ライフサイエンスコーパス: Ca2 induced Ca2 release

1 ow propose to be an amplification mechanism (Ca2+-induced Ca2+ release).

2 (NCX) could enhance Ca2+ influx via NCX (and Ca2+-induced Ca2+ release).

3 eart rates, which may contribute to enhanced Ca2+-induced Ca2+ release.

4 cement of Ca2+ signalling via the process of Ca2+-induced Ca2+ release.

5 trinsically unstable regenerative process of Ca2+-induced Ca2+ release.

6 with an intrinsically higher sensitivity to Ca2+-induced Ca2+ release.

7 lude IP3-dependent and voltage-dependent and Ca2+-induced Ca2+ release.

8 ase in [Ca2+]i may, however, be amplified by Ca2+-induced Ca2+ release.

9 suggest that palmitoyl-CoA may be needed for Ca2+-induced Ca2+ release.

10 ve evolved in parallel with the mechanism of Ca2+-induced Ca2+ release.

11 se ventricular myocytes and are activated on Ca2+ -induced Ca2+ release.

12 this model are compared with those based on Ca2+(-)induced Ca2+ release alone in the bullfrog sympat

13 The Ca2+-induced Ca2+ release amplification factor or gain (

14 synaptic responses, and a transition between Ca2+ -induced Ca2+ release and inositol trisphosphate wa

15 has been developed and its significance for Ca2+(-)induced Ca2+ release and Ca2+ oscillations invest

16 Ca2+ from the ryanodine-sensitive store via Ca2+-induced Ca2+ release, and that depolarization-induc

17 Calcium (Ca2+)-induced Ca2+ release (CICR) in cardiac myocytes ex

18 ction pathway responsible for cAMP-dependent Ca2+-induced Ca2+ release (CICR) from endoplasmic reticu

19 Ca2+-induced Ca2+ release (CICR) from intracellular stor

20 se-fire" model that mimics the properties of Ca2+-induced Ca2+ release (CICR) from isolated sites is

21 ition, we tested the hypothesis that altered Ca2+-induced Ca2+ release (CICR) from ryanodine receptor

22 ed ryanodine receptor type 2 (RyR2)-mediated Ca2+-induced Ca2+ release (CICR) from SR membranes (IC50

23 e-mode Na+-Ca2+ exchange (NCX) in activating Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic r

24 r the graded nature and early termination of Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic r

25 nous cADPR increases the Ca2+ sensitivity of Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic r

26 -adrenergic receptor (betaAR) stimulation of Ca2+-induced Ca2+ release (CICR) in cardiac myocytes.

27 ed [Ca2+]i increases, providing evidence for Ca2+-induced Ca2+ release (CICR) in rods and cones.

28 The effects of modulating Ca2+-induced Ca2+ release (CICR) in single cardiac myocy

29 Ca2+-induced Ca2+ release (CICR) is a well characterized

30 confocal microscopy to provide evidence that Ca2+-induced Ca2+ release (CICR) may contribute to the m

31 Ca2+-induced Ca2+ release (CICR) plays an important role

32 art, to Ca2+ discharge from an intracellular Ca2+-induced Ca2+ release (CICR) pool.

33 ctionally related: they reflect a process of Ca2+-induced Ca2+ release (CICR) that requires activatio

34 The contribution of Ca2+-induced Ca2+ release (CICR) to trigger muscle contr

35 e cytosolic [Ca2+] reached the threshold for Ca2+-induced Ca2+ release (CICR) was able to simulate ea

36 Alternatively, Ca2+-induced Ca2+ release (CICR) was triggered by a rapi

37 IP3Rs display Ca2+-induced Ca2+ release (CICR), but are grouped in clu

38 the inward Ca2+ current (ICa) gives rise to Ca2+-induced Ca2+ release (CICR), the amplifying Ca2+ si

39 n beta-cells indicate that GLP-1 facilitates Ca2+-induced Ca2+ release (CICR), whereby mobilization o

40 depends on the positive feedback process of Ca2+-induced Ca2+ release (CICR).

41 ryanodine receptors (RyRs) in the process of Ca2+-induced Ca2+ release (CICR).

