ライフサイエンスコーパス: mdx mouse

1 e disease that is commonly studied using the mdx mouse.

2 of the dystrophy in the dystrophin-deficient mdx mouse.

3 on is elevated in muscle from the dystrophic mdx mouse.

4 strophin-deficient muscular dystrophy in the mdx mouse.

5 e observed in DMD patients compared with the mdx mouse.

6 e at high levels in the dystrophin-deficient mdx mouse.

7 hways in muscles of the dystrophin-deficient mdx mouse.

8 le growth and improve muscle function in the mdx mouse.

9 e cardiac and skeletal muscles in dystrophic mdx mouse.

10 n and therapeutic interventions has been the mdx mouse.

11 iculum to release Ca2+ may be altered in the mdx mouse.

12 MS) ion channels in skeletal muscle from the mdx mouse, a deletion mutant that lacks the cytoskeletal

13 in several muscle tissues of the dystrophic mdx mouse, a model for continuous muscle degeneration an

14 tively mild dystrophic phenotype) and in the mdx mouse, a model for DMD.

15 liorate aspects of muscular dystrophy in the mdx mouse, a model for Duchenne muscular dystrophy.

16 Using this technique the mdx mouse, a model of Duchenne muscular dystrophy (DMD)

17 pathways in skeletal muscles from normal and mdx mouse, a model of Duchenne muscular dystrophy (DMD),

18 In the mdx mouse, a model of Duchenne muscular dystrophy in whi

19 trophin expression in skeletal muscle in the mdx mouse, a model of Duchenne muscular dystrophy.

20 on coupling in skeletal muscle fibres of the mdx mouse, a model of the human disease Duchenne muscula

21 The mdx mouse, a model of the human disease Duchenne muscula

22 gentamicin on cultured muscle cells from the mdx mouse - an animal model for DMD that possesses a pre

23 and function have benefited from use of the mdx mouse, an animal model for DMD/BMD.

24 cation of muscle-derived stem cells from the mdx mouse, an animal model for Duchenne muscular dystrop

25 f bone marrow transplantation studies in the mdx mouse, an animal model of Duchenne's muscular dystro

26 are also present in the dystrophin-deficient mdx mouse and are believed to result from alternative sp

27 med exon-skipping, has been reported for the mdx mouse and in four DMD patients by local intramuscula

28 Using cells from the mdx mouse as a model system, we show that chimeraplast-m

29 The results substantiate the mdx mouse as an important model system for studies of th

30 orrecting the morphological pathology of the mdx mouse, but still functioned to assemble the DGC at t

31 AAV was delivered to the newborn mdx mouse cardiac cavity.

32 Spontaneous Ca2+ transients in mdx mouse cells are sensitive to depolarization and are

33 In mdx mouse cells the intrinsic gating property of fast vo

34 netic downregulation of Nox2 activity in the mdx mouse decreases reactive oxygen species (ROS) produc

35 These studies in the mdx mouse demonstrate that oral administration of SMT022

36 Data show that mdx mouse EOM contains dystrophin-glycoprotein complex (

37 The mdx/mdx mouse has been widely used to study DMD; this model

38 AIMS: The mdx mouse has proven to be useful in understanding the c

39 ough the increase in MLP and utrophin in the mdx mouse heart was able to compensate for the loss of d

40 efficient and persistent transduction of the mdx mouse heart.

41 mediated microdystrophin gene therapy in the mdx mouse heart.

42 models accumulated desmin and beta-tubulin, mdx mouse hearts accumulated utrophin and MLP, and MLP-n

43 In mdx mouse hearts, LV-to-body weight ratio, cavity volume

44 rmalize blood flow regulation in contracting mdx mouse hindlimb muscles suggests a putative novel tre

45 Analysis of gephyrin -/-, agrin -/-, and mdx mouse hippocampal neurons in culture indicated that

46 Using the mdx mouse homologue, we have shown previously that the a

47 The mdx mouse is a valuable animal model of DMD as it bears

48 The mdx mouse is a widely used animal model of DMD.

49 Heart function of mdx mouse is normal in the absence of external stress.

50 which is unable to prevent dystrophy in the mdx mouse, is able to ameliorate these abnormalities in

51 l model for Duchenne muscular dystrophy, the mdx mouse, loss of dystrophin causes more severe abnorma

52 he symptoms associated with dystrophy in the mdx mouse model for DMD.

