ライフサイエンスコーパス: STIM

1 STIM deficiency did not affect GC B cell proliferation a

2 STIM proteins are Ca(2+) sensors in the endoplasmic reti

3 STIM proteins are endoplasmic reticulum (ER) luminal Ca(

4 STIM proteins are known to mediate Ca(2+) store-sensing

5 STIM proteins are sensors of endoplasmic reticulum (ER)

6 STIM proteins contain an EF-hand in their N-termini that

7 STIM(EF)-expressing cells had normal ER Ca(2+) levels bu

8 STIM-mediated activation of NFAT was required for the ex

9 STIM/ORAI proteins mediate store-operated Ca(2+) entry (

10 r than the distance that can be spanned by a STIM-Orai complex, and STIM1 function should therefore n

11 efects induced by intestinal expression of a STIM-1 Ca(2+)-binding mutant, indicating that the protei

12 A multicenter observational study (A-STIM [According to Stop Imatinib]) evaluating MMR persis

13 at the three major classes of LCCBs activate STIM/ORAI-mediated Ca(2+) entry in VSMCs.

14 t following ER Ca2+ depletion, the activated STIM proteins shift the pattern of IP3R-mediated Ca2+ re

15 on generated sufficient tidal volumes in all STIM animals.

16 or both STIM isoforms we show that although STIM proteins are critical regulators of cell migration,

17 6 mumol L(-1) after 5:20 hrs between CMV and STIM; p < 0.0001), but not the lactate/pyruvate ratio.

18 Orai and STIM have been implicated in the growth and metastasis o

19 he signalling pathways regulated by Orai and STIM in normal and malignant cells, we expose discrepanc

20 More recently Orai and STIM proteins have been proposed to underlie the well-de

21 s little information on the role of Orai and STIM proteins in smooth muscle.

22 ding of the interacting partners of Orai and STIM proteins in the regulation of CRAC channel activity

23 Recently, Orai and STIM proteins were identified as the molecular identitie

24 ted Ca(2+) entry (SOCE) mediated by ORAI and STIM proteins.

25 of key Ca(2+) signalling components, such as STIM proteins and TRP channels.

26 effect involves functional crosstalk between STIM proteins and inositol 1,4,5-trisphosphate receptors

27 i is an essential intracellular link between STIM and the CRAC channel, an accessory protein in the p

28 The loss of both STIM proteins abrogates CRAC channel activity, drastical

29 sing breast cancer cells lacking one or both STIM isoforms we show that although STIM proteins are cr

30 renic nerves to mimic spontaneous breathing (STIM).

31 Antigen presenting BW(STIM) cells expressing human CD1d and CD80 were generate

32 ure of Orai mutants that mimic activation by STIM.

33 e-activated Ca(2+) (CRAC) channels formed by STIM and ORAI proteins is required for the thymic develo

34 t activation of CRAC current is initiated by STIM proteins, which sense ER Ca2+ levels through an EF-

35 activated Ca(2+) (CRAC) channels mediated by STIM and ORAI proteins is a fundamental signaling pathwa

36 ed calcium (Ca(2+)) entry (SOCE) mediated by STIM/Orai proteins is a ubiquitous pathway that controls

37 ruitment of Orai and TRPCs to lipid rafts by STIM, we develop the hypothesis that Orai:TRPC complexes

38 -operated Ca(2+) channel (SOCC) regulated by STIM-1.

39 endoplasmic reticulum (ER) Ca(2+) stores by STIM proteins and coupling to Orai1 channels is well und

40 channels that migrate and become tethered by STIM within the ER-PM junctions, where they mediate exce

41 LCCBs act on the STIM N terminus to cause STIM relocalization to junctions and subsequent ORAI act

42 that induce depletion of ER Ca(2+), causing STIM to activate ORAI.

43 terminal STIM1 antibody blocked constitutive STIM(EF)-mediated Ca(2+) entry, but only in cells expres

44 e that different agonists activate different STIM proteins to sustain Ca(2+) signals and downstream r

45 Panx1, including functions linked to diverse STIM-regulated cellular responses.

46 classical role in store-operated Ca2+ entry, STIM proteins shape the spatial dynamics of IP3R-mediate

47 coupling between endoplasmic reticulum (ER) STIM proteins and plasma membrane (PM) Orai channels, re

48 at organize ER-plasma membrane junctions for STIM-ORAI-dependent calcium signaling.

49 t studies have indicated a critical role for STIM (stromal interacting molecule) proteins in the regu

50 onless (AMN) associates with ORAIs and forms STIM/ORAI/AMN complexes after Ca(2+) store depletion.

51 lot study, followed soon after by the French STIM and Australasian TWISTER studies.

