ライフサイエンスコーパス: model mice

1 specific AMPKalpha isoform suppression in AD model mice.

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

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

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

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

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

7 when used in retinas of retinitis pigmentosa model mice.

8 r reducing Abeta deposition in AD transgenic model mice.

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

10 terns in postmortem human AD patients and AD model mice.

11 athology and alleviate memory deficits in AD model mice.

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

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

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

15 memory deficits in the double transgenic AD model mice.

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

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

18 initiation and elongation regulator, in FXS model mice.

19 s and improved the behavioral patterns of AD model mice.

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

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

22 etter rescue of behavioral impairments in AD model mice.

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

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

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

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

27 cell adhesion using knockout-transgenic SCD model mice.

28 by ex vivo autoradiography in transgenic AD model mice.

29 and VAN group were similar in OVA-induced AD model mice.

30 nsgenic adenocarcinoma of the mouse prostate model mice.

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

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

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

34 saminidase S present in the Sandhoff disease model mice.

35 ion or viral load between wild-type and WHIM model mice.

36 epeats, as well as in the brains of Sod1G93A model mice.

37 x of AAV5-miHTT-treated Huntington's disease model mice.

38 s during the period of MN loss in severe SMA model mice.

39 ctile sensation and improves cognition in AD model mice.

40 hed LBLPS-induced ventricular arrhythmias in model mice.

41 res hearing and inner ear circuitry in DFNB6 model mice.

42 production and improve the SMA phenotype in model mice.

43 tibular histopathological insights in our LF model mice.

44 dentate gyrus in male APP/PS1 transgenic AD model mice.

45 atal cell types of Huntington's disease (HD) model mice.

46 Ube3a-ATS in primary neurons derived from AS model mice.

47 redistribution of AB aggregates in mutant AD model mice.

48 oved cellular and behavioral outcomes of SMA model mice.

49 an CD4 lymphopenia in WHIM patients and WHIM model mice.

50 neurofibrillary tangles in the brains of AD model mice.

51 n DS fibroblasts and in vivo in brains of DS model mice.

52 dontal defect generated in our periodontitis model mice.

53 th phenotypes described in Angelman syndrome model mice.

54 in both B-amyloid-treated and transgenic AD model mice.

55 therapeutic potential of SH-Man-HSA in NASH model mice.

56 b muscles from disease onset to death in ALS model mice.

57 n aged APPswe/PS1DeltaE9 Alzheimer's disease model mice.

58 O) increases SMN production in SMA cells and model mice.

59 uced in excitatory hippocampal neurons of AD model mice.

60 e proepileptogenic plasticity observed in AS model mice.

61 failure displayed in 2 separate lines of AD model mice.

62 muscles from human GNE myopathy patients and model mice.

63 deposition and neuritic dystrophy in amyloid model mice.

64 lomeric functions in cells derived from ICF1 model mice.

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

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

67 fficacy of this approach in Sandhoff disease model mice.

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

69 or affecting cardiorespiratory defects in RS model mice.

70 stasis and other phenotypes exhibited by FXS model mice.

71 nificantly improved cone survival in the LCA model mice.

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

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

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

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

76 asticity and memory deficits exhibited by AS model mice.

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

78 AMD model) and Abca4(-/-)/Rdh8(-/-) (dry-AMD model) mice.

79 bone structure of young Hyp (the XLH animal model) mice.

80 2 -/- [primary sclerosing cholangitis (PSC), model] mice.

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

82 mory impairment and neurodegeneration of FTD-modeling mice.

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

84 on and reduced pathology in the brains of AD-model mice (5xFAD), with a noticeable between-sex effect

85 nal knockout of Shp2 alleles in the ErbB2 BC model mice abrogates mammary tumorigenesis by blocking t

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

87 in both amyotrophic lateral sclerosis (ALS) model mice and ALS patient nerves.

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

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

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

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

92 of D1R-expressing CMs in both heart failure model mice and in heart failure patients with sustained

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

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

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

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

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

98 seizure-driven impairment in cognition in AD model mice and perhaps also in AD.

99 Ras, also are expressed in the blood of FXS model mice and pharmacological treatments previously rep

100 pha has therapeutic effects in transgenic AD model mice and rescues Abeta-dependent impairments.

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

102 y, we compared plasma indicators of the CURD-model mice and the patients with the manic syndrome.

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

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

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

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

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

108 3 proteins in the brain of 5xFAD Alzheimer's model mice, and find reductions in synaptic protein clus

109 l stimulation in tissue samples from colitis-model mice, and impairing glial connexin-43 reduced visc

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

111 t study, we treated the double transgenic AD model mice, APP/PS1, with NOB-containing diets.

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

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

114 In this model, mice are sensitized with inactivated Schistosoma

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

116 tive/memory impairments of 3- to 4-mo-old AD model mice as measured by their performance in the Barne

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

118 tro and further significantly reduced CDI in model mice, as evidenced by a 100% survival rate and imp

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

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

121 ld type and APP/PS1 Alzheimer's disease (AD) model mice at different ages, indicating their strong co

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

123 ingle-cell atlas of brain immune cells in AD model mice bearing the three common human APOE alleles.

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

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

126 drial ceramide levels in vitro and in animal models (mice, C57BL/6J) (under chow and high-fat diet) i

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

128 t that brain-based de novo proteomics in FXS model mice can be used to find altered expression of pro

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

130 In our model, mice clustered in two groups displaying high or l

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

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

133 er abundance of nonfibrillar AB plaque in AD-model mice contributes importantly to the PET signal.

134 abundance of nonfibrillar Abeta plaque in AD-model mice contributes importantly to the PET signal.

