ライフサイエンスコーパス: STIM1

1 STIM1 (stromal interaction molecule 1) regulates Ca(2+)

2 STIM1 and Orai1 are the main components of a widely cons

3 STIM1 and STIM2 are calcium-sensing molecules that link

4 STIM1 can associate with Orai in cardiac myocytes to pro

5 STIM1 effects were eliminated by either BTP2 or by coexp

6 STIM1 expression also increased spark rates and induced

7 STIM1 expression produced an increase in the amount of C

8 STIM1 is a calcium sensor, which oligomerizes and activa

9 STIM1 is known to be involved in the chemoattractant sig

10 STIM1 is thought to act as an initiator of cardiac hyper

11 STIM1 overexpression in CRC was significantly associated

12 STIM1-KO and ORAI1-KO cell lines were generated by CRISP

13 STIM1-mediated channel activation occurs through rotatio

14 STIM1/ORAI1 colocalizes with clathrin, but not with cave

15 activated by stromal interaction molecule 1 (STIM1) after depletion of intracellular calcium stores.

16 sociation of stromal interaction molecule 1 (STIM1) and Orai1 and is even required for the full activ

17 report that stromal interaction molecule 1 (STIM1) and Orai1 channels, key components of store-opera

18 iated by the stromal interaction molecule 1 (STIM1) and the Ca(2+) channel Orai1 as well as store ope

19 sing protein stromal interaction molecule 1 (STIM1) and the channel pore-forming protein Orai1.

20 ts activator stromal interaction molecule 1 (STIM1) are immunodeficient and prone to chronic infectio

21 the role of stromal interaction molecule 1 (STIM1) in coupling store depletion to this activation pa

22 Stromal interaction molecule 1 (STIM1) is a Ca(2+) sensor protein that initiates store-o

23 Stromal interaction molecule 1 (STIM1) is a dynamic calcium signal transducer implicated

24 itable cells stromal interaction molecule 1 (STIM1) is a key element in the generation of Ca(2+) sign

25 Stromal interaction molecule 1 (STIM1) regulates store-operated Ca(2+) entry (SOCE) and

26 a(2+) sensor stromal interaction molecule 1 (STIM1) to ER-plasma membrane (PM) junctions.

27 a(2+) sensor stromal interacting molecule 1 (STIM1) via association with the plasma membrane Ca(2+)/A

28 roteins, the stromal interaction molecule 1 (STIM1), a Ca(2+) sensor in the endoplasmic reticulum, an

29 function of stromal interaction molecule 1 (STIM1), an endo/sarcoplasmic reticulum (ER/SR) Ca(2+) se

30 the role of stromal interaction molecule 1 (STIM1), an endo/sarcoplasmic reticulum Ca(2+) sensor.

31 activated by stromal interacting molecule 1 (STIM1), an endoplasmic reticulum (ER)-resident calcium s

32 ene encoding stromal interaction molecule 1 (STIM1), the endoplasmic reticulum calcium (Ca(2+)) senso

33 Stromal-interaction molecule 1 (STIM1), upon sensing the depletion of (Ca(2+)) from the

34 ntly express stromal interacting molecule 1 (STIM1), whereas STIM2 is mainly confined to the outer pl

35 s activator, stromal interacting molecule 1 (STIM1).

36 lated by the stromal-interacting molecule-1 (STIM1) protein, two distinct pools of this protein are r

37 a(2+) sensor stromal interacting molecule-1 (STIM1), whereas sphingosine-1-phosphate-mediated enhance

38 ediate SOCE: stromal interaction molecule-1 (STIM1), which functions as the SR Ca(2+) sensor, and Ora

39 or (SARAF) has recently been identified as a STIM1 regulatory protein that facilitates slow Ca(2+)-de

40 Using a STIM1 promoter luciferase vector, we found that the zinc

41 location, which was associated with aberrant STIM1 O-GlycNAcylation.

42 oplasmic STIM1 oligomerization and abolishes STIM1-ORAI1 interactions.

43 -2 with ibuprofen and indomethacin abrogated STIM1-mediated CRC cell motility.