53 skeletal muscle pathological lesions in the mdx mouse model for DMD.

54 phin expression into skeletal muscles of the mdx mouse model for Duchenne muscular dystrophy (DMD).

55 n the development of muscle pathology in the mdx mouse model for Duchenne muscular dystrophy, but non

56 responsible for the death of muscles in the mdx mouse model of DMD and human DMD lymphoblasts.

57 Here, we used the mdx mouse model of DMD and non-invasive spectroscopy to

58 is a highly potent therapeutic agent for the mdx mouse model of DMD and represents a paradigm for the

59 c silencing of the klotho gene occurs in the mdx mouse model of DMD and whether klotho silencing is a

60 gative muscle cell line established from the mdx mouse model of DMD but not in normal myoblasts, expo

61 Injection of laminin-111 protein into the mdx mouse model of DMD increased expression of alpha(7)-

62 indromic repeats (CRISPR)-Cas9 system to the mdx mouse model of DMD to remove the mutated exon 23 fro

63 ne muscular dystrophy (DMD) and the standard mdx mouse model of DMD, dystrophin deficiency causes los

64 Studies in mice, including the mdx mouse model of DMD, have demonstrated that circulati

65 l muscle mass and functional strength in the mdx mouse model of DMD, providing a therapeutic rational

66 In the mdx mouse model of DMD, the pharmacological reduction of

67 eurogenesis in the dentate gyrus (DG) in the mdx mouse model of DMD, using bromodeoxyuridine incorpor

68 n binding and amelioration of disease in the mdx mouse model of DMD.

69 itophagy pathway, would be beneficial in the mdx mouse model of DMD.

70 ion and recover dystrophin expression in the mdx mouse model of DMD.

71 rcolemma and reduces muscle pathology in the mdx mouse model of DMD.

72 of Duchenne muscular dystrophy (DMD) and the mdx mouse model of DMD.

73 rtant role in promoting the pathology in the mdx mouse model of DMD.

74 mediates salutary therapeutic effects in the mdx mouse model of DMD.

75 A expression in the tibialis anterior of the mdx mouse model of DMD.

76 on to IgG-Fc improved pathophysiology of the mdx mouse model of DMD.

77 n to improve the dystrophic phenotype in the mdx mouse model of DMD.

78 o ameliorate the dystrophic phenotype in the mdx mouse model of Duchenne muscular dystrophy (DMD).

79 ic streptomycin from onset of disease in the mdx mouse model of Duchenne muscular dystrophy (DMD).

80 expression is also normally increased in the mdx mouse model of Duchenne muscular dystrophy compared

81 Deletion of MSTN in the mdx mouse model of Duchenne muscular dystrophy enhances

82 portantly, genetically deleting S1PR3 in the mdx mouse model of Duchenne muscular dystrophy produced

83 major role in worsening muscle injury in the mdx mouse model of Duchenne muscular dystrophy.

84 iomyopathy by reducing SR Ca(2+) leak in the mdx mouse model of Duchenne muscular dystrophy.

85 bit regeneration in the dystrophin-deficient mdx mouse model of Duchenne muscular dystrophy.

86 In the mdx mouse model of dystrophinopathy, this protective mec

87 Previous studies in the mdx mouse model of muscular dystrophy demonstrate that i

88 asmic reticulum Ca2+ release channel, in the mdx mouse model of muscular dystrophy that contributes t

89 reatment of dystrophic DMD muscles using the mdx mouse model, and found that Wnt7a treatment efficien

90 been identified in the Dystrophin-deficient mdx mouse model, in vivo evidence of pathology based on

91 In the dystrophic mdx mouse model, overexpression of ML1 decreased muscle

92 ates both in cell culture and in vivo in the mdx mouse model.

