ライフサイエンスコーパス: CRACM1

1 le interaction of STIM1-mRFP and AcGFP-Orai1/CRACM1.

2 membrane (PM)-localized Ca2+ channel, Orai1/CRACM1.

3 um channels are functional in the absence of CRACM1.

4 CRACM1, -2, and -3 mRNA transcripts and CRACM1 and -2 pr

5 release-activated Ca(2+) channels (Orai1-3, CRACM1-3) in the plasma membrane.

6 We characterized the human ortholog of CRACM1, a plasma membrane-resident protein encoded by ge

7 CRACM1 (also called Orai1) constitutes the pore subunit

8 m release-activated calcium (CRAC) modulator CRACM1 (also known as Orai1) in the plasma membrane have

9 CRACM1, -2, and -3 mRNA transcripts and CRACM1 and -2 proteins were detectable in HLMCs.

10 A secondary patch-clamp screen identified CRACM1 and CRACM2 (CRAC modulators 1 and 2) as modulator

11 ith STIM1 and activated via store depletion, CRACM1 and CRACM2 are facilitated at low 2-APB concentra

12 st for CRACM3 and a potentiating agonist for CRACM1 and CRACM2 following store-operated and STIM1-dep

13 oglobulin E receptors causes much less Orai1/CRACM1 and STIM1 association, but strong interaction is

14 (2+) sensor in endoplasmic reticulum, Orai1 (CRACM1) as a plasma membrane channel that is activated b

15 oplasmic reticulum Ca2+ sensor, and ORAI1 or CRACM1--both of which may function as I(crac) channels o

16 The inhibition of CRACM1 channels by high concentrations of 2-APB appears

17 M regulation, which indicates that the STIM2/CRACM1 complex may be under the control of both luminal

18 nsmembrane (TM) and extracellular domains of CRACM1 contribute to the ionic selectivity of the CRAC-c

19 CRACM1 could be the CRAC channel itself, a subunit of it

20 riments with the three CRAC channel subtypes CRACM1, CRACM2 and CRACM3 have indicated that they might

21 ding site in the first extracellular loop of CRACM1 (D110/112A) enhances monovalent cation permeation

22 Here we generated CRACM1-deficient mice in which beta-galactosidase activi

23 Mast cells derived from CRACM1-deficient mice showed grossly defective degranula

24 CRACM1-deficient mice were smaller in size.

25 reactions elicited in vivo were inhibited in CRACM1-deficient mice.

26 influx and development and proliferation of CRACM1-deficient T cells was unaffected.

27 Mutations in CRACM1 determine the selectivity of CRAC currents, demon

28 Although overexpression of CRACM1 did not affect CRAC currents, RNAi-mediated knock

29 A nonconducting mutation of CRACM1 (E106Q) acts as a dominant negative for all three

30 We detected robust CRACM1 expression in skeletal muscles and some regions o

31 which beta-galactosidase activity 'reported' CRACM1 expression.

32 We show here that CRACM1 forms multimeric assemblies that bind STIM1 and t

33 ctivity of CRAC currents, demonstrating that CRACM1 forms the CRAC channel's ion-selective pore, but

34 e CRAC channel's ion-selective pore, but the CRACM1 homologs CRACM2 and CRACM3 are less well characte

35 pore (E106D and E190A) enable 2-APB to gate CRACM1 in a STIM1-independent manner, suggesting that 2-

36 STIM1 in the endoplasmic reticulum and CRACM1 in the plasma membrane are essential molecular co

37 Here, we show that STIM1 and CRACM1 interact functionally.

38 A point mutation in the gene encoding CRACM1 is associated with severe combined immunodeficien

39 Thus, CRACM1 is crucial in mouse mast cell effector function,

40 self is completely unresponsive to 2-APB and CRACM1 is only very weakly activated.

41 plasma membrane junctions that contain Orai1/CRACM1, labeled with monomeric Aequorea coerulescens gre

42 lum (ER), and calcium channel subunit (Orai1/CRACM1), localized to the plasma membrane.

43 ually limit store-operated currents and that CRACM1 may be the long-sought CRAC channel.

44 Our data provide unequivocal evidence that CRACM1 multimers form the Ca(2+)-selective CRAC-channel

45 tentiates I(CRAC), suggesting that STIM1 and CRACM1 mutually limit store-operated currents and that C

46 STIM1 and CRACM1 (or Orai1) are essential molecular components med

47 d STIM1 as the putative ER Ca(2+) sensor and CRACM1 (Orai1; ) as the putative store-operated Ca(2+) c

48 amino acids in the selectivity filter of the CRACM1 pore (E106D and E190A) enable 2-APB to gate CRACM

49 CRACM1 proteins multimerize and bind STIM1, and the comb

50 and the combined overexpression of STIM1 and CRACM1 reconstitutes amplified CRAC currents.

51 el and an additional uncoupling of STIM1 and CRACM1, since the compound reversed the store-dependent

52 residues in the cytoplasmic segment of Orai1/CRACM1, suggesting a role for electrostatic interactions

53 lecular interactions between STIM1 and Orai1/CRACM1 that depend quantitatively on electrostatic inter

54 ortant molecular components of SOC channels, CRACM1 (the pore-forming subunit) and STIM1 (the sensor

55 via these residues in the coupling of Orai1/CRACM1 to STIM1.

56 te in position 106 of the first TM domain of CRACM1 with glutamine (E106Q) acts as a dominant-negativ