maintained by the intermolecular interactions between its coiled-coil domains in the resting state (①). Depletion of ER luminal Ca2+ causes Ca2+ dissociation from the STIM1 N-terminal canonical EF hand, leading to STIM1 oligomerization due to the intermolecular interactions between EF-SAM domains (②). This activated STIM1 puncta interacts with the plasma membrane (PM) by the C-terminal polybasic K-rich clusters and accumulates in the ER-PM junctions (③). Orai1 tetramers diffusing in the PM (④) are tethered and trapped in junctions by the electrostatic interaction between CAD/SOAR domain in STIM1 and basic domains in the C-terminus of Orai1. The formation of the active STIM1/Orai1 complex conformationally gates the opening of SOC channel Orai1, thereby allowing Ca2+ entry (⑤). Upon store refilling, re-association of Ca2+ with STIM1 reverses EF-SAM oligomerization, causing STIM1-Orai1 uncoupling, Orai1 deactivation and the release of resting STIM1 dimers from puncta to redistribute throughout the ER (⑥).

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