93 phic environment has been established in the mdx mouse model.

94 e skeletal muscle of DMD patients and in the mdx mouse model.

95 elta-sarcoglycan (Sgcd(-/-)), Dysf(-/-), and mdx mouse models of muscular dystrophy.

96 muscle size and absolute muscle strength in mdx mouse muscle along with a significant decrease in mu

97 arcolemma isolated from dystrophin-deficient mdx mouse muscle even though it was localized to costame

98 long-term OVL are detrimental for hind limb mdx mouse muscle, a murine model of Duchene muscular dys

99 ndogenously corrected myogenic precursors in mdx mouse muscle.

100 ed to confer protection on Dag1(Y890F/Y890F)/mdx mouse muscle.

101 dystrophin promoters results in a series of mdx mouse mutants that differ in their repertoire of iso

102 canine myocytes than in the mildly affected mdx mouse myocytes, and this was associated with a lack

103 ds also demonstrated readthrough activity in mdx mouse myotube cells carrying a nonsense mutation and

104 MSCs in patches from mdx mouse myotubes have higher levels of resting activit

105 ong exon-skipping activity in differentiated mdx mouse myotubes in culture in the absence of an added

106 in individual resting normal and dystrophic mdx mouse myotubes in culture.

107 1beta and tumor necrosis factor alpha in the mdx mouse precede the onset of muscular dystrophy.

108 The dystrophin gene in the mdx mouse provides a favored system for study of exon sk

109 y in healthy (wild-type, WT) and dystrophic (mdx) mouse quadriceps muscles and evaluated transcript l

110 Genetic crosses with the mdx mouse showed that neither transgenic syntrophin coul

111 rophin transgene in the dystrophin-deficient mdx mouse significantly improves the dystrophic muscle p

112 The mdx mouse strain has a point mutation in the dystrophin

113 We have recently shown in the dystrophic mdx mouse that exon 23, bearing a nonsense mutation, can

114 rcolemmal membrane of skeletal muscle of the mdx mouse that lacks dystrophin.

115 c mouse models to identify phenotypes of the mdx mouse that remain despite transgenic utrophin overex

116 roximately 20 years of investigations of the mdx mouse, the impact of the disease on the life span of

117 Our results suggest that in myofibers of the mdx mouse, the membrane- associated cytoskeleton, but no

118 The mdx mouse, the most widely used animal model of DMD, has

119 rove aspects of the disease phenotype in the mdx mouse; therefore, utrophin up-regulation is under in

120 regeneration of dystrophin in the muscle of mdx mouse through a 2'O-methyl phosphorothioate-mediated

121 mprovement, we used in situ protocols in the mdx mouse to measure muscle strength and resistance to e

122 of stop codons, successfully achieved in the mdx mouse using gentamicin, represents an important evol

123 Consequently, a life span study of the mdx mouse was designed that included cohorts of male and

124 , but muscle fibre degeneration found in the mdx mouse was reduced almost to wild-type levels.

125 for Duchenne muscular dystrophy, the mutant mdx mouse, was used to determine whether disruption of t

126 Obviation of such a blockage is seen in the mdx mouse, where despite a nonsense mutation in exon 23

127 In the mdx mouse, where muscular dystrophy is due to a nonsense

128 In a transgenic mdx mouse, where utrophin was over expressed in the skel

129 ed in the dystrophin-deficient model of DMD (mdx mouse), which may explain the relatively mild dystro

130 e studied the expression of myoferlin in the mdx mouse, which lacks dystrophin and whose muscles unde

131 nsive protein biomarkers in the serum of the mdx mouse with potential utility in DMD patients.

132 lecular signature of dystrophinopathy in the mdx mouse, with evidence that secondary mechanisms are k

133 body-wide skeletal muscles of the dystrophic mdx mouse, with resulting improvement in muscle function