ライフサイエンスコーパス: model mice

1 deposition and neuritic dystrophy in amyloid model mice.

2 anced long-term contextual fear memory in AS model mice.

3 initiation and elongation regulator, in FXS model mice.

4 activation of NF-kappaB in WT and progeroid model mice.

5 TD), weight gain, and macro-orchidism in FXS model mice.

6 l circuitry in spinal muscular atrophy (SMA) model mice.

7 tured cells and in peripheral tissues of SMA model mice.

8 SMN levels and improves the lifespan of SMA model mice.

9 tively depleting SMN in the motor neurons of model mice.

10 cell adhesion using knockout-transgenic SCD model mice.

11 by ex vivo autoradiography in transgenic AD model mice.

12 nsgenic adenocarcinoma of the mouse prostate model mice.

13 mprove cognition in Alzheimer's disease (AD) model mice.

14 i) reminiscent of the asymptomatic Tay-Sachs model mice.

15 chs (Hexa-/-) and Sandhoff (Hexb-/-) disease model mice.

16 saminidase S present in the Sandhoff disease model mice.

17 perexcitability, and perhaps epilepsy, in AS model mice.

18 ined plaques ex vivo in brain tissue from AD model mice.

19 fficacy of this approach in Sandhoff disease model mice.

20 enance is reduced in the visual cortex of AS model mice.

21 or affecting cardiorespiratory defects in RS model mice.

22 stasis and other phenotypes exhibited by FXS model mice.

23 nificantly improved cone survival in the LCA model mice.

24 echanisms that are known to be reduced in HD model mice.

25 ecover the ER instability and necrosis in HD model mice.

26 napse loss in Alzheimer's disease transgenic model mice.

27 ct cognitive impairment and bone loss in DMD model mice.

28 asticity and memory deficits exhibited by AS model mice.

29 ts in contextual fear memory exhibited by AS model mice.

30 d a correction of behavioral features in DMD model mice.

31 ed seizure susceptibility of the LGI1(E383A) model mice.

32 otor coordination of AMI-treated N171-82Q HD model mice.

33 escues the memory impairment of the ApoE4 AD model mice.

34 were studied in APPSW /PS1dE9 AD transgenic model mice.

35 when used in retinas of retinitis pigmentosa model mice.

36 r reducing Abeta deposition in AD transgenic model mice.

37 ally in the brains of familial AD transgenic model mice.

38 athology and alleviate memory deficits in AD model mice.

39 muscles from human GNE myopathy patients and model mice.

40 memory exhibited by the Alzheimer's disease model mice.

41 cues AD pathology (up to 70-80%) in 5XFAD AD model mice.

42 r's disease patients and Alzheimer's disease model mice.

43 memory deficits in the double transgenic AD model mice.

44 y and memory deficits in Alzheimer's disease model mice.

45 D, and reduced disease phenotypes in R6/2 HD modeled mice.

46 In an ischemic cardiomyopathy model, mice 4 weeks post-myocardial infarction were rand

47 d CBS into the circulation of homocystinuria model mice alters the extra- and intracellular equilibri

48 We reduced IGF signaling in Alzheimer's model mice and discovered that these animals are protect

49 lin-ErbB4 signaling in the hippocampus of AS model mice and found that ErbB inhibitors could reverse

50 from brain synaptosomes of presymptomatic HD model mice and from mutant Htt-expressing primary neuron

51 NDelta7, provides a protective effect in SMA model mice and human motor neuron cell culture systems.

52 gic receptor expression in Alexander disease model mice and in postmortem brain tissue from Alexander

53 re we show that atrogenes are induced in SMA model mice and in SMA patient muscle in association with

54 gnificantly reduced in both the brains of RS model mice and in the motor cortex of human RS autopsy s

55 idal neurons in hippocampal area CA1 from AS model mice and observed alterations in resting membrane

56 beta2AR activation protected model mice and patient-derived cells.

57 ributes to hippocampal pathophysiology in AS model mice and that targeting mitochondrial ROS pharmaco

58 smaller number of studies using small animal models (mice and rats), no abnormal behaviour or tissue

59 eferoxamine (Df)-pembrolizumab in two rodent models (mice and rats).

60 tested its protective efficacy in two animal models, mice and guinea pigs.

61 While these are standard biomedical research models, mice and rats provide a limited perspective to e

62 cross-reactive immune response in two animal models: mice and ferrets.

63 ong-term depression in the hippocampus of RS model mice, and that administration of a novel mGlu5 pos

64 find that axons within the WM pathways of AS model mice are abnormally small in caliber.

65 hat the enhanced nociceptive responses in AS model mice are due to loss of maternal Ube3a in the cent

66 In this model, mice are sensitized with inactivated Schistosoma

67 ered by the lack of appropriate small animal models; mice are naturally not susceptible to DENV and o

68 glia/macrophages and RPE cells isolated from model mice as well as wild-type mice.

