ライフサイエンスコーパス: STIM2

1 eveals direct interactions between STIM1 and STIM2.

2 -depletion-mediated Ca(2+) influx, STIM1 and STIM2.

3 way is controlled by the ER resident protein STIM2.

4 max channels are activated by both STIM1 and STIM2.

5 doplasmic reticulum Ca(2+) sensors STIM1 and STIM2.

6 -Orai-activating regions (SOAR) of STIM1 and STIM2.

7 essential role of STIM1 partially rescued by STIM2.

8 by stromal interaction molecule (STIM) 1 and STIM2.

9 by stromal interaction molecule (STIM) 1 and STIM2.

10 ceptor-mediated depletion of ER Ca2+ stores, STIM2 activated Ca2+ influx upon smaller decreases in ER

11 In the absence of STIM1 and STIM2, acute viral infections became chronic.

12 +) entry is mediated initially by endogenous STIM2 and incrementally by STIM1, enabling differential

13 Changes in the ratio between active STIM2 and STIM1 proteins can switch the regulation of Im

14 gene expression through recruitment of both STIM2 and STIM1.

15 new data about cross-talk between STIM1 and STIM2 and their different roles in store-operated channe

16 Together, our data indicate that STIM1, STIM2, and CRAC channel function play distinct but syner

17 n KGM-H display enhancement of Orai1, STIM1, STIM2, and nuclear factor of activated T cells 1 (NFAT1)

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

19 phology, in part due to its association with STIM2, and that modulation of EB3 expression is a potent

20 generate smooth muscle (sm)-targeted STIM1-, STIM2-, and double STIM1/STIM2-knockout (KO) mouse model

21 STIM1 and STIM2 are calcium-sensing molecules that link calcium de

22 STIM1 and STIM2 are dynamic transmembrane endoplasmic reticulum Ca

23 STIM1 and STIM2 are widely expressed endoplasmic reticulum (ER) Ca

24 mal interaction molecules 1 and 2 (STIM1 and STIM2) are key modulators of store-operated calcium entr

25 Stromal interaction molecules (STIM1 and STIM2) are single pass transmembrane proteins located ma

26 kdown approach, we identified both STIM1 and STIM2 as important mediators of SOCE and SOC current, an

27 lators of basal Ca2+ concentration and found STIM2 as the strongest positive regulator.

28 Our study places STIM2 at the center of a feedback module that keeps basa

29 43-amino-acid STIM1 N terminus with that of STIM2 attenuates Orai1-mediated Ca(2+) entry and drastic

30 ver, neutrophil cytokine production required STIM2, but not STIM1, at least in part as a result of re

31 Molecular silencing of STIM2 by siRNA or inhibition by G418 suppresses store-op

32 Independent of store depletion, STIM2 colocalizes with and blocks the function of a STIM

33 -terminal random coil sequences of STIM1 and STIM2 confer profoundly different activation properties.

34 Here we report that while both STIM1 and STIM2 contribute to store-refilling during Ca(2+) oscill

35 onclude that a reciprocal shift in TRPC1 and STIM2 contributes to Ca(2+) remodeling and tumor feature

36 and CaM regulation, which indicates that the STIM2/CRACM1 complex may be under the control of both lu

37 is a highly specific and potent inhibitor of STIM2-dependent CRAC channel activation.

38 suggest EVP4593 and other inhibitors of the STIM2-dependent nSOC pathway as promising leads for HD t

39 , contributes to synaptotoxic enhancement of STIM2-dependent store-operated calcium (SOC) entry.

40 scued loss of mushroom spines resulting from STIM2 depletion.

41 he results of this study show that STIM1 and STIM2 differ in the ability to activate these store-oper

42 of Stromal Interaction Molecule (STIM) 1 and STIM2 [double-knockout (DKO)] mice develop spontaneous a

43 tional S1ct-Orai1 coupling occurred in STIM1/STIM2(-/-) DT40 chicken B cells, indicating ct fragments

44 e-Pro aminoacid motif and that disruption of STIM2-EB3 interaction resulted in loss of mushroom spine

45 ucine-replacement of this crucial residue in STIM2 endows it with partial agonist properties, which m

46 We discovered that STIM2 expression is elevated in aged YAC128 striatal cul

47 We showed that STIM2 forms an endoplasmic reticulum (ER) Ca(2+) -depend

48 Conditional deletion of Stim1 and Stim2 genes in T cells abolished SOCE and strongly reduc

49 mice with conditional deletion of Stim1 and Stim2 genes, and therefore complete inhibition of SOCE,

50 ux, whereas deficiency in the calcium sensor STIM2 had a smaller effect.

51 However, T cells lacking either STIM1 or STIM2 had much less cytokine production and nuclear tran

52 Here we reveal that STIM2 has two distinct modes of activating CRAC channels

53 D8+ T cells required expression of STIM1 and STIM2 in CD4+ T cells.

54 inct but cooperative functions for STIM1 and STIM2 in modulating neutrophil bactericidal and cytokine

55 tim1 and/or Stim2 to investigate the role of STIM2 in neutrophil activation.

56 onditional deletion of Stim1 and its homolog Stim2 in T cells, we determined that both components are

57 by stromal interaction molecule (STIM)1 and STIM2 in the endoplasmic reticulum.

58 tiated by calcium sensor proteins, STIM1 and STIM2, in the endoplasmic reticulum [3].