44 pletion of Ca(2+)stores, sigma1R accompanied STIM1 to ER-plasma membrane (PM) junctions where STIM1 s

45 says revealed that store depletion activated STIM1 translocation from within the cell to the plasma m

46 of sarcoplasmic reticulum calcium activates STIM1/Orai1-dependent store-operated calcium entry.

47 been mapped, signaling mechanisms activating STIM1 recruitment of Orai1 and STIM1-Orai1 interaction r

48 r the full activity of constitutively active STIM1 variants that bind Orai1 independently of ER Ca(2+

49 TIM1, or an Orai1 mutation (L273D) affecting STIM1 association.

50 Although STIM1-deficient T cells exhibited markedly reduced IFN-g

51 We conclude that although STIM1 is required for GPCR-mediated disruption of barrie

52 1 suppresses Cav1.3 activity by providing an STIM1-based scaffold, which is essential for DA neuron s

53 inhibited by TRPC1 and STIM1 antibodies and STIM1 short hairpin RNA (shRNA) in wild-type VSMCs, and

54 e identified an interaction between CSQ1 and STIM1 in HEK293 cells.

55 tion between low polymeric forms of CSQ1 and STIM1 likely acts by interfering with STIM1 oligimerizat

56 actin flow corrals ER tubule extensions and STIM1/Orai1 complexes to the synapse center, creating a

57 ctivated Ca2+ (CRAC) channel genes ORAI1 and STIM1 abolish store-operated Ca2+ entry (SOCE), and pati

58 Mutations in the ORAI1 and STIM1 genes that abolish SOCE cause a combined immunodef

59 Mutations in ORAI1 and STIM1 genes that abolish SOCE cause severe immunodeficie

60 ed Ca(2+) entry (SOCE) components, Orai1 and STIM1, did not reduce Tg cytotoxicity, indicating that S

61 ms activating STIM1 recruitment of Orai1 and STIM1-Orai1 interaction remains enigmatic.

62 Ca(2+) (CRAC) channels encoded by Orai1 and STIM1.

63 nal STIM1 antibodies on TRPC1-based SOCs and STIM1 staining suggest that channel activation may invol

64 hanges in the ratio between active STIM2 and STIM1 proteins can switch the regulation of Imin channel

65 channel activity was inhibited by TRPC1 and STIM1 antibodies and STIM1 short hairpin RNA (shRNA) in

66 ernary complex composed of Orai1, TRPC1, and STIM1, the key proteins involved in the formation of SOC

67 Orai1, TRPC1, TRPC3 and STIM1 have been identified as critical components of SOC

68 I-Orai1 probes reveal local Ca(2+) influx at STIM1-Orai1 puncta.

69 We conclude that sigma1R attenuates STIM1 coupling to Orai1 and thereby inhibits SOCE.

70 an unexpected unimolecular coupling between STIM1 and Orai1 and argues against recent evidence sugge

71 as supported by a direct interaction between STIM1 and Rictor, a specific component of mTOR complex 2

72 dence suggesting dimeric interaction between STIM1 and two adjacent Orai1 channel subunits.

73 Store depletion induced interactions between STIM1 and TRPC1, Galphaq and PLCbeta1, which required ST

74 These new data about cross-talk between STIM1 and STIM2 and their different roles in store-opera

75 composed Imax channels are activated by both STIM1 and STIM2.

76 OCs and that these channels are activated by STIM1 in response to thapsigargin or ACh.

77 ated by CAD, and small Orai1 puncta gated by STIM1, exhibit repetitive fluctuations in single-channel

78 TRPC3-containing INS channels are induced by STIM1, and TRPC1-composed Imax channels are activated by

79 alphaq and PLCbeta1, which were inhibited by STIM1 knockdown.

80 el and PLCbeta1 activities were inhibited by STIM1 short hairpin RNA (shRNA) and absent in TRPC1(-/-)

81 KC phosphorylation of TRPC1 was inhibited by STIM1 shRNA.

82 ated if Ca(2+) clearance is not inhibited by STIM1.

83 Store-operated Ca(2+) entry mediated by STIM1 and ORAI1 constitutes one of the major Ca(2+) entr

84 te biosensor GFP-PLCdelta1-PH was reduced by STIM1 shRNA and absent in TRPC1(-/-) cells.

