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A Ca2+ Release-activated Ca2+ (CRAC) Modulatory Domain (CMD) within STIM1 Mediates Fast Ca2+-dependent Inactivation of ORAI1 Channels
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Brief Report: STIM1 Mutation Associated with a Syndrome of Immunodeficiency and Autoimmunity.
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Oligomerization of STIM1 couples ER calcium depletion to CRAC channel activation
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STIM1 signalling controls store-operated calcium entry required for development and contractile function in skeletal muscle
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Orai1 and STIM1 move to the immunological synapse and are up-regulated during T cell activation
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Defective mast cell effector functions in mice lacking the CRACM1 pore subunit of store-operated calcium release-activated calcium channels
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STIM2 is a feedback regulator that stabilizes basal cytosolic and endoplasmic reticulum Ca2+ levels
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Mapping the interacting domains of STIM1 and Orai1 in Ca2+ release-activated Ca2+ channel activation
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Biochemical properties and cellular localisation of STIM proteins
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Live-cell imaging reveals sequential oligomerization and local plasma membrane targeting of stromal interaction molecule 1 after Ca2+ store depletion
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STIM1 knockdown reveals that store-operated Ca2+ channels located close to sarco/endoplasmic Ca2+ ATPases (SERCA) pumps silently refill the endoplasmic reticulum
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Calcium sources used by post-natal human myoblasts during initial differentiation
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Orai1 and STIM reconstitute store-operated calcium channel function
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Loss of myogenin in postnatal life leads to normal skeletal muscle but reduced body size
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Membrane hyperpolarization triggers myogenin and myocyte enhancer factor-2 expression during human myoblast differentiation
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