69 Molecular genetic analyses of these model mice, as well as primary human disease, demonstrat

70 wild-type (WT) and Huntington's disease (HD) model mice at ages not accompanied by overt astrogliosis

71 Here we report the establishment of AD model mice, B6Tg2576, that are prone to atherosclerosis.

72 ncentration of mutant SOD1 (SOD1G37R) in ALS model mice, but paradoxically improved locomotor functio

73 ncing mean survival in severely affected SMA model mice by approximately 40%.

74 of stab-injured or Alzheimer's disease (AD) model mice can be directly reprogrammed into functional

75 Here we show that the intestines of CAPS model mice carrying an Nlrp3 (R258W) mutation maintain h

76 In the UTI model, mice coinfected with the two species exhibited hi

77 nt epithelium (RPE) in Abca4 (-/-) Stargardt model mice compared to their relevant background strain.

78 ime evidence, using Alzheimer's disease (AD) model mice deficient in neural exosome secretion due to

79 s was severely impaired in Angelman syndrome model mice deficient in Ube3a.

80 In a second model, mice deficient in both Nur77 and ApoE (ApoE(-/-)N

81 In a bleomycin-induced PF model, mice deficient in p-rex1 had well-preserved alveo

82 Consistent with this model, mice deficient in SLP76 have a complete block at

83 FNs in this process in an infectious disease model, mice deficient in the type I IFN receptor (CD118(

84 ar responses, by using genetic knockout (KO) models (mice deficient in A(2A)Rs or D(2)Rs or both).

85 le KO mouse model of Tcap deficiency and our model mice demonstrate a dystrophic phenotype comparable

86 We show here that FX model mice display substantial deficits in a PFC-depende

87 For the in vivo models, mice either were sham treated or were given Flu

88 In this novel model, mice engrafted with beta-globin-null (Hbb(th3/th3

89 he human Abeta originated from transgenic AD model mice entered the circulation and accumulated in th

90 ly stops the decline of motor function of HD model mice even after the onset of symptom.

91 Herein, we report that AS model mice exhibit elevated levels of mitochondria-deriv

92 demonstrate that, in a diet-induced obesity model, mice exhibit resistance to peripherally administe

93 erebroventricularly for 7 d in transgenic AD model mice expressing green fluorescent protein specific

94 In ALS model mice expressing mutant superoxide dismutase (SOD1)

95 FAP-V(12)Ha-ras transgenic mouse astrocytoma model, mice expressing both activated RAS and EGFR were

96 To test this possibility, we used a mouse model (mice fed a choline-deficient diet) that develops

97 between AS and schizophrenia, we examined AS model mice for alterations in the neuregulin-ErbB4 pathw

98 er nociceptive responses were affected in AS model mice (global deletion of maternal Ube3a allele; Ub

99 antial amounts of dopamine to be produced in model mice harboring the S250F mutation.

100 ng upper motor neuron pathology in these ALS model mice has hindered both molecular-pathophysiologic

101 an species in which complex behaviors may be modeled, mice have been the focus of much attention for

102 stimuli were enhanced in male and female AS model mice; however, nociceptive responses were not alte

103 umor regression in an inducible RAS melanoma model, mice implanted with VEGF-expressing tumors sustai

104 r bases for neurodevelopmental impairment in model mice in vivoSIGNIFICANCE STATEMENT Our understandi

105 nally, we find that chronic treatment of FXS model mice, in adulthood, also restores the level of mGl

106 eterious to disease course in transgenic ALS model mice, in contrast to astrocytes and microglia.

107 ultiple disease-associated phenotypes in FXS model mice including exaggerated protein synthesis, inap

108 isoform of Agrin in the motor neurons of SMA model mice increases muscle fiber size, enhances the pos

109 ver-expressing amyotrophic lateral sclerosis model mice indicate that initiation of disease is intrin

110 egions that control circadian behavior of AS-model mice, indicating an important role for Ube3a in mo

111 In addition, cognition was tested in AD model mice intravenously injected with young blood plasm

112 Neuromuscular weakness in the model mice is accompanied by peripheral as well as centr

113 e mitochondria of cyst-lining cells in ADPKD model mice (Ksp-Cre PKD1 (flox/flox)) and rats (Han:SPRD

114 Melanocytes from HPS model mice lacking a different protein complex, BLOC-2,

115 We found that AS model mice lacking maternal Ube3a (Ube3a(m-/p+) mice) ex

116 In an allergen-induced asthma model, mice lacking Arg2 had greater Th2 inflammation th

117 In this model, mice lacking IL-17C exhibited exacerbated disease

118 , a mitochondria-specific antioxidant, to AS model mice normalizes synaptic plasticity and restores m

119 When applied to model mice of another neuromuscular disorder, autosomal

120 In our nonhealing model, mice on a C57BL/6 background which have a targete

121 by the relatively mild SMA phenotype in our model mice, one explanation for which is the presence of

122 ot seen in the Tay-Sachs or Sandhoff disease model mice or in the corresponding human patients.

123 In mouse genetic models, mice over-expressing CRF show anxiogenic-like re

124 Here, we ask whether SMA model mice possess such phenotypes.

125 ilial Alzheimer disease mutant transgenes in model mice prevents protein-protein interaction changes

126 rtical neurons from AD patients and APP23 AD model mice produce more TTR is unknown.

