ライフサイエンスコーパス: transgenic animal

1 T(-)B(+)NK(-) SCID phenotype of the original transgenic animal.

2 eads to synaptic and cognitive impairment in transgenic animals.

3 oinjected than traditional methods to obtain transgenic animals.

4 enhanced in lungs from Chit1 overexpressing transgenic animals.

5 nces in SPE-38 are required for fertility in transgenic animals.

6 ME normalized pressure-dependent drainage in transgenic animals.

7 ty of the PNKD protein in cultured cells and transgenic animals.

8 ts, and efficient and flexible generation of transgenic animals.

9 uorescent imaging or to the cost of building transgenic animals.

10 ncrease in circulating IGFBP-3 levels in the transgenic animals.

11 l culture and in virally infected tissue and transgenic animals.

12 s are expressed in the body columns of these transgenic animals.

13 y-a problem common to most cell types in non-transgenic animals.

14 D8(+) AI4 T-cell clones from T-cell receptor transgenic animals.

15 or neurons in spinal cord gray matter in all transgenic animals.

16 enotypes, leaving autoregulation impaired in transgenic animals.

17 and liver function tests were unaffected in transgenic animals.

18 defects resulting in retinal degeneration in transgenic animals.

19 tB site, which facilitates the production of transgenic animals.

20 n 7 inclusion in the liver and kidney of the transgenic animals.

21 murine pancreatic islets, derived from egfp transgenic animals.

22 homeostasis was not grossly perturbed in the transgenic animals.

23 30 min after induction and last for 24 h in transgenic animals.

24 origenesis was significantly dampened in the transgenic animals.

25 ated apolipoprotein L-I does not function in transgenic animals.

26 embryogenesis and for efficiently generating transgenic animals.

27 lized using pancreatic explants from MIP-GFP transgenic animals.

28 he ovary, and cells of the adrenal cortex in transgenic animals.

29 the frequency of cardiac arrhythmias in Ras transgenic animals.

30 ase the cellular specificity of silencing in transgenic animals.

31 gnaling, an activity that we corroborated in transgenic animals.

32 , to modify BAC/PAC sequences for generating transgenic animals.

33 be transmitted for many generations in these transgenic animals.

34 i detected in liver and lungs of >86% of all transgenic animals.

35 edominates in freshly isolated NK cells from transgenic animals.

36 n and rapidly accelerates tumor formation in transgenic animals.

37 events in mixed cell cultures and tissues of transgenic animals.

38 ith Abeta12-28P prevents a memory deficit in transgenic animals.

39 of the nontransgenic cows but in none of the transgenic animals.

40 significantly higher scaling exponent in the transgenic animals.

41 xpression of abu-11 extends the life span of transgenic animals.

42 domain is dispensable for LIN-42 function in transgenic animals.

43 ased in size selectively in the 24-month-old transgenic animals.

44 nos, dominant-negative mutants, and knockout transgenic animals.

45 production in cell culture manufacturing or transgenic animals.

46 increases of Abeta deposits in these double transgenic animals.

47 kout (NSG) human leucocyte antigen (HLA)-DQ8 transgenic animals.

48 ecreased Akt and MAPK phosphorylation in the transgenic animals.

49 insertion into the genome to produce stable transgenic animals.

50 and enteric nervous system function in these transgenic animals.

51 of producing human proinsulin in the milk of transgenic animals.

52 evels were not associated with malignancy in transgenic animals.

53 permanent genomic insertion produces stable transgenic animals.

54 stably transmitted to a third generation of transgenic animals.

55 ermanent genomic insertion to produce stable transgenic animals.

56 out the nervous system of transgenic and non-transgenic animals.

57 TDP-43-dependent neurodegeneration in TDP-43-transgenic animals.

58 nduces pigment formation in cell culture and transgenic animals.

59 to distinguish heterozygous from homozygous transgenic animals.

60 ted using advanced model systems, especially transgenic animals.

61 ing streptozotocin in wild-type and netrin-1 transgenic animals.