85 rotein STIM1, CRAC channels are regulated by STIM1 in the endoplasmic reticulum, whilst ARC channels

86 rai1 and TRPC1, which form SOCs regulated by STIM1, play a key role in the effect of ACh on GSIS, a p

87 E and KATP channel activity are regulated by STIM1.

88 ulated Ca(2+)(ARC) channels are regulated by STIM1.

89 Pore helix rotation by STIM1 also explains the dynamic coupling between CRAC ch

90 signals, how gating of Orai1 is triggered by STIM1 remains unknown.

91 aintenance and reveals a second phase of CAD/STIM1 binding after channel opening.

92 In cardiomyocytes, STIM1 acts by tuning Akt kinase activity through activat

93 ons formed during exercise, and that contain STIM1 and Orai1, function as Ca (2+) Entry Units (CEUs),

94 membrane (PM) function: [Ca(2+)]ER controls STIM1 activation in presynaptic terminals, which results

95 ute to the interaction with STIM1 and couple STIM1 binding with channel gating and modulation of ion

96 CRAC-/STIM1-mediated Orai channel currents display characteris

97 rther increased CSQ1 monomerization and CSQ1-STIM1 interaction, but reduced the association of STIM1

98 Q folding and aggregation, enhanced the CSQ1-STIM1 interaction.

99 ctive conformational state, (ii) cytoplasmic STIM1 oligomerization, and (iii) STIM1-ORAI1 binding req

100 wever, the mutation also impairs cytoplasmic STIM1 oligomerization and abolishes STIM1-ORAI1 interact

101 -operated calcium entry (SOCE) by decreasing STIM1 puncta formation near the plasma membrane upon cal

102 Surprisingly, the phospho-defective STIM1-Y361F mutant formed puncta but failed to recruit O

103 +) currents, decreased stimulation-dependent STIM1-Cav1.3 interaction, and decreased DA neurons.

104 After Ca(2+) store depletion, STIM1 and Orai couple to each other, allowing Ca(2+) inf

105 The dimeric STIM1 protein contains a small STIM-Orai-activating regi

106 ai1 channel without the necessity for direct STIM1 contact with the pore-forming helix.

107 ation within the STIM1 transmembrane domain (STIM1-TM), here we show that local rearrangement, rather

108 g expression of STIM1, the gene that encodes STIM1, in insulin-secreting MIN6 beta-cells with RNA int

109 We found that endogenous STIM1 was expressed at low but measureable levels along

110 To gate Orai1 channels, the exposed STIM1-activating domain binds to two sites in Orai1, one

111 tion of the Orai N terminus is essential for STIM1, as it fine-tunes the open Orai channel gating, th

112 efine distinct but cooperative functions for STIM1 and STIM2 in modulating neutrophil bactericidal an

113 er Orai channels are obligatory partners for STIM1 in these processes using a clinically relevant lar

114 s) due to a T cell-intrinsic requirement for STIM1 in iTreg differentiation and excessive production

115 Although a role for STIM1 in neutrophil SOCE and activation has been establi

116 C1-based SOCs in VSMCs, and a novel role for STIM1, in which store-operated STIM1-TRPC1 interactions

117 C1-based SOCs in VSMCs, and a novel role for STIM1, where store-operated STIM1-TRPC1 interactions sti

118 These findings reveal a critical role for STIM1-mediated control of Ca(2+) clearance in NFAT induc

119 rovided clinicopathological significance for STIM1 and SOCE in CRC progression, and implicated a role

120 Orai C terminus, the main coupling site for STIM1, the Orai N terminus is indispensable for Orai cha

121 to the plasma membrane (PM) where it formed STIM1-TRPC1 complexes, which then associated with Galpha

122 cular mechanisms by which a loss-of-function STIM1 mutation (R429C) in human patients abolishes SOCE.

123 nts with mutations in the CRAC channel genes STIM1 and ORAI1 show abnormal enamel mineralization, we

124 These results highlight how STIM1-dependent Ca(2+) microdomains have a major impact

125 ide new insights to our understanding of how STIM1 orchestrates the cellular behavior underlying chem

126 o this modulation mechanism would reveal how STIM1-dependent channel gating is enhanced, and benefit

127 During the chronic phase, however, STIM1-deficient T cells displayed enhanced IFN-gamma pro

128 rus gene shuttle vector that expressed human STIM1 Immunoprecipitation studies revealed that STIM1 bi

129 cytoplasmic STIM1 oligomerization, and (iii) STIM1-ORAI1 binding required for ORAI1 activation.