59 Only a few studies have recorded STIM2-induced CRAC (calcium release-activated calcium) c

60 The close STIM1 homologue, STIM2, inhibited SOCE when expressed alone but coexpress

61 M1 is a required mediator of SOC activation, STIM2 is a powerful inhibitor of this process, interferi

62 We reveal that STIM2 is a powerful SOC inhibitor when expressed in HEK2

63 STIM2 is activated by changes in endoplasmic reticulum c

64 hannels, but it has remained unclear whether STIM2 is capable of regulating store-operated non-CRAC c

65 xpressed in both the ER and plasma membrane, STIM2 is expressed only intracellularly.

66 omal interacting molecule 1 (STIM1), whereas STIM2 is mainly confined to the outer plexiform and RGC

67 Thus, STIM2 is preferentially activated by low-level physiolog

68 vation has been established, the function of STIM2 is unknown.

69 In addition, STIM2 knockdown decreases SOCE and Ca(2+) store content

70 m)-targeted STIM1-, STIM2-, and double STIM1/STIM2-knockout (KO) mouse models, which reveal the essen

71 While sm-STIM2-KO was without detectable phenotype, the STIM1/STI

72 STIM2, like STIM1, caused Ca2+ influx via activation of

73 These data suggest that loss of STIM2 may underlie Ca(2+) store depletion and apoptosis

74 stabilization of mushroom spines depends on STIM2-mediated neuronal store-operated calcium influx (n

75 We demonstrate that STIM2-nSOC-CaMKII pathway is compromised in KI neurons,

76 Our results identify STIM2-nSOC-CaMKII synaptic maintenance pathway as a nove

77 Knockdown of STIM1, STIM2 or Orai1 decreased resting Ca(2+) levels.

78 Knockdown of Stim1, Stim2, or Orai1 inhibited EC proliferation and caused ce

79 ic VSMC proliferation and migration, whereas STIM2, Orai2, and Orai3 knockdown had no effect.

80 STIM2 overexpression failed to restore mushroom dendriti

81 ctive activation of native STIM2 proteins or STIM2 overexpression results in store-operated activatio

82 We conclude that both STIM1 and STIM2 promote store-operated Ca2+ entry into T cells and

83 7]; however, the role of the closely related STIM2 protein remains undetermined.

84 In contrast, STIM2 protein was nearly depleted in tumor cells.

85 nSOC) in hippocampal neurons is regulated by STIM2 protein.

86 sporadic AD brains due to downregulation of STIM2 protein.

87 previously unreported link between STIM1 and STIM2 proteins and pSS.

88 Thus, deficiency of STIM1 and STIM2 proteins in T cells, and consequent defects in Ca(

89 HEK293 cells, selective activation of native STIM2 proteins or STIM2 overexpression results in store-

90 nstrated significant reductions in STIM1 and STIM2 proteins.

91 Knockdown of PKCdelta with siRNA increased STIM2 punctum formation and enhanced basal calcium entry

92 nce for the existence of endogenous non-CRAC STIM2-regulated channels.

93 d in pathology, but available data on native STIM2-regulated plasma membrane channels are scarce.

94 endoplasmic reticulum (ER), the function of STIM2 remains unclear.

95 We further establish that overexpression of STIM2 rescues synaptic nSOC, CaMKII activity, and mushro

96 T cell-specific ablation of both STIM1 and STIM2 resulted in a notable lymphoproliferative phenotyp

97 igonucleotides or knock-down or knock-out of STIM2 resulted in normalization of nSOC and rescue of sp

98 We demonstrate that loss of STIM2 results in decreased SOCE, particularly at lower d

99 In vivo loss of STIM2 results in lower cytokine levels and protection fr

100 cytoplasmic C-terminal domains of STIM1 and STIM2 (S1ct and S2ct) and identifying a fundamental acti

101 STIM1 and STIM2 sense the depletion of ER Ca(2+) stores, whereas O

102 independent of ER Ca(2+) stores or STIM1 and STIM2 sensors and uncoupled from Ca(2+)-ATPase activity

103 romal cell-interaction molecule (STIM) 1 and STIM2 serve as endoplasmic reticulum Ca(2+) sensors that

104 deletion of Orai1 (Orai1K14Cre) or Stim1 and Stim2 (Stim1/2K14Cre) failed to sweat despite normal swe

105 The opposing functions of STIM1 and STIM2 suggest they may play a coordinated role in contro

106 nd phagocytosis are normal in the absence of STIM2, suggesting STIM1 is the dominant calcium sensor r

107 Conversely, the 55-amino-acid STIM2 terminus substituted within STIM1 strikingly enhan

108 show that, surprisingly, it is STIM1 and not STIM2 that is exclusively involved in calcium entry duri

109 a novel bimodal control of CRAC channels by STIM2, the store dependence and CaM regulation, which in

110 powerful coupling modifiers, functioning in STIM2 to "brake" the otherwise constitutive activation o

111 ce with conditional ablation of Stim1 and/or Stim2 to investigate the role of STIM2 in neutrophil act

112 istribution of STIM1 into distinct "puncta." STIM2 translocates into puncta upon store depletion only

113 ted channels; Imin channels are regulated by STIM2, TRPC3-containing INS channels are induced by STIM

114 Early during infection, STIM1 and STIM2 were required for the differentiation of naive CD8

115 CD4+ T cells lacking STIM1 and STIM2 were unable to provide "help" to CD8+ T cells due

116 f CRAC channels (ORAI1, ORAI2, ORAI3, STIM1, STIM2) were expressed and most abundant during the matur

117 uble labeling shows coincidence of STIM1 and STIM2 within puncta, and immunoprecipitation reveals dir