ライフサイエンスコーパス: calcium handling

1 l relaxation resulting from abnormal myocyte calcium handling.

2 -induced VT/VF under conditions of defective calcium handling.

3 r cardiomyocytes exhibited markedly improved calcium handling.

4 associated with alterations in intracellular calcium handling.

5 function, leading to disturbed intracellular calcium handling.

6 on, myocardial energetics, and intracellular calcium handling.

7 activity is decreased, resulting in abnormal calcium handling.

8 ted with alterations in proteins involved in calcium handling.

9 ll EP by changing both membrane currents and calcium handling.

10 keletal proteins, and proteins that regulate calcium handling.

11 s for alterations in cellular morphology and calcium handling.

12 disrupted transverse tubule organization and calcium handling.

13 o need to postulate defects in intracellular calcium handling.

14 eling of excitation-contraction coupling and calcium handling.

15 ed cytochrome oxidase activity and defective calcium handling.

16 sphorylation (S16), consistent with improved calcium handling.

17 g human hearts are characterized by abnormal calcium handling, a negative force-frequency relationshi

18 y regulating the intracellular structure and calcium handling ability.

19 including cell survival, cytokine signaling, calcium handling, adrenergic receptor signaling, cytoske

20 Altered muscle SR calcium handling also rendered these mice exercise intol

21 ersensitivity, which may include receptor or calcium-handling alterations within the vasculature.

22 cardiac dysfunction, dampened intracellular calcium handling, alterations in cardiac morphology, and

23 ting possibility that sarcoplasmic reticulum calcium handling and cardiac contractility may be regula

24 ed pathways linked to abnormal intracellular calcium handling and cardiac neurotransmission.

25 ort and cell cycle genes, leading to altered calcium handling and cell cycle defects.

26 NO is known to modulate calcium handling and cellular signaling in the myocardiu

27 activity is decreased, resulting in abnormal calcium handling and contractile dysfunction.

28 d to functional alterations in intracellular calcium handling and contractile function.

29 Functional analysis of calcium handling and contractile parameters in isolated

30 by increased myofiber diameter and improved calcium handling and contractile strength.

31 ar O-GlcNAcylation has beneficial effects on calcium handling and diabetic cardiac function.

32 ical genes involved in contractile function, calcium handling and energy metabolism underpins this co

33 Properties of calcium handling and exchanger currents are altered to a

34 ral and transchamber expression gradients of calcium handling and gap junction proteins that may wors

35 se 2a (SERCA2a) in the regulation of overall calcium handling and heart muscle contractility.

36 r of contractile function through effects on calcium handling and hypertrophy through protein kinase

37 There were also changes in calcium handling and in action potential waveforms, and

38 gnaling events would be predicted to promote calcium handling and increase contractile function of th

39 ad to proteasome impairment, such as altered calcium handling and increased oxidative stress due to m

40 m ATPase (SERCA) plays a key role in cardiac calcium handling and is considered a high-value target f

41 To study the effect of VF on calcium handling and its modulation by dantrolene, heart

42 Although calcium handling and myofibrillar proteins have been imp

43 effects are modulated by phosphorylation of calcium handling and myofilament proteins such as tropon

44 s may produce heterogeneity of intracellular calcium handling and pacemaker activity across the SAN.

45 of SR Ca(2+)-ATPase can modify intracellular calcium handling and shortening in myocardial cells.

46 -dependent cardiovascular functions, such as calcium handling and vascular tone.

47 However, heterogeneity of intracellular calcium handling and, in particular, its effect on the e

48 es in gene expression, myocyte architecture, calcium handling, and contractile function and compared

49 pecific information on ion channel kinetics, calcium handling, and dynamic changes in the intracellul

50 to changes in sarcomeric proteins, abnormal calcium handling, and fibrosis.

51 Action potentials, calcium handling, and ion currents were recorded in vent

52 Furthermore, respiratory variables, calcium handling, and membrane potentials of synaptosome

53 ense mutation showed impaired contractility, calcium handling, and metabolic activity.