62 aRIIb levels, this change is blunted in BAFF-transgenic animals.

63 In contrast, adult transgenic animals (12 months) displayed decreased level

64 of granulocyte colony-stimulating factor in transgenic animals after wounding.

65 r, enhanced PRX1 activity, and protected the transgenic animals against alcohol-induced, ROS-mediated

66 gher baseline BCG organ load in this CD8 TCR transgenic animal allowed us to demonstrate that OVA imm

67 Transgenic animals also failed to show an increased pred

68 Significantly, RNF5 loss in F508del-CFTR transgenic animals ameliorated intestinal malabsorption

69 tumors and a cell line were derived from the transgenic animals and are sensitive to inhibition by a

70 erated two independent strains of nestin-tTA transgenic animals and crossed founder mice from both li

71 c plaque burden in the hippocampus of double-transgenic animals and elevated steady-state Abeta level

72 ient to induce mammary transformation in all transgenic animals and is associated with a high degree

73 etely functionally ablate EGFP expression in transgenic animals and recapitulate developmental phenot

74 used the Tol2 transposon system to generate transgenic animals and rescue the mutant phenotype.

75 In HLA-A2 transgenic animals and similar to human EBV carriers, T

76 We investigated the ability of both our transgenic animals and their wild-type littermate to lea

77 Primary mouse hepatocytes from both the SV1 transgenic animals and those with hepatocyte-specific Kl

78 was increased in the ONL of larval and adult transgenic animals, and an elevation of rod precursor pr

79 The plethora of models of cardiac function, transgenic animals, and drug screens based on variable E

80 naturally occurring developmental disorders, transgenic animals, and highly specific lesion studies a

81 es and from studies involving cell cultures, transgenic animals, and human tissue provide initial evi

82 gulated in human PD brain, in A30P alpha-syn transgenic animals, and in a cell culture model for alph

83 -/-) CD8(+) T cells were transferred into HA transgenic animals, and lung injury was not observed, th

84 ifferences across drug treatments, diseases, transgenic animals, and others.

85 Using a transgenic animal approach we have extended dentin sialo

86 Transgenic animals are extensively used to model human d

87 Once transgenic animals are obtained, the entire experimental

88 Transgenic animals are produced by introducing 'foreign'

89 found only in the spinal cord of symptomatic transgenic animals, are not observed in unafflicted tiss

90 Using clone 4 TCR transgenic animals as a source of naive CD8 T cells, we

91 d the regenerative capacity of muscle in the transgenic animals as determined by fusion of BrdUrd-lab

92 ermined in specific pathogen-free B6 and TCR transgenic animals, as well as in germ-free B6 mice.

93 he ability to express an exogenous gene in a transgenic animal at a defined level and in a spatially

94 ls, they were found to be increased in older transgenic animals at the age at which selective neurode

95 city in Torpedo acetylcholine receptor-alpha-transgenic animals bear distinct tolerance imprints.

96 Middle-aged (9-11 months) transgenic animals (both male and female) displayed mild

97 ught to bypass the laborious generation of a transgenic animal by exploiting placental trophoblast-sp

98 kRASG12D can be conditionally induced within transgenic animals by heat shock treatment.

99 t highly efficient, technique for generating transgenic animals by transducing spermatozoa with lenti

100 as been selected such that double and triple transgenic animals can be visually identified and that f

101 acts containing amyloid or tau aggregates in transgenic animals can induce cerebral amyloidosis and t

102 along the endothelial lining of lesions from transgenic animals compared with controls.