52 the independence of T cell development from STIM and Orai, despite compelling evidence that it requi

53 Hence, STIM N termini are powerful coupling modifiers, function

54 While the escape probability at high STIM:Orai expression ratios is <1%, it is significantly

55 ing on the open state of the channel and how STIM proteins may exert remote allosteric control of cha

56 But how STIM proteins bind to the channel periphery and remotely

57 This difference in STIM proteins was associated with distinct time courses

58 ease increased in CMV transiently whereas in STIM lactate dropped during this same time point (2.6 vs

59 However, the precise mechanisms involving STIM-dependent Ca(2+) signaling in the heart are not cle

60 ticulum stores, and a second phase involving STIM 1 (stromal interaction molecule 1) clustering and C

61 o cells, but little is known about how local STIM-ORAI signalling at junctions is coordinated with ov

62 Ist2 lysine-rich tail are found in mammalian STIM proteins that reversibly induce the formation of cE

63 1, and a few proteins that directly modulate STIM-ORAI function.

64 nts and have been found recently to modulate STIM-ORAI signalling.

65 Stromal interacting molecule (STIM) 1 acts as a sensor for the level of Ca(2+) stored

66 Stromal interacting molecule (STIM) and Orai proteins constitute the core machinery of

67 reticulum (ER) stromal-interacting molecule (STIM) Ca(2+) sensor proteins and the plasma membrane ORA

68 ed deletion of Stromal Interaction Molecule (STIM) 1 and STIM2 [double-knockout (DKO)] mice develop s

69 Stromal cell-interaction molecule (STIM) 1 and STIM2 serve as endoplasmic reticulum Ca(2+)

70 d activated by stromal interaction molecule (STIM) 1 and STIM2.

71 e activated by stromal interaction molecule (STIM) 1 and STIM2.

72 ervations, the stromal interaction molecule (STIM) 1 and the calcium release-activated calcium modula

73 domain in the stromal interaction molecule (STIM) 1 is distinct in that it is ordered in the monomer

74 Ca(2+) sensor stromal interaction molecule (STIM) 1.

75 Ca(2+) sensor stromal interaction molecule (STIM) 1.

76 Stromal interaction molecule (STIM) 2, but not STIM1, was arranged in puncta in restin

77 In T cells, stromal interaction molecule (STIM) and Orai are dispensable for conventional T cell d

78 ntification of stromal interaction molecule (STIM) and ORAI, two essential regulators of CRAC channel

79 Ca(2+)-sensing stromal interaction molecule (STIM) proteins are crucial Ca(2+) signal coordinators.

80 he Ca2+ sensor Stromal Interaction Molecule (STIM) proteins of the endoplasmic reticulum (ER).

81 nd mediated by stromal interaction molecule (STIM) proteins.

82 nding protein, stromal interaction molecule (STIM), plays an essential role in the activation of thes

83 nflux mediator stromal interaction molecule (STIM), the plasma membrane Ca(2+) pump plasma membrane C

84 is mediated by stromal interaction molecule (STIM), which senses the depletion of endoplasmic reticul

85 The stromal interaction molecule (STIM)-ORAI calcium release-activated calcium modulator (

86 d activated by stromal interaction molecule (STIM)1 and STIM2 in the endoplasmic reticulum.

87 Orai1 and stromal interaction molecule (STIM)1 are critical components of Ca(2+) release-activat

88 trate that the stromal interaction molecule (STIM)2, a calcium sensor, acts as a novel regulator of C

89 activated by stromal interaction molecules (STIM) 1 and 2 in response to depletion of endoplasmic re

90 activated by stromal interaction molecules (STIM) located in the endoplasmic reticulum (ER).

91 ct fragments operate independently of native STIM proteins.

92 vation, thereby identifying a model of NMDAR-STIM-Panx1 signaling in neurons.

93 This review focuses on novel STIM-dependent mechanisms for control of Ca(2+) signals

94 from this domain induces the aggregation of STIM to regions of the ER immediately adjacent to the pl

95 larify the mechanism and the contribution of STIM proteins to Ca(2+) oscillations in T-cells.

96 B cell-specific deletion of STIM proteins decreased the number of high-affinity B ce

97 not in DT40 STIM1 knock-out cells devoid of STIM(WT).

98 s of store-operated Ca2+ entry downstream of STIM.

99 However, the possible effects of STIM on other modes of receptor-activated Ca2+ entry hav

100 In PC2-defective cells, the interaction of STIM-1 with Orai channels is uncoupled, whereas coupling

101 ze or disrupt intramolecular interactions of STIM C termini, we show that the increased flexibility o

102 f cardiovascular remodeling, where levels of STIM and ORAI are elevated.

103 Current models emphasize the role of STIM located in the endoplasmic reticulum membrane, wher

104 e models, which reveal the essential role of STIM proteins in Ca(2+) homeostasis and their crucial ro

105 M1 knockout, demonstrating a central role of STIM/Orai-mediated calcium signaling.

106 is little or no information on the roles of STIM and Orai proteins in primary cells.

107 l discuss results pertaining to the roles of STIM and Orai proteins in smooth muscle Ca(2+) entry pat

108 the immune system, focusing on the roles of STIM and ORAI proteins in store-operated Ca(2+) entry.