130 port the final results of the Stop Imatinib (STIM1) study with a long follow-up.

131 ntly diminished SOCE as a result of impaired STIM1 translocation, which was associated with aberrant

132 gression, and implicated a role for COX-2 in STIM1-mediated CRC metastasis.

133 iggers a series of conformational changes in STIM1 that unmask a minimal Orai1-activating domain (CRA

134 PGE2 were able to rescue migration defect in STIM1 knockdown CRC cells, and inhibition of COX-2 with

135 Primary hepatocytes deficient in STIM1 exhibited elevated cellular stress as well as impa

136 Reduction in STIM1 expression promoted a rapid transition to heart fa

137 phorylation status of this single residue in STIM1 represents a key molecular determinant of the rela

138 Therefore, Y361 in STIM1 represents a novel target for limiting SOCE-associ

139 Hypertrophied myocytes had increased STIM1 expression and activity, which correlated with alt

140 at ER Ca(2+)-store depletion rapidly induces STIM1 phosphorylation at Y361 via proline-rich kinase 2

141 Chronically Mtb-infected, STIM1-deficient mice had reduced levels of inducible reg

142 ies also suggested a new approach to inhibit STIM1-mediated metastasis with COX-2 inhibitors.

143 ring with STIM1 oligimerization and inhibits STIM1-Orai1 interaction, providing a brake to SOCE under

144 main in regulating intra- and intermolecular STIM1 interactions that control (i) transition of STIM1

145 ho-switch enabling recruitment of Orai1 into STIM1 puncta leading to SOCE.

146 A widely held gating model invokes STIM1 binding directly to Orai1 pore-forming helix.

147 used conditional knockout (KO) mice lacking STIM1 in cells of myeloid lineage (STIM1(fl/fl) LysM-cre

148 Indeed, mice lacking STIM1 showed less adverse structural remodeling in respo

149 e results are recapitulated with full length STIM1.

150 e lacking STIM1 in cells of myeloid lineage (STIM1(fl/fl) LysM-cre).

151 transition to heart failure, we manipulated STIM1 expression in mice cardiomyocytes by using in vivo

152 ased TRPC1 expression, inhibited Tg-mediated STIM1-Cav1.3 interaction, and induced caspase activation

153 ty, whilst the minor pool of plasma membrane STIM1 regulates ARC channel activity.

154 diated by the association of plasma membrane STIM1 with the scaffolding protein AKAP79.

155 m (ER)-located stromal interaction molecue1 (STIM1) and the plasma membrane-located Ca(2+) channel su

156 Moreover, STIM1 influenced SAN function by regulating ionic fluxes

157 tive localization at ER-PM junctions, mutant STIM1 fails to activate SOCE.

158 yopathy (ACTA1), tubular aggregate myopathy (STIM1), myofibrillar myopathy (FLNC), and mutation of CH

159 We further found that neither STIM1 nor PMCA4 is up-regulated when both EGR1 and EGR4

160 Nevertheless, STIM1 overexpressing cells show increased SR Ca(2+) cont

161 cytokine production required STIM2, but not STIM1, at least in part as a result of redox regulation

162 of Ip requires the open state of Orai1, not STIM1 itself.

163 Novel STIM1-dependent control of Ca(2+) clearance regulates NF

164 ame residue actually inhibits the ability of STIM1 to activate the CRAC channels.

165 h inducible, cardiac-restricted, ablation of STIM1 exhibited left ventricular reduced contractility,

166 y open state exactly mimicking the action of STIM1.

167 We demonstrate a functional association of STIM1 and SOAR to cholesterol, indicating a close proxim

168 interaction, but reduced the association of STIM1 with Orai1 and SOCE.