42 discussed with respect to the properties of Ca2+-induced Ca2+-release (CICR) and the local control t

43 ine receptors (RyRs) and release of Ca2+ via Ca2+-induced Ca2+ release(CICR).

44 t Ca2+ release, VDCR) and Ca2+ influx-gated (Ca2+-induced Ca2+ release, CICR) sarcoplasmic reticulum

45 Our results suggest that Ca2+-induced Ca2+ release contributes little to the elev

46 closure approach to study the restitution of Ca2+-induced Ca2+ release during simulated two-pulse vol

47 tage-dependent Ca2+ channels and followed by Ca2+ -induced Ca2+ release from the endoplasmic reticulu

48 gh plasma membrane Ca2+ channels, as well as Ca2+-induced Ca2+ release from cytoplasmic stores.

49 Activation of Ca2+-induced Ca2+ release from internal stores with a gr

50 ors, voltage-dependent calcium channels, and Ca2+-induced Ca2+ release from internal stores.

51 Ca2+-induced Ca2+ release from presynaptic endoplasmic r

52 reverse Na+-Ca2+ exchange, and the resulting Ca2+-induced Ca2+ release from SR.

53 phosphorylation as a homeostatic response by Ca2+-induced Ca2+ release from the ER.

54 m is required to counteract the regenerative Ca2+-induced Ca2+ release from the sarcoplasmic reticulu

55 action and that the contractions depended on Ca2+-induced Ca2+ release from the sarcoplasmic reticulu

56 xtracellular Ca2+ or on the classic model of Ca2+ -induced Ca2+ release in cardiac myocytes.

57 s that accurately represent local control of Ca2+-induced Ca2+ release in cardiac myocytes can reprod

58 ensity approach to modeling local control of Ca2+-induced Ca2+ release in cardiac myocytes, where we

59 ort that 2-aminoethoxydiphenyl borate blocks Ca2+-induced Ca2+ release in isolated, non-synaptosomal

60 hyperpolarization and arterial dilation via Ca2+-induced Ca2+ release in response to an endothelial-

61 ing enhances SR release channel activity and Ca2+-induced Ca2+ release in TG4 cardiac myocytes, and t

62 dence validating the local control theory of Ca2+-induced Ca2+ release in the heart.

63 ulator of ryanodine receptors also amplified Ca2+-induced Ca2+ release in these neurons.

64 d the model is inconsistent with the data if Ca2+-induced Ca2+ release is a dominating factor.

65 Ca2+-induced Ca2+ release is a general mechanism that mo

66 We find that Ca2+-induced Ca2+ release is not necessary to explain th

67 try across the plasma membrane (50%) whereas Ca2+-induced Ca2+ release is the major contributor to Ca

68 g and release functions and destabilizes the Ca2+-induced Ca2+ release mechanism by reducing the effe

69 zed Ca2+ influx via L-type Ca2+ channels and Ca2+-induced Ca2+ release mediated by clusters of ryanod

70 odine-sensitive stores are implicated in the Ca2+-induced Ca2+ release, NO can be expected to potenti

71 Waves of Ca2+-induced Ca2+ release occur in various cell types an

72 hat depolarization-induced Ca2+ entry evoked Ca2+-induced Ca2+ release only from the ryanodine-sensit

73 y serve to augment the existing regenerative Ca2+-induced Ca2+-release process; however, the sensitiv

74 This process, called Ca2+-induced Ca2+ release, relies on the properties of t

75 Ca2+-induced Ca2+ release, resulting in concerted openin

76 cycles of Ca2+ uptake into and release from Ca2+-induced Ca2+ release stores (pool 2).

77 om this Ca2+ pool, the amount of Ca2+ in the Ca2+-induced Ca2+ release stores was increased.

78 ows that the inherently positive feedback of Ca2+-induced Ca2+ release terminates, despite a large re

79 e intracellular Ca2+signals are amplified by Ca2+-induced Ca2+ release via both ryanodine and IP3 rec

80 ux through T-type Ca2+ channels, followed by Ca2+-induced Ca2+ release via RyRs, contributes to the g

81 ess how i(Ca) and NP(o) separately influence Ca2+-induced Ca2+ release, we measured I(Ca) and junctio

82 ction coupling in cardiac myocytes occurs by Ca2+-induced Ca2+ release, where L-type Ca2+ current evo