109 tion of ER calcium triggers translocation of STIM proteins, which serve as calcium sensors in the ER,

110 In recent years, studies on STIM and Orai tissue-specific knockout mice and gain- an

111 ain-of-function approach with an optogenetic STIM lentivirus, we demonstrate that independent activat

112 se line drawings for 3s ('stimulus phase' or STIM).

113 n cancer is presently indisputable, how Orai-STIM-controlled Ca(2+) signals affect malignant transfor

114 Here, we review recent studies linking Orai-STIM Ca(2+) channels with cancer, with a particular focu

115 s physiological/pathological functions, Orai/STIM channels may be an important mediator for various p

116 rane Orai1-SNP leads to a mis-match in Orai1-STIM stoichiometry, resulting in inhibition of Ca2+ entr

117 rane Orai1-SNP leads to a mis-match in Orai1:STIM stoichiometry, resulting in inhibition of Ca2+ entr

118 In a recently discovered signaling process, STIM (stromal-interacting molecule) proteins sense a dro

119 lex and the microtubule cytoskeleton promote STIM 1 clustering at sites of plasma membrane apposition

120 The proteins STIM and ORAI were discovered through limited and genome

121 ling between two distinct membrane proteins, STIM and Orai.

122 We found that reduced STIM-mediated ER-plasma membrane contacts underlie presy

123 d directly by endoplasmic reticulum-resident STIM proteins to generate the Ca(2+)-selective, Ca(2+) r

124 volving endoplasmic reticulum Ca(2+) sensing STIM proteins and plasma membrane Orai1 channels, is a w

125 Upon store depletion, the ER Ca(2+)-sensing STIM proteins aggregate and gain extended conformations

126 Whereas ORAI1 activation by Ca(2+)-sensing STIM proteins is known, still obscure is how ORAI1 is tu

127 The endoplasmic reticulum Ca(2+)-sensing STIM proteins mediate Ca(2+) entry signals by coupling t

128 termembrane coupling with the Ca(2+)-sensing STIM proteins.

129 s mediated by the ubiquitous calcium-sensing STIM proteins.

130 E) by causing the ER localized Ca(2+) sensor STIM to unfurl domains that activate Orai channels in th

131 Both actions are mediated by the short STIM-Orai activating region (SOAR) of STIM1.

132 cal differences in the function of the short STIM-Orai-activating regions (SOAR) of STIM1 and STIM2.

133 The dimeric STIM1 protein contains a small STIM-Orai-activating region (SOAR)--the minimal sequence

134 terminants underlying activation of specific STIM isoforms, insights that are potentially useful for

135 was without detectable phenotype, the STIM1/STIM double-KO was perinatally lethal, revealing an esse

136 Targeted STIM deletion impairs calcium homeostasis, NFAT activati

137 entry into T cells and fibroblasts and that STIM proteins are required for the development and funct

138 Our results provide direct evidence that STIM-Orai complexes are trapped by their physical connec

139 ticity is indicated by the observations that STIM-1, the sensor of calcium concentration in stores, a

140 New studies reveal that STIM proteins - sensors of endoplasmic reticulum Ca(2+)

141 We reveal that STIM-Orai coupling is rapidly blocked by hypoxia and the

142 in Panx1 knockout (KO) neurons, we show that STIM recruitment couples Ca(2+) entry via NMDARs to Panx

143 Here, we showed that STIM-deficient B cells have reduced B cell competitivene

144 These findings suggest that STIM-mediated survival signals after antigen capture reg

145 Our study suggests that STIM proteins function as Ca(2+) store sensors in the si

146 Dissecting the STIM-Orai coupling process is restricted by the abstruse

147 Despite extensive sequence homology, the STIM proteins are functionally distinct.

148 o recent studies independently implicate the STIM protein family as essential components in this coup

149 pstream and downstream of Ca(2+) influx (the STIM/ORAI and calcineurin/NFAT pathways, respectively).

150 key role in SOCE activation and inhibits the STIM-dependent activation of AC6 by ER Ca(2+) depletion.

151 such entry, the recent identification of the STIM and Orai proteins has focused attention on the chan

152 LCCBs act on the STIM N terminus to cause STIM relocalization to junction

153 ER luminal Ca(2+) concentrations through the STIM proteins and facilitates import of the ion from the

154 multimerization is essential to unleash the STIM C-terminal binding site for Orai1 channels.

155 at LCCBs promote vascular remodeling through STIM-mediated activation of ORAI.

156 e this problem, we studied coupling by using STIM chimera and cytoplasmic C-terminal domains of STIM1

157 ore operated calcium entry (SOCE) likely via STIM/ORAI-based channels.

158 ORAI-1 GFP reporters are co-expressed with STIM-1 in the gonad and intestine.

159 to junctions solely through interaction with STIM proteins, while septins regulate the number of ER-P

160 d to as STIM1-Ctl) and for Cre(tg/-) without STIM deletion (referred to as Cre-Ctl).