54 lectrophysiology, dysregulated intracellular calcium handling, and proarrhythmic behavior in isolated

55 and altered expression of genes involved in calcium handling, angiogenesis, and glucose metabolism.

56 Remarkable new roles for mitochondria in calcium handling, apoptosis, heme turnover, inflammation

57 We conclude that cardiac ion channel and calcium handling are abnormal in CKD rats, leading to in

58 The alterations in calcium handling are due at least in part to direct down

59 chanism whereby alterations in intracellular calcium handling are linked to the expression of hypertr

60 nt view is that instabilities in subcellular calcium handling are the main underlying mechanism.

61 cardiomyocyte contractility and dysregulated calcium handling associated with high-fat diet.

62 decreased myocyte and myofilament function, calcium handling, beta-adrenergic responsiveness, mitoch

63 ransition pore, we used an in vitro assay of calcium handling by isolated brain mitochondria.

64 th triadin suggest that HRCBP is involved in calcium handling by the SR.

65 use model appears to be related to decreased calcium handling by the SR.

66 stent with earlier results that indicate the calcium handling capacity of a range of tissues includin

67 n species (ROS) negatively affect myocardial calcium handling, cause arrhythmia, and contribute to ca

68 as fibrosis, cardiomyocyte hypertrophy, and calcium handling (Col1a2, Nppa, and Serca2).

69 dent adjustment of membrane excitability and calcium handling, compromising the enhancement of cardia

70 oliferation and for protein synthesis of the calcium handling constituents required for tissue contra

71 , we hypothesized that altered mitochondrial calcium handling contributes to dendritic retraction eli

72 tochondrial and metabolic function, impaired calcium handling, decreased antioxidant pathway activity

73 (HF) is associated with impaired myocardial calcium handling, deficient SERCA2a, and increased susce

74 CMs with a homozygous PKP2 mutation also had calcium-handling deficits.

75 Podocyte depletion may result from improper calcium handling due to abnormal activation of the calci

76 er myofibril density and alignment, improved calcium handling, enhanced contractility, and more physi

77 rent ER compartments specialize in different calcium-handling functions (Ca(2+) release and Ca(2+) re

78 on and alternative splicing transitions, and calcium-handling functions are significantly enriched am

79 by marked reduction of energy/metabolism and calcium-handling gene expression (eg, PGC1-alpha, peroxi

80 (lncRNA) required for the expression of the calcium-handling gene Ryr2.

81 Pitx2 target genes that include channel and calcium handling genes, as well as genes that stabilize

82 ia on hECT-developed force and expression of calcium-handling genes (eg, SERCA2a, L-type calcium chan

83 lar drive train pattern on the expression of calcium-handling genes and proteins in rat ventricular m

84 de of mitochondrial depolarization, aberrant calcium handling, impaired ATP synthesis, and activation

85 evated serum aldosterone levels, and altered calcium handling in a controlled experimental model of h

86 eling of excitation-contraction coupling and calcium handling in failing and nonfailing human hearts.

87 identify miRNAs that suppress intracellular calcium handling in heart muscle by interacting with mes

88 A signaling and was reversed for effects on calcium handling in HL-1 cells.

89 neity of excitation-contraction coupling and calcium handling in human hearts.

90 estigate the arrhythmogenic role of abnormal calcium handling in many pathological settings.

91 Calcium handling in pancreatic beta-cells is important f

92 c phenotype of these mice and that different calcium handling in PCs and type II UBCs may account for

93 hus thyroid hormone improves LV function and calcium handling in pressure overload hypertrophy, and t

94 Altered calcium handling in these diseases is evidenced by chang

95 nsistent with a regulatory role for HRCBP in calcium handling in vivo and suggests that mutations in

96 Changes in intracellular calcium handling, including a reduced activity of the sa

97 d that Pkd2(+/-) cardiomyocytes have altered calcium handling, independent of desensitized calcium-co

98 incipal role of mitochondria in pre-synaptic calcium handling is to take up Ca2+ directly or to fuel

99 This is due to profoundly abnormal calcium handling, leading to an inability to normalize c

100 6 had abnormal contraction, relaxation, and calcium handling (LVHdecomp).

