ライフサイエンスコーパス: InsP3 receptor

1 ed Ca2+ release from internal stores via the InsP3 receptor.

2 e apical pole, in the region of the type III InsP3 receptor.

3 ndreds of micromolar, without activating the InsP3 receptor.

4 he myocytes contain the high affinity type 2 InsP3 receptor.

5 es calcium from intracellular stores via the InsP3 receptor.

6 n from the inner nuclear envelope by nuclear InsP3 receptors.

7 ght to be found in the vicinity of activated InsP3 receptors.

8 ly selective calpain-mediated degradation of InsP3 receptors.

9 s was not due to the localised expression of InsP3 receptors.

10 Purkinje neurons, which have a high level of InsP3 receptors.

11 ddition of native or recombinant InsP3-bound InsP3 receptors.

12 e in a tight functional interaction with the InsP3 receptors.

13 strated the presence of types I, II, and III InsP3 receptors.

14 Different regions of the heart also express InsP3 receptors.

15 edback signal on the inositol trisphosphate (InsP3) receptor.

16 ase C and opening of inositol trisphosphate (InsP3) receptors.

17 idence for the coupling hypothesis, in which InsP3 receptors activated by InsP3 interact with SOC and

18 InsP3 receptor aggregation may be a characteristic cellu

19 rgeting of Na/K ATPase, Na/Ca exchanger, and InsP3 receptor (all ankyrin-binding proteins) to cardiom

20 quantal behaviour of inositol trisphosphate (InsP3) receptors allows rapid graded release of Ca2+ fro

21 ing of platelet internal membranes with anti-InsP3 receptor and anti-actin binding protein antibodies

22 The role of the InsP3 receptor and its interaction with Ca2+ in shaping

23 s revealed that the platelet contains type 1 InsP3 receptor and that it is distinct from actin bindin

24 ith antisera specific to types I, II, or III InsP3 receptors and analyzed by confocal fluorescence mi

25 he possibility that zymogen granules express InsP3 receptors and are thus Ca2+ release sites.

26 ncluded that zymogen granules do not express InsP3 receptors and thus are not a site of Ca2+ release

27 proteolysis of inositol 1,4,5-trisphosphate (InsP3) receptors and, thus, lead to InsP3 receptor down-

28 Pre-treatment with the membrane-permeable InsP3 receptor antagonist 2-APB blocked the activation o

29 Studies with the more conventional InsP3 receptor antagonist heparin revealed that occupati

30 In the presence of heparin, an InsP3 receptor antagonist, repeated activation of PF+Del

31 xception of the dendritic spines, where only InsP3 receptors are found, InsP3 and Ry receptors are pr

32 re both metabotropic glutamate receptors and InsP3 receptors are located, or to multiple spines and a

33 The requirements for activation of InsP3 receptors are more stringent (InsP3 and then Ca2+

34 regulate calcium influx and that functional InsP3 receptors are not required for activation of I(CRA

35 In summary, these data show that all InsP3 receptors are phosphorylated by PKA, albeit with m

36 Inositol 1,4,5-trisphosphate (InsP3) receptors are down-regulated in response to chron

37 I, II, and III inositol-1,4,5-trisphosphate (InsP3) receptors are expressed selectively in different

38 clusters of inositol 1 ,4,5,-trisphosphate (InsP3) receptors are the building blocks for local and g

39 indicating that G-kinase phosphorylates the InsP3 receptor at sites targeted by PKA.

40 Thus, InsP3 receptor binding affinity seems to influence the p

41 (-/-) mice) and inositol 1,4,5-triphosphate (InsP3) receptor-binding protein released with InsP3 (Irb

42 the basal pole, in the region of the type I InsP3 receptor, but only subtle or absent apically.

43 Prior phosphorylation of the insP3 receptor by endogenous kinases inhibited additiona

44 indicate that phosphorylation of the hepatic InsP3 receptor by G-kinase increases the sensitivity to

45 Blockade of the InsP3 receptor, by microinjection of single cells with l

46 ine the structure-function properties of the InsP3 receptor channel family.

47 involving, respectively, single and multiple InsP3 receptor channels.

48 bitory action of cytosolic Ca2+ on gating of InsP3 receptor-channels.

49 InsP3 receptor clustering occurs within 5-10 min of stim

50 hus, cysteine protease activity accounts for InsP3 receptor degradation and analysis of proteolysis i

51 nto this process, we examined whether or not InsP3 receptor degradation is a direct consequence of In

52 ed by brefeldin A and NH4Cl, indicating that InsP3 receptor degradation occurs without removal of rec

53 nclude that InsP3 binding directly activates InsP3 receptor degradation.

54 We examined whether type I, II, and III InsP3 receptors differ in ligand-binding affinity and wh

55 While types I and III InsP3 receptors displayed a similar luminal distribution

56 Thus, InsP3 receptor down-regulation appears to result from th

57 InsP3 receptor down-regulation was not accompanied by pa

58 osphate (InsP3) receptors and, thus, lead to InsP3 receptor down-regulation.

59 oncentrations, InsP4 acts as an inhibitor of InsP3 receptors, enabling InsP4 to act as a potent bi-mo

60 enous wild-type and binding-defective mutant InsP3 receptors expressed in SH-SY5Y human neuroblastoma

61 down-regulatory process selectively targets InsP3 receptors for degradation.

62 ogen treatment of osteoblasts affects type I InsP3 receptor gene expression, signal transduction, and

63 This is the first study of the type I InsP3 receptor gene promoter, and the results suggest a

64 nd proximal DNA segments of the human type I InsP3 receptor gene.