135 Here, we show that in diet-induced NASH model mice, decrease of fecal alpha-defensin along with

136 asma gondii infection of Alzheimer's disease model mice decreases amyloid beta plaques.

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

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

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

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

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

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

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

144 In transgenic AD model mice, deletion of Pyk2 rescues synaptic loss and l

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

146 electrophysiological properties in tauopathy model mice despite a paradoxical evolution of biomarker

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

148 DOK7-CMS model mice displayed a severe phenotype with reduced wei

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

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

151 ly, systemic blockade of ErbB function in MI model mice enhanced senescence and apoptosis of cardiac

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

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

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

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

156 22qDS model mice exhibited CA1 excitatory ensemble hyperexcita

157 In a gut colonization model, mice exposed to the SPAR deletion mutant showed s

158 Female and male transgenic AD model mice expressing APPswe/PSEN1DeltaE9 require Pyk2 f

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

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

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

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

163 mulated in kidneys and plasma in a CKD mouse model (mice fed an adenine-rich diet).

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

165 In APP/PS1 AD model mice, GIRK-dependent signaling was diminished in h

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

167 Correspondingly, model mice had fewer acetylcholine receptor-stained NMJs

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

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

170 Whereas AS model mice have associated synaptic dysfunction and alte

171 Type 2 diabetes model mice have elevated plasma glycerol, which is a pre

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

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

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

175 ed levels of rabphilin-3A (RPH3A) in 3xTg-AD model mice, implying its role in disease pathogenesis.

176 ATV:TREM2 treatment in AD model mice improved energy metabolism and microglial fun

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

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

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

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

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

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

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

184 g the delta and theta rhythms observed in AS model mice, indicating that CBD administration could als

185 , peripheral delivery of (S)-PHA533533 in AS model mice induces widespread neuronal UBE3A expression.

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

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

188 hat the de novo translational profile in FXS model mice is altered at steady state and in response to

189 AS model mice kindled similarly to wild-type mice, but they

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

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

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

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

194 In a GAS-induced NF model, mice lacking hepcidin in keratinocytes failed to

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

196 In two epilepsy models, mice lacking HCA1R (lactate receptor) were more

197 Upon breeding with amyloid model mice, liver-expressed apoE4 exacerbated brain amyl

198 In humanized SLE model mice, MDSC depletion decreased the levels of Th17

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

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

201 ed a significant dysfunction in CF cells and model mice of the transcription factor nuclear-factor-E2

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

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

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

205 N levels and improves pathophysiology of SMA model mice over individual treatment.

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

207 tis observed in classical TNF overexpression models, mice overexpressing tmTNF developed axial and pe

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

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

210 In the parabiosis model, mice previously exposed intranasally to OVA with

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

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

213 2B antagonism differs between wt and disease model mice, provide critical insight into the therapeuti

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

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

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

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

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

219 an ACC->BLA circuit in female breast cancer model mice, reducing anxiety, norepinephrine, and tumor

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

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

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

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

224 nduced LC ROS production is reduced in lupus model mice, restored by anti-IFNAR, and is cytoplasmic i

225 e and human LCs, and IFNAR blockade in lupus model mice restores LC ADAM17 sheddase activity, all wit

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

227 In vivo administration in murine sepsis model mice results in near complete survival.

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

229 imaging of the brains of Parkinson's disease model mice revealed significant alternations in mobile C

230 In the CNV model mice, S1P1 tended to decrease in expression immedi

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

232 Here, AS model mice showed abnormal responses to familiar visual

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

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

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

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

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

238 In AD model mice, SuM neurons targeting dDG or vDG display abe

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

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

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

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

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

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

245 he C-boutons are frequently performed in ALS model mice, the mice perform better than their untreated

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

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

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

249 Gardasil 9, vaccination of wild-type and EV model mice (Tmc6(Delta/Delta) or Tmc8(Delta/Delta)) with

250 flurothyl kindling and retest paradigm in AS model mice to assess epileptogenesis and to gain mechani

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

252 We used model mice to map and identify an Hspa8(G470R) synaptic

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

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

255 ng of hippocampal tissue from a rat epilepsy model, mice treated with the antiseizure medicine cannab

256 manized alpha-synuclein overexpressing mouse model; mice treated at 12 months of age when motor defec

257 On the other hand, work in animal models (mice, typically) has led to fundamental insight

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

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

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

261 Using the SAUNA model, mice underwent HFpEF induction by uninephrectomy,

262 au P301L variant in precisely engineered FTD-modeling mice unveils a transiently protective effect of

263 enetic constructs in 34 control and 24 22qDS model mice via adeno-associated viral vectors, driven by

264 The concentration of SCFAs in feces of IBS model mice was higher compared to the control group.

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

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

267 In AD model mice, we identifed pericytes throughout the capill

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

269 Our SMA model mice were generated by deletion of exon 7 of Smn g

270 A total of 16 SMA model mice were injected with 1 x 10(5) hAFSC in uterus,

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

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

273 Three-month-old 5xFAD (AD model) mice were injected with T. gondii or with phospha

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

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

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

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

278 In a passive sensitization model, mice were injected with IgE to Dermatophagoides p

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

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

281 the cardiac immune infiltrate profile in our model, mice were randomized to receive the sodium glucos

282 As a disease model, mice were subjected to pressure overload for 6 an

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

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

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

286 expression was found in the BNST of anxiety model mice, whereas pharmacological activation or local

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

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

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

290 Temporally resolved imaging of AKI-disease model mice with KNP-1 suggests a gradual increase in ren

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

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

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

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

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

296 In orthotopic mouse GBM models, mice with chronic and acute Trem2 loss of functi

297 In both models, mice with endothelium-specific overexpression of

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

299 on method for distinguishing control and mdx model mice, with a strong potential for clinical diagnos