169 The association of STIM1 with sigma1R slowed the recruitment of STIM1 to ER

170 M1 to ER-PM junctions and reduced binding of STIM1 to PM Orai1.

171 Binding of STIM1 to SUR1 was enhanced by poly-lysine.

172 rai1 and the CRAC-activating domain (CAD) of STIM1 were coexpressed at low levels and imaged using a

173 The molecular choreography of STIM1-ORAI1 coupling is initiated by endoplasmic reticul

174 single Orai1 channel with small clusters of STIM1 molecules.

175 tivated Ca(2+) (CRAC) channels, comprised of STIM1 and Orai1 proteins.

176 To define the contributions of STIM1-mediated Ca(2+) influx on electrical and mechanica

177 itionally, mice with acute liver deletion of STIM1 displayed systemic glucose intolerance.

178 omoted CRC cell motility, while depletion of STIM1 with short hairpin RNA inhibited CRC cell migratio

179 al residues within the cytoplasmic domain of STIM1 (STIM1-CT) that entail autoinhibition.

180 (T389) in the extensive cytosolic domain of STIM1 by protein kinase A.

181 proximately 450 residue) cytosolic domain of STIM1.

182 The effects of STIM1 knockdown were reversed by transduction of MIN6 ce

183 Forced expression of STIM1 in cultured adult feline ventricular myocytes incr

184 Conversely, over-expression of STIM1 in obese mice led to increased SOCE, which was suf

185 Furthermore, ectopic expression of STIM1 promoted CRC cell motility, while depletion of STI

186 We report that lowering expression of STIM1, the gene that encodes STIM1, in insulin-secreting

187 try (SOCE) that was rescued by expression of STIM1-mCherry and ORAI1-mCherry.

188 ctive Orai1-V102C/A/G mutants independent of STIM1.

189 ial barrier function occurs independently of STIM1.

190 Extended molecules, indicative of STIM1, decorated the cytoplasmic surface of ER, bridged

191 ch actually caused significant inhibition of STIM1-mediated Orai currents.

192 channel activation may involve insertion of STIM1 into the PM.

193 We investigated the involvement of STIM1 in neutrophil chemotaxis in vitro, as well as duri

194 Pharmacological blockage or knockdown of STIM1 or ORAI1 reduced ENO-1-dependent migration of MDA-

195 ylation of TRPC1 was reduced by knockdown of STIM1.

196 Thus, KO of STIM1 impairs neutrophil contribution to psoriatic infla

197 The lack of STIM1 in T cells was associated with impaired activation

198 from Cmpt mice, endogenous protein levels of STIM1 and Orai1 were reduced, and consequently, SOCE aft

199 on without altering the expression levels of STIM1, Orai1, and TRPC1.

200 ,5]P2) levels, important for localization of STIM1 and E-Syts at ER-PM junctions, were reduced in RAS

201 naling and to track the cellular movement of STIM1 with mCherry and immunofluorescence in freshly iso

202 Hence, Pyk2-dependent phosphorylation of STIM1 at Y361 is a critical phospho-switch enabling recr

203 tein are responsible, with the major pool of STIM1 in the endoplasmic reticulum membrane regulating C

204 s constitutively associated with the pool of STIM1 in the plasma membrane.

205 annel activity required both the presence of STIM1 and the conserved Orai N-terminal portion.

206 The spatial properties of STIM1-dependent Ca(2+) signals determine restricted Ca(2

207 STIM1 with sigma1R slowed the recruitment of STIM1 to ER-PM junctions and reduced binding of STIM1 to

208 mechanisms regulating both up-regulation of STIM1 and PMCA4 and assessing how this up-regulation con

209 ork contributes to understanding the role of STIM1 and ORAI1 in the promotion of membrane ruffling by

210 To determine the mechanistic role of STIM1 in cardiac hypertrophy and during the transition t

211 However, the role of STIM1 in insulin-secreting beta-cells is unresolved.

212 ompared with control cells, thin sections of STIM1-transfected cells possessed far more ER elements,

213 d found that 2-APB enlarged the pore size of STIM1-activated Orai1 from 3.8 to 4.6 A.