103 Third, Prdm1:TVB-mRFP transgenic animals could provide an invaluable tool for

104 ntly elevated prostaglandin I2 levels in the transgenic animals, coupled with significantly decreased

105 Dsg3 (hDSG3) murine model utilizing a hDsg3 transgenic animal crossed to the mDsg3 knockout line.

106 trophil phagocytosis of P. gingivalis in the transgenic animals; cutaneous fat deposition was reduced

107 The survival of the transgenic animal delineates requirements for gene thera

108 At 4 months of age, K303R ERalpha transgenic animals demonstrate precocious alveolar buddi

109 autosomes can be compatible with viability, transgenic animals demonstrate reduced fitness, subferti

110 The resistance to microsphere leakage in transgenic animals demonstrated a protective role agains

111 Mcl-1 transgenic animals demonstrated little to no acute liver

112 xamination of mhc2dab:GFP; cd45:DsRed double-transgenic animals demonstrated that kidney mhc2dab:GFP(

113 Functional studies using transgenic animals demonstrated that this modular system

114 Existing TDP-43 transgenic animals develop a limited loss of motor neuro

115 On Ras activation, the transgenic animal developed ventricular hypertrophy and

116 The IL-22R1 transgenic animals developed neutrophilia that correlate

117 At 6 months of age, most transgenic animals developed premalignant ductal lesions

118 These transgenic animals display a nuclear lamin aggregation p

119 We show that these transgenic animals display dosage-dependent, repeat-leng

120 DeltaNp63 transgenic animals display dramatic defects in hair foll

121 Despite expanded eWAT, transgenic animals display improved systemic insulin sen

122 duction and extracellular remodeling, MKK6bE transgenic animals displayed impaired hemodynamic functi

123 Transgenic animals displayed increased energy expenditur

124 ll cycle, and stimulation via the TCR in TCR transgenic animals does not enhance or decrease cell dea

125 found that over-activation of Cdk5 in young transgenic animals does not induce tau hyperphosphorylat

126 ue metabolism, which was increased in 4E-BP1 transgenic animals during normal aging and in a response

127 Populations of RGCs labeled in transgenic animals establish distinct dendritic strata s

128 Moreover, DeltaNp63 transgenic animals exhibit a depleted hair follicle stem

129 monstrated that these macrophage adiponectin transgenic animals exhibit reduced macrophage foam cell

130 hydroxybutyl) nitrosamine (OH-BBN), survivin transgenic animals exhibited accelerated tumor progressi

131 Transgenic animals exhibited higher and inheritable resi

132 Muc1 and pregnant mammary glands from c-Neu transgenic animals expressed high levels of Muc1.

133 Likewise, muscle-specific transgenic animals expressing a SNARK dominant-negative

134 Transgenic animals expressing both human proteins exhibi

135 minant CORD phenotype was observed in double transgenic animals expressing both mutant P351Delta12 an

136 Finally, transgenic animals expressing constitutively active Akt

137 Previous research in acute brain slices of transgenic animals expressing constitutively active CREB

138 Transgenic animals expressing Drosophila Fig4 missense m

139 on of these discoveries are now in progress; transgenic animals expressing either baboon or minimally

140 ynapsin during synaptic growth, we generated transgenic animals expressing fluorescently tagged synap

141 In transgenic animals expressing GAR-3 variants that are no

142 Transgenic animals expressing GFP regulated by the glial

143 e of C. elegans promoters needed to generate transgenic animals expressing localization markers such

144 Transgenic animals expressing mutations that disrupt Ca(

145 Indeed, transgenic animals expressing vGPCR manifest vascular tu

146 In lysates from hearts of heterozygous transgenic animals expressing wild type and unphosphoryl

147 Double-transgenic animals for hPSA and TAU(P301L) transgenes de

148 genic animals had normal survival rates, but transgenic animals had an impaired response to erythropo

149 Septic bi-transgenic animals had decreased crypt apoptosis but had

150 or milk compositions were unchanged, and the transgenic animals had no apparent health defects.

151 The resulting transgenic animals had normal numbers of MCs in their ti

152 Circulating erythrocytes in transgenic animals had normal survival rates, but transg

153 he spectrum, generation of a multiplicity of transgenic animals has allowed analysis of the physiolog

154 Research performed on transgenic animals has led to numerous advances in biolo

155 Dsp transgenic animals have been engineered with superior en

156 Transgenic animals have enabled Ca(2+) signalling to be

157 Transgenic animals heterozygous for the germline Stat5 n

158 Tau transgenic animals homozygous for loss of these enhancer

159 CD40 expression in the livers of transgenic animals, however, resulted in CD80 and CD86 e

160 Ablation of these interneurons in transgenic animals impairs escape responses, indicating

161 n and ethics implications will prevent using transgenic animals in the short term.

