ライフサイエンスコーパス: STIM1

1 STIM1 (stromal interaction molecule 1) is a calcium (Ca(

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

3 STIM1 also interacts with microtubule plus-end binding p

4 STIM1 and STIM2 are calcium-sensing molecules that link

5 STIM1 can associate with Orai in cardiac myocytes to pro

6 STIM1 effects were eliminated by either BTP2 or by coexp

7 STIM1 expression also increased spark rates and induced

8 STIM1 expression produced an increase in the amount of C

9 STIM1 interacts with the cochaperone BAG3 and localizes

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

11 STIM1 phosphorylation has been suggested to mediate this

12 STIM1 protein serves as one of the main calcium sensors

13 STIM1 translocates to the ER-plasma membrane (PM) juncti

14 STIM1-KD but not STIM1-Ctl or Cre-Ctl hearts exhibited a

15 STIM1-KD mice (N=23) exhibited poor survival compared wi

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

17 STIM1-mediated channel activation occurs through rotatio

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

19 STIM1/STIM2 chimeric constructs indicated that coordinat

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

21 lusters with stromal interaction molecule 1 (STIM1) and Ca2+-release-activated Ca2+ channel 1 (Orai1)

22 tion between stromal interaction molecule 1 (STIM1) and L-type Ca(2+) channels, and thus stronger STI

23 ing proteins stromal interaction molecule 1 (STIM1) and STIM2, which transition into an active confor

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

25 a(2+) sensor stromal interaction molecule 1 (STIM1) and the plasma membrane (PM) channel Orai1, is in

26 a(2+) sensor stromal interaction molecule 1 (STIM1) caused spontaneous activation of STING and enhanc

27 The stromal interaction molecule 1 (STIM1) has two important functions, Ca(2+) sensing withi

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

29 vel role for stromal interacting molecule 1 (STIM1) in regulating microtubule and subsequent ER remod

30 a(2+) sensor stromal interaction molecule 1 (STIM1) in response to store depletion triggered by stimu

31 Stromal interaction molecule 1 (STIM1) is a calcium sensor and regulatory protein locali

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

33 cium sensor, stromal interacting molecule 1 (STIM1) is necessary for growth cone steering toward the

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

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

36 mains of the stromal interaction molecule 1 (STIM1) to manipulate protein activity and faithfully rec

37 Ca2+ sensor stromal interaction molecule 1 (STIM1) triggers SOCE by forming punctate structures with

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

39 a(2+) sensor stromal interaction molecule 1 (STIM1) with the PMCA4b splice variant further enhanced N

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

41 eticulin and stromal interaction molecule 1 (STIM1), a protein of the SOCE machinery that leads to Ca

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

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

44 pitated with stromal interaction molecule 1 (STIM1), the Ca(2+) sensor SOC channel subunit in the ER.

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

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

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

48 is sensed by stromal interaction molecule 1 (STIM1).

49 of Orai1 and stromal interaction molecule 1 (STIM1).

50 ls formed by stromal interaction molecule 1 (STIM1)/Orai complexes, attenuates acinar cell pathology

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

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

53 nsors, stromal interaction molecule 1 and 2 (STIM1 and STIM2), in basophil activation.

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

55 This work delineates a STIM1-STING circuit that maintains the resting state of

56 ed SOCE to the level seen in control EC in a STIM1-dependent manner.

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

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

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

60 es L-type Ca(2+) channel current to activate STIM1, and betaAR activity extends the range along the s

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

62 Ca(2+)-induced Ca(2+) release and activates STIM1 feedback inhibition of L-type Ca(2+) channels.

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

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

65 ditional deletion of Orai1 (or its activator STIM1) in the brain.

66 ese gating checkpoints are required to allow STIM1 coupling and Orai1 pore opening.