214 r than alteration in the oligomeric state of STIM1-TM, prompts conformational changes in the cytosoli

215 A (PKA)-mediated phosphorylation of T389 of STIM1 is necessary for effective activation of the ARC c

216 CC3) domain of the cytoplasmic C terminus of STIM1.

217 interactions that control (i) transition of STIM1 from a quiescent to an active conformational state

218 These images offer dramatic, direct views of STIM1 aggregation and Orai1 clustering in store-depleted

219 esearch on calcium signaling has centered on STIM1, ORAI1, and a few proteins that directly modulate

220 , combined with previous studies focusing on STIM1, define distinct but cooperative functions for STI

221 a novel role for STIM1, where store-operated STIM1-TRPC1 interactions stimulate Galphaq/PLCbeta1/PKC

222 ovel role for STIM1, in which store-operated STIM1-TRPC1 interactions stimulate PLCbeta1 activity to

223 no store-operated Ca(2+) entry in control or STIM1 overexpressing ventricular myocytes.

224 and human sweat gland cells lacking ORAI1 or STIM1 expression.

225 re depletion and the loss of either TRPC1 or STIM1 led to DA cell death, which was prevented by inhib

226 those in KGM-H display enhancement of Orai1, STIM1, STIM2, and nuclear factor of activated T cells 1

227 intracellular pH (pHi) sensitivity of Orai1/STIM1 is not fully understood.

228 H155 is the intracellular pH sensor of Orai1/STIM1, the molecular mechanism of external pH sensitivit

229 is responsible for pHi sensitivity of Orai1/STIM1.

230 nents of CRAC channels (ORAI1, ORAI2, ORAI3, STIM1, STIM2) were expressed and most abundant during th

231 leading edge of cells, and that both phospho-STIM1 and ORAI1 co-localize with cortactin (CTTN), a reg

232 of membrane ruffling by showing that phospho-STIM1 localizes at the leading edge of cells, and that b

233 mouse lungs, expression of phosphodefective STIM1-Y361F mutant in ECs prevented the increase in vasc

234 y releasing a polybasic domain that promotes STIM1 recruitment to ER-PM junctions.

235 ts of the pathway are the regulatory protein STIM1, located in the endoplasmic reticulum (ER) membran

236 Orai channel and the Ca(2+)-sensing protein STIM1.

237 nt ARC channels are regulated by the protein STIM1, CRAC channels are regulated by STIM1 in the endop

238 JC formation required STIM1 expression but not store depletion, induced here b

239 TRPC1, Galphaq and PLCbeta1, which required STIM1 and TRPC1.

240 the endoplasmic reticulum (ER) Ca(2+) sensor STIM1 to Orai1, the pore-forming subunit of the Ca(2+) r

241 d by the endoplasmic reticulum Ca(2+) sensor STIM1.

242 he endoplasmic reticulum (ER) Ca(2+) sensor, STIM1, becomes activated when ER-stored Ca(2+) is deplet

243 and the endoplasmic reticulum Ca(2+) sensors STIM1 and STIM2.

244 dues within the cytoplasmic domain of STIM1 (STIM1-CT) that entail autoinhibition.

245 e normal in the absence of STIM2, suggesting STIM1 is the dominant calcium sensor required for classi

246 el in which STIM1-TM reorganization switches STIM1-CT into an extended conformation, thereby projecti

247 Effects of N-terminal and C-terminal STIM1 antibodies on TRPC1-based SOCs and STIM1 staining

248 n Orai1 connecting the peripheral C-terminal STIM1-binding site to the Orai1 core helices.

249 Here we report that an Orai1 C-terminal STIM1-binding site, situated far from the N-terminal por

250 l change in the inner core helices, and that STIM1 remotely gates the Orai1 channel without the neces

251 We conclude that STIM1 binding to phospholamban contributes to the regula

252 We demonstrate that STIM1 is required for chemotaxis because of multiple che

253 Here, we demonstrate that STIM1 is required for T cell-mediated immune regulation

254 Our findings demonstrate that STIM1, STIM2, and SOCE are dispensable for many critical

255 In this study we provide clear evidence that STIM1 has a cholesterol-binding domain located inside th

256 The model predicts that STIM1 dimers may be involved in crosslinking between Ora

257 The series of molecular rearrangements that STIM1 undergoes until final activation of Orai1 require

258 In conclusion, these studies reveal that STIM1 is a multifunctional regulator of Ca(2+) dynamics

259 M1 Immunoprecipitation studies revealed that STIM1 binds to nucleotide binding fold-1 (NBF1) of the s

260 The results of this study show that STIM1 and STIM2 differ in the ability to activate these

261 oresis and coimmunoprecipitation showed that STIM1 in the heart exists mainly as a large protein comp