162 The contribution of transgenic animals in this field is emphasized, and the

163 Relative to wild-type mice, transgenic animals in which the NR2B subunit was over-ex

164 rs of neurodegeneration and neurotoxicity in transgenic animals, including analysis of both males and

165 Low phytate transgenic plants and transgenic animals increased P availability by 14% and 5

166 f exogenous genes inserted in the genomes of transgenic animals is critical for the success of a wide

167 The production of transgenic animals is one of several new and developing

168 The most important benefit from using transgenic animals is the capability to perform in vivo

169 We previously showed with ex vivo studies on transgenic animals lacking NOS3 that adverse intrauterin

170 Compared to wild-type (WT) control mice, transgenic animals lacking the IL-33 receptor ST2 exhibi

171 urther elevation of GFAP via crosses to GFAP transgenic animals leads to a shift in GFAP solubility,

172 ta TK mice, and we show that after treatment transgenic animals lose lymphoid, erythroid, and myeloid

173 ue mouse model was developed by breeding two transgenic animals: mice with reduced selenoprotein leve

174 The triple transgenic animals (moAPP x APPswe/PS1dE9) produced 20%

175 mutant in mammary epithelium cells and in a transgenic animal model caused apoptosis and accelerated

176 dings, cellular studies, and various in vivo transgenic animal model experiments.

177 es in mutant amyloid precursor protein (APP)-transgenic animal model of Alzheimer's disease (AD) that

178 results demonstrate for the first time in a transgenic animal model of schizophrenia a dissociation

179 Here we report a transgenic animal model that expresses the green fluores

180 o regulation of human UGT1A1 by chrysin in a transgenic animal model.

181 ngiopathy (CAA)-related microhemorrhage in a transgenic animal model.

182 eloped to assess the behavioral phenotype in transgenic animal models (rodent and fly).

183 of CRAC channels at an organism level using transgenic animal models and at a molecular level using

184 rticularly with RAGE, was studied in various transgenic animal models and by pharmacological blockade

185 -MSI), statistical analysis, and conditional transgenic animal models and cell samples to investigate

186 r's disease (AD) is supported by findings in transgenic animal models and forms the basis of clinical

187 es of Parkinson's disease and development of transgenic animal models bearing these mutations should

188 However, recent transgenic animal models cast doubt on their direct role

189 homeotic transformations, which can occur in transgenic animal models during embryonic development as

190 Transgenic animal models expressing rhodopsin glycosylat

191 These studies illustrate the utility of transgenic animal models for investigation of factors in

192 However, we have no suitable transgenic animal models for surgical interventions.

193 d genome editing and the rapid generation of transgenic animal models for the study of human genetic

194 ardiovascular diseases, yet lack of specific transgenic animal models has prevented it's in vivo anal

195 Although P23H cultured cell and transgenic animal models have been developed, there rema

196 In vitro expression of mutations and transgenic animal models have been instrumental in enhan

197 ropathologic and genetics studies as well as transgenic animal models have provided strong evidence l

198 One of the most widely used transgenic animal models in biology is Drosophila melano

199 id burden, astrocytosis, and microgliosis in transgenic animal models of Alzheimer's disease.

200 atients with LRRK2 mutations, and in several transgenic animal models of LRRK2, tau hyperphosphorylat

201 The generation of transgenic animal models of MSA coupled with an increasi

202 Transgenic animal models of Pompe disease mirroring the

203 Most transgenic animal models of retinal degeneration caused

204 ce and highlight similarities between AD and transgenic animal models of the disease.