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

68 1 suppresses Cav1.3 activity by providing an STIM1-based scaffold, which is essential for DA neuron s

69 tion in TRPC1/6-deficient (TRPC1/6(-/-)) and STIM1/2- deficient (STIM1/2(DeltapmLF)) primary murine l

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

71 ions between mutant calreticulin, ERp57, and STIM1 activated SOCE and generated spontaneous cytosolic

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

73 is essential for STIM1-STIM1 interaction and STIM1-Orai1 interaction and channel activation at a ER/P

74 ulum (ER)-plasma membrane (PM) junctions and STIM1 translocation to these junctions.

75 localizes to autophagosomes in mitosis, and STIM1 protein levels are reduced.

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

77 Ca(2+) (CRAC) channels encoded by Orai1 and STIM1 as a major route of Ca(2+) entry for driving susta

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

79 Brain-specific Orai1 and STIM1 knockout (KO) mice exhibited significantly stronge

80 oss-of-function (LOF) mutations in ORAI1 and STIM1 that abolish Ca(2+) influx cause a unique disease

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

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

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

84 n of the molecular SOCE components ORAI1 and STIM1.

85 RPC1/6 channels are not involved in SOCE and STIM1/2 deficiency resulted in decreased cell proliferat

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

87 Cas9 to generate STIM1(-/-), STIM2(-/-), and STIM1/2(-/-) knockouts in HEK293 and colorectal HCT116 c

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

89 ontrols for STIM1(flox/flox) (referred to as STIM1-Ctl) and for Cre(tg/-) without STIM deletion (refe

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

91 2+) signals, reflecting their enhanced basal STIM1-binding and heightened Ca(2+)-dependent inactivati

92 Because STIM1 binding to phospholamban increases sarcoplasmic re

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

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

95 ulation of spatially discordant alternans by STIM1.

96 els in the plasma membrane (PM) are gated by STIM1 at endoplasmic reticulum (ER)-PM junctions to effe

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

98 (i) increases comparable to those induced by STIM1 activation of Orai1.

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

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

101 KC phosphorylation of TRPC1 was inhibited by STIM1 shRNA.

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

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

104 E and KATP channel activity are regulated by STIM1.

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

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

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

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

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

110 hobic cleft yielded constitutively clustered STIM1, which was associated with activation of Ca(2+) en

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

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

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

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

115 that, in response to multiple guidance cues, STIM1 couples microtubule organization and ER-derived ca

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

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

118 IP3R function in combination with defective STIM1-mediated SOC channel activation, while Ca2+ store

119 cient (TRPC1/6(-/-)) and STIM1/2- deficient (STIM1/2(DeltapmLF)) primary murine lung fibroblasts (pmL

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

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

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

123 ate the structural properties distinguishing STIM1 and STIM2 activation of ORAI1 channels under nativ

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

125 te the number of ER-PM junctions and enhance STIM1-ORAI1 interactions within junctions.

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

127 )(/-) (STIM1-KD) and littermate controls for STIM1(flox/flox) (referred to as STIM1-Ctl) and for Cre(

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

129 of the ER/PM junctions that is essential for STIM1-STIM1 interaction and STIM1-Orai1 interaction and

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

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

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

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

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

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

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

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

138 itions, here we used CRISPR/Cas9 to generate STIM1(-/-), STIM2(-/-), and STIM1/2(-/-) knockouts in HE

139 Although structurally homologous, STIM1 and STIM2 generate distinct Ca(2+) signatures in r

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

141 However, STIM1 is also required for growth cone steering away fro

142 However, STIM1 variants with enhanced flexibility in the C termin

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

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

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

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

147 As expected, SOCE was decreased in STIM1/2- deficient pmLF and ROCE was decreased in TRPC1/

148 Furthermore, deficiency in STIM1 strongly enhanced the expression of type I interfe

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

150 No PMCA4 splice variant dependence in STIM1 association was observed, whereas partner of STIM1

151 increased AP duration (APD) heterogeneity in STIM1-KD.

152 Early mortality in STIM1-KD mice is likely related to enhanced susceptibili

153 a spatially discordant alternans profile in STIM1-KD hearts.