65 e fertilization calcium transient, while the InsP3 receptor generates the subsequent mitotic calcium

66 Analysis of InsP3 receptor immunofluorescence confirmed that the rec

67 These data show a different distribution of InsP3 receptor in the catfish retina compared to that of

68 to store depletion; in an alternative model, InsP3 receptors in the stores are coupled to SOC and I(c

69 ryanodine or inositol 1,4, 5-trisphosphate (InsP3) receptors, increases both cytosolic and mitochond

70 d back phosphorylation of the hepatic type-1 InsP3 receptor, indicating that G-kinase phosphorylates

71 Similarly, the InsP3 receptor inhibitor caffeine failed to alter the ra

72 ructing this model were the mechanism of the InsP3-receptor, InsP3 degradation, calcium buffering in

73 proteins acting synergistically to increase InsP3 receptor (InsP3R) activity and sensitivity.

74 of intracellular Ca2+ levels as a result of InsP3 receptor (InsP3R) activity represents a ubiquitous

75 In Drosophila, only one InsP3 receptor (InsP3R) gene is known, and it is express

76 nsP3) dependent, and cells lacking the three InsP3 receptor (InsP3R) isoforms failed to display the [

77 fects may be due to Ca2+ release mediated by InsP3 receptors (InsP3Rs) [1-3].

78 3), this requires local interactions between InsP3 receptors (InsP3Rs) mediated by their rapid stimul

79 ith the inhibition of Ca(2+) release through InsP3 receptors (InsP3Rs), Na2S reversibly inhibited ace

80 Inositol 1,4,5-trisphosphate (InsP3) receptors (InsP3Rs) are channels responsible for

81 titive Ca2+ release events, and the type III InsP3 receptor instead is suited to initiate Ca2+ signal

82 In resting cells, Irbit was sequestered by InsP3 receptors (IP3Rs) in the endoplasmic reticulum.

83 Because the type I InsP3 receptor is thought to be responsible for repetiti

84 Redistribution of type II InsP3 receptors is also seen after treatment of RBL-2H3

85 The inositol 1,4,5-trisphosphate (InsP3) receptor is essential for signal Ca2+ release fro

86 We conclude that the predominant InsP3 receptor isoform expressed in cardiac myocytes is

87 Differential subcellular expression of InsP3 receptor isoforms may be an important molecular me

88 ional blockade or genetic deletion of type 1 InsP3 receptors led to a conversion of LTD to LTP and el

89 ese three cell types leads to a reduction in InsP3 receptor levels only in AR4-2J cells, indicating t

90 An InsP3 receptor ligand binding domain truncation lacking

91 alcium release from intracellular stores via InsP3 receptors may be important in the induction of LTD

92 The calcium-dependent aggregation of InsP3 receptors may contribute to the previously observe

93 e fall in luminal [Ca2+] after activation of InsP3 receptors may, therefore, cause their inactivation

94 hat L-CaBP1 is able to specifically regulate InsP3 receptor-mediated alterations in [Ca2+]i during ag

95 These data indicate a new mode of InsP3 receptor modulation and hence control of intracell

96 s are discussed in terms of a model in which InsP3 receptors must undergo a slow transition after bin

97 e neurite and soma of a neuronal cell of the InsP3 receptor on the endoplasmic reticulum; estimation

98 ereby enabling inositol 1,4,5-trisphosphate (InsP3) receptors on the stores to bind to, and thus acti

99 Gq-coupled cell surface receptors to effect InsP3 receptor phosphorylation by PKA suggests that this

100 DeltaV failed to induce LTD, suggesting that InsP3 receptors play an important role in LTD induction

101 + from internal stores through ryanodine and InsP3 receptors, regulates both the polarity and input s

102 anodine receptors and inositol triphosphate (InsP3) receptors, respectively.

103 Ca2+ may regulate the local [Ca2+]c near the InsP3 receptor so maintaining the sensitivity of the Ins

104 soforms of the inositol 1,4,5-trisphosphate (InsP3) receptor, the relationship between the distributi

105 sphate (InsP3) production or blockade of the InsP3 receptor, therefore representing a novel form of [

106 nding induces a conformational change in the InsP3 receptor, these data suggest that this change prov

107 ceptor so maintaining the sensitivity of the InsP3 receptor to release Ca2+ from the SR.

108 We have immunolocalized the InsP3 receptor to the inner nuclear layer and limiting m

109 munostaining of the rat retina localized the InsP3 receptor to the plexiform layers.

110 interacts with inositol 1,4,5-trisphosphate (InsP3) receptors to elicit channel activation in the abs

111 The inositol 1,4,5-trisphosphate (InsP3) receptor type I (InsP3R-I) is the principle chann

112 al fluorescence microscopy revealed that all InsP3 receptor types were present in acinar cells.

113 lasmids encoding the InsP3-binding domain of InsP3 receptors (types 1-3) between cyan fluorescent pro

114 It is concluded that InsP3 receptors use the same functional Ca2+ pool as tha

115 The type I InsP3 receptor was concentrated at the basal pole of NPE

116 The localization of InsP3 receptor was in marked contrast to the distributio

117 The type II InsP3 receptor was not expressed in detectable amounts.

118 The platelet InsP3 receptor was shown to be phosphorylated by endogen

119 I, II, and III inositol 1,4,5-trisphosphate (InsP3) receptors was examined.

120 he distributions of the types I, II, and III InsP3 receptors were determined in NPE cells by immunofl

121 on of Ca2+ puff sites was also observed when InsP3 receptors were directly stimulated with thimerosal

122 were further purified on a Percoll gradient, InsP3 receptors were undetectable, and InsP3 failed to r

123 These results suggest that the InsP3 receptor within intact platelets is phosphorylated

124 e accompanied by a redistribution of type II InsP3 receptors within the endoplasmic reticulum and nuc