262 Previous reports suggest that STIM1 may play a role in cardiac hypertrophy, but its ro

263 Our data further suggested that STIM1 promoted CRC cell migration through increasing the

264 This suggests that STIM1 is a multifunctional signaling effector that parti

265 A growing body of literature suggests that STIM1 plays a key role in the development of pathologica

266 The STIM1 protein regulates not only CRAC but also transient

267 um, whilst ARC channels are regulated by the STIM1 constitutively resident in the plasma membrane.

268 6 years after treatment discontinuation, the STIM1 study demonstrates that IM can safely be discontin

269 Here, we have investigated the STIM1-associated Ca(2+) signals in cardiomyocytes and th

270 apsigargin (2-10 microM) changed neither the STIM1 distribution pattern nor its mobilization rate, ev

271 structure and alters the conformation of the STIM1 C terminus, thereby releasing a polybasic domain t

272 CAD), and can promote the association of the STIM1 CAD with Orai1.

273 of Orai1 require the direct exposure of the STIM1 domain known as SOAR (Stim Orai Activating Region)

274 etion with subsequent oligomerization of the STIM1 ER-luminal domain, followed by its redistribution

275 In addition, blockage of the STIM1-Orai pathway effectively abolishes neurite outgrow

276 Here we reported that the STIM1 was overexpressed in colorectal cancer (CRC) patie

277 suggest that the Orai1 nexus transduces the STIM1-binding signal through a conformational change in

278 While the STIM1 and Orai1 binding interfaces have been mapped, sig

279 ncta and linear segments consistent with the STIM1 localizing to the junctional SR (jSR).

280 unique gain-of-function mutation within the STIM1 transmembrane domain (STIM1-TM), here we show that

281 Thus, STIM1 controls multiple aspects of T cell-mediated immun

282 (2+) signaling in the SR appear to be due to STIM1 binding to phospholamban and thereby indirectly ac

283 nel activity and associations between TRPC1, STIM1, Galphaq and PLCbeta1, which were inhibited by STI

284 Increased interaction between Cav1.3-TRPC1-STIM1 was observed upon store depletion and the loss of

285 vity in DA neurons is inhibited by the TRPC1-STIM1 complex.

286 R-A3 result from the expression of truncated STIM1.

287 increased Cav1.3 currents were observed upon STIM1 or TRPC1 silencing.

288 uires the influx of extracellular Ca(2+) via STIM1-dependent Ca(2+) release-activated Ca(2+)/Orai cha

289 Store depletion that activates TRPC1, via STIM1, inhibits the frequency and amplitude of the rhyth

290 ze-fracture electron microscopy to visualize STIM1 and Orai1 at endoplasmic reticulum (ER)-plasma mem

291 1 to ER-plasma membrane (PM) junctions where STIM1 stimulated opening of the Ca(2+)channel, Orai1.

292 alongside ER-plasma membrane junctions where STIM1, which regulates store-operated Ca(2+) entry, accu

293 perated activation of Imin channels, whereas STIM1 activation blocks this process.

294 These data support a model whereby STIM1 is critical to deactivate a key negative regulator

295 these findings, we propose a model in which STIM1-TM reorganization switches STIM1-CT into an extend

296 smic reticulum (ER), sigma1R associated with STIM1, the ER Ca(2+)sensor that regulates SOCE.

297 SPPL3 associates with STIM1 through at least two independent domains, the tran

298 hanged by store depletion, coexpression with STIM1, or an Orai1 mutation (L273D) affecting STIM1 asso

299 istically contribute to the interaction with STIM1 and couple STIM1 binding with channel gating and m

300 Q1 and STIM1 likely acts by interfering with STIM1 oligimerization and inhibits STIM1-Orai1 interacti

301 ithin the Orai N terminus that together with STIM1 maintained the typical CRAC channel hallmarks were