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

155 in TRPC1/6(-/-) pmLF and ROCE was similar in STIM1/2-deficient pmLF compared to Wt cells.

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

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

158 al (AP) mapping ex vivo in tamoxifen-induced STIM1(flox/flox)-Cre(tg)(/-) (STIM1-KD) and littermate c

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

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

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

162 Inducible myocyte-restricted STIM1-KD (STIM1 knockdown) was achieved in adult mice using an alp

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

164 ER membrane, and coexpression of full-length STIM1 or a STING-interacting fragment of STIM1 suppresse

165 ion was sufficient to stabilize the luminal STIM1 complex.

166 a(2+)-dependent conformations of the luminal STIM1 domain upon activation.

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

168 Mechanistically, STIM1 associated with STING to retain it in the ER membr

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

170 s regulated by stromal interaction molecules STIM1 and STIM2 within endoplasmic reticulum (ER)-plasma

171 Stromal interaction molecules (STIM1, 2) are acting as sensors for Ca(2+) in intracellu

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

173 approaches, including a nonphosphorylatable STIM1 knock-in mouse, that STIM1 phosphorylation is not

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

175 stimulated with IL-3, loss of STIM2, but not STIM1, reduced basophil IL-4 production.

176 STIM1-KD but not STIM1-Ctl or Cre-Ctl hearts exhibited a proclivity for a

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

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

179 Stimulation evokes numerous STIM1-Orai1 clusters but whether distinct signal transdu

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

181 Tc1 and c3) were decreased after ablation of STIM1/2 proteins in pmLF.

182 In the absence of STIM1/STIM2 in Treg cells, mice develop a broad spectrum

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

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

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

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

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

188 Replacing the PIP(2)-binding domain of STIM1 with that of STIM2 eliminated the requirement of S

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

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

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

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

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

194 gth STIM1 or a STING-interacting fragment of STIM1 suppressed the function of dominant STING mutants

195 um release, suggesting multiple functions of STIM1 within growth cones (Mitchell et al., 2012).

196 ial barrier function occurs independently of STIM1.

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

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

199 ylation of TRPC1 was reduced by knockdown of STIM1.

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

201 ,5]P2) levels, important for localization of STIM1 and E-Syts at ER-PM junctions, were reduced in RAS

202 We found that loss of STIM1, but not STIM2, impaired basophil IL-4 production

203 basis of our results, we present a model of STIM1 Ca(2+) binding and refine the currently known init

204 Variations in the number of STIM1-Orai1 clusters and Ca(2+) flux through them regula

205 ave different requirements for the number of STIM1-Orai1 clusters and on the Ca(2+) flux through them

206 association was observed, whereas partner of STIM1 (POST) preferentially associated with PMCA4b over

207 grator 2 (BIN2) as an interaction partner of STIM1 and IP3R in platelets.

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

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

210 Transcriptional profiling of STIM1/STIM2-deficient Treg cells reveals that Ca(2+) sig

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

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

213 trate that TRIC-A is a negative regulator of STIM1/Orai1 function.

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

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

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

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

218 refine the currently known initial steps of STIM1 activation on a molecular level.

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

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

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

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

223 e show by super-resolution imaging of ORAI1, STIM1, and septin 4 in living cells that septins facilit

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

225 store-operated Ca(2+) entry (SOCE) and ORAI1-STIM1 clustering in Jurkat T cells.

226 We report that STIM2 recruitment of Orai1/STIM1 to ER-PM junctions in response to depletion of ER-

227 ession had relatively little effect on Orai1/STIM1 clustering or local and global [Ca(2+)](i) increas

228 MCs) and rodent PaSCs, indicating that Orai1/STIM1 channels participate in the inflammatory responses

229 In outline, STIM1 senses an ER-luminal calcium decrease, relocalizes

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

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

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

233 core Ca(2+) signaling proteins: Orai1, PMCA, STIM1, IP(3) receptors, and SERCA2 at the ER/PM junction

234 duced in mitosis, thus physically preventing STIM1 and Orai1 from interacting to activate SOCE.