101 Intracellular calcium handling, measured by Rhod 2 spectrofluorometry,

102 Analyses of calcium-handling measures demonstrate that RanBP9 select

103 heart muscle cells by boosting intracellular calcium handling might be an effective therapy.

104 pression of genes associated with signaling, calcium handling, mitochondria function and biogenesis,

105 Forced expression of NCX1h or other calcium-handling molecules restored synchronized heartbe

106 onal relationship among proteins involved in calcium handling, myofibrils, and energy production may

107 ions in sarcomere genes may distinctly alter calcium handling pathways.

108 logical and pathophysiological intracellular calcium handling phenomena at the whole-cell.

109 as well, demonstrating the novel and unique calcium handling profile of TOT cardiomyocytes.

110 ium affects the anatomy, gene expression and calcium handling properties of trigeminal sensory affere

111 r calcium signalling was recorded to compare calcium-handling properties among cardiomyocytes differe

112 action and relaxation with minimal effect on calcium-handling properties in vitro, and that contracti

113 In conjunction, calcium-handling protein expression was examined in left

114 Gene expression of calcium handling proteins (SERCA, phospholamban) and str

115 of gene expression and protein synthesis of calcium handling proteins compared to the 2D constructs

116 he gene expressions and protein synthesis of calcium handling proteins decreased significantly during

117 Levels of these calcium handling proteins in SR get altered under diseas

118 Although several calcium handling proteins that control differentiation o

119 unction, expression of hypertrophic markers, calcium handling proteins, and cardiac fibrosis were the

120 AR pathway balance and changed expression of calcium handling proteins, which resulted in altered car

121 f beta1-adrenergic receptor (ADRB1) or other calcium handling proteins.

122 sponse to calcium that is independent of the calcium handling proteins.

123 logical roles of sarcoplasmic reticulum (SR) calcium handling proteins.

124 sed in Sgcg muscle focused on those encoding calcium-handling proteins and responsive to TGFbeta sinc

125 Several other abnormal calcium-handling proteins in the failing heart are candi

126 reased cell capacity, and alterations in the calcium-handling proteins that were similar for RV free

127 estigations, and examinations of connexin43, calcium-handling proteins, and histomorphology were carr

128 We investigated whether alterations in calcium-handling proteins, beta-adrenoceptor density, or

129 s sodium channels, transcription factors and calcium-handling proteins, but also point to previously

130 changes were seen in the expression of other calcium-handling proteins.

131 tered myocyte calcium cycling and changes in calcium-handling proteins.

132 skeletal, nucleoskeletal, mitochondrial, and calcium-handling proteins.

133 altering the expression and activity of key calcium-handling proteins.

134 rial morphology, transcriptional signatures, calcium handling, responses to hypoxia, neurohormonal st

135 ere correlated with changes in intracellular calcium handling, resulting in increased nitric oxide bi

136 to known gene expression changes, additional calcium-handling, sarcomeric, adrenergic signaling, and

137 cardiac remodeling as a result of changes in calcium handling, separate from renal complications.

138 evels of some of the other genes involved in calcium handling, such as the ryanodine receptor and cal

139 s associated with progressive changes in the calcium handling system of atrial myocytes.

140 tion of impaired cardiac cAMP generation and calcium handling that result from AC6 deletion underlies

141 e, Ang-(1-9) directly affected cardiomyocyte calcium handling through a protein kinase A-dependent me

142 a-adrenergic-stimulated myocyte function and calcium handling, upregulating beta(1) receptors and ade

143 ent with mislocalization of Serca1 and Ryr1, calcium handling was drastically altered in Rbfox1(-/-)

144 he phosphorylation of substrates involved in calcium handling were disrupted in AKAP5 knockout cardio

145 lar tuft contractility and macula densa cell calcium handling were observed.

146 pha-Tm mutants can be corrected by modifying calcium handling with Parv.

147 liver, we observe an additive impairment in calcium handling without adversely impacting mitochondri