205 sease are poorly understood, but research in transgenic animal models of the disorder is providing in

206 associate with early onset cases of PD; and transgenic animal models overexpressing alpha-synuclein

207 ne locus leads to autosomal dominant PD, and transgenic animal models overexpressing human alpha-synu

208 Evidence from humans and from transgenic animal models suggests that this strategy may

209 We addressed this issue by using transgenic animal models to modify the activity of enter

210 nd permanent neonatal diabetes mellitus, and transgenic animal models to study them, are exciting mil

211 In transgenic animal models, ADM and PanINs are initiated b

212 evaluation of conventional cell culture and transgenic animal models.

213 n oncogene sufficient to produce lymphoma in transgenic animal models.

214 ficking were studied in several knockout and transgenic animal models.

215 al diagnosis in humans and drug discovery in transgenic animal models.

216 e (SOD1) reduction prolongs survival in SOD1-transgenic animal models.

217 In experiments involving transgenic animals or animals treated with transgenic ce

218 ating genomes have allowed the generation of transgenic animals other than mice.

219 It has been reported that transgenic animals overexpressing human alpha-syn develo

220 3-kinase activity in the skeletal muscle of transgenic animals overexpressing human placental growth

221 82, P<0.05) and were significantly higher in transgenic animals (P<0.01).

222 Since the late 1990s, the use of transgenic animal platforms has transformed the discover

223 lication to the propagation of livestock and transgenic animal production, and of its scientific prom

224 rterial myocytes (prepared from wild-type or transgenic animals) provide a useful model for studying

225 luding in vitro mammalian tissue culture and transgenic animals, provide only limited quantities at h

226 RK phosphorylation among LT-resistant MEK1DD transgenic animals provided additional confirmation of t

227 ngly, chronic administration of leptin to AD-transgenic animals reduced the brain Abeta load, underly

228 are markedly suppressed in tumors from ErbB2 transgenic animals relative to normal tissue.

229 transgenic animals was determined, and RRM1 transgenic animals repaired chemically induced DNA damag

230 determine the outcome of ALI, and CREMalpha transgenic animals represent a model in which proinflamm

231 n subcortical monoaminergic systems, because transgenic animals responded to both amphetamine and gua

232 Reduction of Akt activity in transgenic animals resulted in impaired glucose toleranc

233 Unexpectedly, transgenic animals revealed an additional series of phot

234 oter-green fluorescent protein constructs in transgenic animals revealed that unc-94a is expressed in

235 ated DNA breakage-repair by sequencing seven transgenic animals, revealing extensive rearrangement of

236 zebrafish and it will be useful for imaging transgenic animals, screening for tumor engraftment, and

237 These transgenic animals should be useful in the study of homo

238 Allospecific cell lines generated from GNLY transgenic animals showed enhanced killing of target cel

239 v-1 null(-/-)/mouse mammary tumor virus-CR-1 transgenic animals showed enhanced motility and activati

240 Wild-type and transgenic animals showed little difference in constitut

241 Livers from the TSLP transgenic animals showed mild to moderate liver injury,

242 Transgenic animals showed varied degrees of phenotype ma

243 Analysis of neonatal pancreas in both transgenic animals shows each beta-cell stained positive

244 r, when the expression level of QKI-6 in the transgenic animal significantly exceeds what is needed f

245 bserved a significant increased incidence of transgenic animal solid tumors, which were not seen in l

246 Transgenic animal studies have demonstrated that hepatic

247 Based on transgenic animal studies, it is suggested that (CAG)(n)

248 Previous work using B cell antigen receptor transgenic animals suggested that self-antigen-specific

249 d in frequency equivalently in old and young transgenic animals, suggesting that immune regulation in

250 Consistently, coexpression of miR-11 in transgenic animals suppressed dE2F1-induced apoptosis in

251 city was also significantly decreased in the transgenic animals (tg+ = 0.4 +/- 0.5 versus wild-type =

252 pproximately 2 orders of magnitude higher in transgenic animals than in nontransgenic animals 2 to 4

253 Recent data deriving from transgenic animals that are deficient in LCs have begun

254 extended ex vivo manipulation by generating transgenic animals that express DeltaCD34-tk in the peri

255 delta cells, we generated and characterized transgenic animals that express Pax4 specifically in som

256 l-dependent increases are more pronounced in transgenic animals that express the HCV NS5A protein tha

257 er of vertebrate regeneration, and generated transgenic animals that fluorescently report RA signalin

258 Mating of these animals with transgenic animals that overexpress the BMP inhibitor no

259 kinson's disease and by neurodegeneration in transgenic animals that overexpress this protein.