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

236 the activation of the Ca(2+)-sensor protein STIM1 upon Ca(2+) store depletion of the endoplasmic ret

237 protein activity and faithfully recapitulate STIM1-mediated signaling events.

238 nant isoform of E-Syt2 in T cells, recruited STIM1 to the junctions via a direct interaction.

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

240 nduced promotion of VSMC remodeling requires STIM1, which is up-regulated in VSMCs from hypertensive

241 fter only 8-days of cardiomyocyte-restricted STIM1-KD.

242 Inducible myocyte-restricted STIM1-KD (STIM1 knockdown) was achieved in adult mice us

243 ns, are the sites where the ER Ca(2+) sensor STIM1 and the PM Ca(2+) influx channel Orai1 cluster.

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

245 ed by the endoplasmic reticulum (ER) sensors STIM1 and STIM2.

246 Similarly, basophil-specific STIM1 expression was required for IgE-driven chronic all

247 ne model with inducible and myocyte-specific STIM1 depletion, we demonstrate for the first time the r

248 nd L-type Ca(2+) channels, and thus stronger STIM1 inhibition of these channels.

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

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

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

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

253 oxifen-induced STIM1(flox/flox)-Cre(tg)(/-) (STIM1-KD) and littermate controls for STIM1(flox/flox) (

254 s often considered to be less important than STIM1.

255 ciates with EB1/EB3 in growth cones and that STIM1 expression is critical for microtubule recruitment

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

257 t did not directly test, the hypothesis that STIM1-mediated Orai1 pore opening is accompanied by a gl

258 These data indicate that STIM1 and STIM2 have differential roles in the productio

259 nphosphorylatable STIM1 knock-in mouse, that STIM1 phosphorylation is not required for SOCE inhibitio

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

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

262 Here, we show that STIM1 associates with EB1/EB3 in growth cones and that S

263 We show that STIM1, an activator of store-operated calcium entry, reg

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

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

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

267 The STIM1-microtubule-ER interaction provides a new model fo

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

269 m-store depletion, and particularly into the STIM1 conformational change that is the basis for commun

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

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

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

273 e (PM) junctions and impairs assembly of the STIM1/Orai1 complex, causing a decrease in Orai1-mediate

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

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

276 However, in contrast to STIM1, STIM1DeltaK induced less NFAT1 activation and att

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

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

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

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

281 (by 80%, P<0.05) in VT/VF(+) versus VT/VF(-) STIM1-KD hearts.

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

283 Here, we show that Ca(2+) influx via STIM1/Orai1 calcium channels, which cluster near FAs, le

284 robe further the mechanisms whereby SOCE via STIM1/Orai complexes contributes to the disease in pancr

285 Using CM4620, we show that SOCE via STIM1/Orai complexes promotes activation and fibroinflam

286 Using CM4620, we show that SOCE via STIM1/Orai complexes promotes neutrophil oxidative burst

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

288 1 to ER-plasma membrane (PM) junctions where STIM1 stimulated opening of the Ca(2+)channel, Orai1.

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

290 signals, thereby providing a mechanism where STIM1-mediated ER remodeling, particularly in filopodia,

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

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

293 he calcium-dependent guidance cue BDNF, with STIM1 functioning to sustain calcium signals through sto

294 articularly when PMCA4b was coexpressed with STIM1.

295 Thus septins communicate with STIM1 and ORAI1 through protein or lipid intermediaries,

296 When compared with STIM1, STIM2 is a weak activator of Orai1, but it has be

297 (N=23) exhibited poor survival compared with STIM1-Ctl (N=22) and Cre-Ctl (N=11) with >50% mortality

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

299 suggest that in the ER, PMP22 interacts with STIM1 and increases Ca(2+) influx through SOC channels.

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