127 A, a drug known to benefit phenotypes of SMA model mice, produces prolonged maturation of the SMA hea

128 2B antagonism differs between wt and disease model mice, provide critical insight into the therapeuti

129 of lipidoids were evaluated in three animal models: mice, rats and nonhuman primates.

130 In a second model, mice received a methionin-choline-deficient (MCD)

131 of increased nitric oxide synthesis in this model, mice received daily i.p. injections of NG-nitro-L

132 ng muscarinic receptors in Alexander disease model mice reduces oxidative stress, emphasizing the tra

133 phosphorylated tau epitope, in P301L tangle model mice, reduces aggregated tau in the brain and slow

134 indicates that decreased spine density in AS model mice reflects impaired experience-driven spine mai

135 H and higher lactate levels in the brains of model mice relative to controls, as well as a significan

136 ated impaired healing in an impaired healing model (mice rendered hypogonadal) associated with increa

137 In slices prepared from FXS model mice, repeated stimulation of recurrent CA3 pyrami

138 richostatin A (TSA) in nontransgenic and SMA model mice resulted in increased levels of acetylated H3

139 hippocampus/neocortex in normal aging and AD model mice revealed intense calcineurin immunostaining t

140 In this model, mice sensitized to OVA by i.p. and intranasal (i.

141 In contrast, in HD model mice, spontaneous Ca(2+)signals were significantly

142 s and leukocytes to endothelial cells in SCD model mice, suggesting a critical role for P-selectin in

143 er BM from either wild-type or WHIM syndrome model mice, suggesting a potential mechanism for the pat

144 ptic plasticity and memory impairments in AS model mice, suggesting that ErbB inhibitors have therape

145 down-regulate inflammatory bowel disease in model mice, suggesting that stimulation with PSA results

146 teria were maximally attenuated in the mouse model; mice survived, without visible signs of illness,

147 Here, we immunized AD model mice (Tg2576) with Abeta1-30[E18E19] or with K6Abe

148 Transgenic HD model mice that express a portion of the disease-causing

149 /BxN serum transfer-induced arthritis (STIA) model, mice that lacked HK, pKal, or bradykinin receptor

150 In mouse models, mice that overexpressed HIF1alpha or HIF2alpha s

151 tivity are impaired in sensory systems in DS model mice, that such defects may contribute to function

152 ver, and in vivo in Alzheimer's disease (AD) model mice, the peptide specifically inhibits the Cdk5/p

153 In model mice these synapses appear disorganized, fail to m

154 Unlike the NP-C model mice, these double mutant mice did not exhibit cen

155 We used model mice to demonstrate that low Glut1 protein arrests

156 oxidase (anti-MPO) antibody-mediated disease model, mice transplanted with either gp91(phox)-deficien

157 In a disseminated CAG MM model, mice treated with Flu had a significantly decreas

158 the primary visual cortex of control and AS model mice (Ube3a(m-/p+) mice).

159 Here we extend evidence in AS model mice (Ube3a(m-/p+)) of paternal UBE3A expression w

160 We found that neurons in AS model mice undergo a greater elimination of dendritic sp

161 glutamate signaling that was observed in HD model mice was largely, but not completely, rescued by a

162 In both types of HD model mice, we determined biochemical changes, including

163 ization of cysteine in PEGylated CBS-treated model mice were accompanied by improvement of histopatho

164 Alzheimer disease model mice were then treated either by surgically connec

165 Transgenic HIT model mice were treated with KKO, a mouse monoclonal HIT

166 For the influenza virus model, mice were challenged with virus via the intranasa

167 imeric SCID mouse/human synovial tissue (ST) model, mice were engrafted subcutaneously with human ST,

168 In a separate model, mice were given injections of cerulein for 10 wee

169 nce of serotype-specific immunity in a mouse model, mice were immunized with rhesus rotavirus (RRV: G

170 In this model, mice were inoculated subcutaneously with a non-sm

171 In the infection model, mice were orally inoculated with S. enterica 24 h

172 nd dextran sulfate sodium (DSS) as an injury model, mice were treated with COG112 by intraperitoneal

173 In both models, mice were reconstituted with cells from CD154-de

174 nsory cortex layer I was smaller for the FAD model mice, when compared to the corresponding region of

175 AS model mice, which carry a maternal Ube3a null mutation (

176 ere indistinguishable between control and AS model mice, which indicates that decreased spine density

177 d olfactory sensory systems in Down syndrome model mice, which provide insight into defects in the fu

178 al factor in neuropathogenesis, we bred NP-C model mice with mice carrying a targeted mutation in Gal

179 In the second model, mice with a liver-specific knockout of the insuli

180 Utilizing the AOM-DSS model, mice with a myeloid-specific deletion of Egfr had

181 eas in a chemically induced tumor initiation model, mice with conditional ST6Gal-I overexpression exh

182 In the s.c. U87 model, mice with established xenografts were treated wit

183 In two chemically induced seizure models, mice with reduced tau protein had less severe se