260 Transgenic animals that were homozygous rather than hemi

261 However, in old transgenic animals the inhibition of GSK3 is lost and re

262 ed in the alpha-Tm E180G/S283A double mutant transgenic animals; these mice exhibited no signs of car

263 d with the expression of human antibodies in transgenic animals, this technique allowed upon immuniza

264 tion of autophagic structures in patient and transgenic animal tissue.

265 We used a gata2:eGFP transgenic animal to enable prospective isolation and ch

266 ibed that allow large numbers of fluorescent transgenic animals to be imaged simultaneously, facilita

267 on the use of molecular blocking agents and transgenic animals to elucidate disease pathways.

268 udy, we examined the response of the RasGRP1 transgenic animals to full-thickness incision wounding o

269 ensitivity of dopamine-signaling mutants and transgenic animals to the acetylcholinesterase inhibitor

270 When these lines are crossed, doubly transgenic animals uniformly develop a disease similar t

271 utase 1-yellow fluorescent protein (SOD1YFP) transgenic animals up to 6 mo of age.

272 ogy and electrophysiology appeared normal in transgenic animals up to 7 months of age.

273 um signaling in neurons, we generated mGluR5 transgenic animals using a Thy1 promoter to drive expres

274 e we have exploited lentiviruses to generate transgenic animals via the male germline.

275 The resultant EGFP expression pattern in the transgenic animals was analyzed by fluorescence microsco

276 Cellular toxicity in the retinas of transgenic animals was detected by a post-translational

277 DNA damage repair capacity in transgenic animals was determined, and RRM1 transgenic a

278 Through the use of transgenic animals, we also demonstrate that HMP-1 resid

279 nd FAD mutant PS1, which are co-expressed in transgenic animals, we expressed the PS1 M146V knock-in

280 Using transgenic animals, we previously showed that adverse in

281 ion of whole kidney marrow cells from double transgenic animals, we were able to generate specificall

282 Eight transgenic animals were born and shown to have stable an

283 Healthy transgenic animals were born with a functional heart pre

284 Ihh-overexpressing transgenic animals were generated and analyzed.

285 However, when transgenic animals were generated that overexpressed con

286 ugh spontaneous tumorigenesis did not occur, transgenic animals were highly susceptible to progestin/

287 s of muscle physiological performance in the transgenic animals were not different from wild type.

288 The muscle weights of transgenic animals were substantially increased compared

289 Transgenic animals were then bred with animals lacking m

290 rden, we observed a reduced number of double transgenic animals when treated with high-level doxycycl

291 rdiomyopathy, and arrhythmia inducibility in transgenic animals, which correlated with premature mort

292 hes has been stimulated by the generation of transgenic animals, which facilitates analysis of the im

293 t hyperactivation of IGF1-R signaling in p44 transgenic animals, which show an accelerated form of ag

294 Lastly, immunization of human-antibody transgenic animals with a lead mimetic evokes nAbs with

295 Using mutant and transgenic animals with a monospecific TCR, we discovere

296 rneuron classification, we took advantage of transgenic animals with fluorescently labeled PV interne

297 o gross or histological changes were seen in transgenic animals with increased iron in the epidermis.

298 After inoculation of transgenic animals with infectious PERV supernatants, vi

299 Treatment of transgenic animals with the Gi/o inhibitor pertussis tox

300 ology compared with AD transgenic mice or AD transgenic animals with type 1 diabetes (T1D).