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

3 nduces pigment formation in cell culture and transgenic animals.

4 to distinguish heterozygous from homozygous transgenic animals.

5 ted using advanced model systems, especially transgenic animals.

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

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

8 e interrogation that decreases dependency on transgenic animals.

9 eads to synaptic and cognitive impairment in transgenic animals.

10 oinjected than traditional methods to obtain transgenic animals.

11 t neurodegenerative changes in the Abeta;tau transgenic animals.

12 enhanced in lungs from Chit1 overexpressing transgenic animals.

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

14 ME normalized pressure-dependent drainage in transgenic animals.

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

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

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

18 d with altered protein levels in 4-month-old transgenic animals.

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

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

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

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

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

24 enotypes, leaving autoregulation impaired in transgenic animals.

25 and liver function tests were unaffected in transgenic animals.

26 defects resulting in retinal degeneration in transgenic animals.

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

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

29 ed to it confer greater ethanol tolerance on transgenic animals.

30 murine pancreatic islets, derived from egfp transgenic animals.

31 homeostasis was not grossly perturbed in the transgenic animals.

32 30 min after induction and last for 24 h in transgenic animals.

33 origenesis was significantly dampened in the transgenic animals.

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

35 embryogenesis and for efficiently generating transgenic animals.

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

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

38 the frequency of cardiac arrhythmias in Ras transgenic animals.

39 ase the cellular specificity of silencing in transgenic animals.

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

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

42 be transmitted for many generations in these transgenic animals.

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

44 edominates in freshly isolated NK cells from transgenic animals.

45 n and rapidly accelerates tumor formation in transgenic animals.

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

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

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

49 significantly higher scaling exponent in the transgenic animals.

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

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

52 umanness" assessment of BCR repertoires from transgenic animals.

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

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

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

56 ecreased Akt and MAPK phosphorylation in the transgenic animals.

57 insertion into the genome to produce stable transgenic animals.

58 and enteric nervous system function in these transgenic animals.

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

60 evels were not associated with malignancy in transgenic animals.

61 permanent genomic insertion produces stable transgenic animals.

62 stably transmitted to a third generation of transgenic animals.

63 ermanent genomic insertion to produce stable transgenic animals.

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

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

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

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

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 due to high circulating levels of IL-23, as transgenic animals and controls had similar levels of th

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 d molecular imaging in rodents, including AD transgenic animals, and macaques, which revealed that ou

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

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

93 her, these changes occurred in the Abeta;tau transgenic animals at greater levels than worms harborin

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 We show that transgenic animals containing Hap-I have increased blood

104 ngly to chromatin obtained from the liver of transgenic animals containing Hap-I than to liver chroma

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

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

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

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

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

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

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

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

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

114 Functional studies using transgenic animals demonstrated that this modular system

115 A transgenic animal derived mAb (PCa75) targeted against a

116 is rather prevalent, 18 out the 21 approved transgenic animal-derived antibodies have at least one '

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

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

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

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

121 etween 2 and 3 months of exercise 3 out of 6 transgenic animals developed self-terminating spontaneou

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

123 DeltaNp63 transgenic animals display dramatic defects in hair foll

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

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

126 Transgenic animals displayed increased energy expenditur

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

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

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

130 oral control over MITO-Tag expression, these transgenic animals enable the rapid, cell-type-specific

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

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

133 We demonstrate that MK4 transgenic animals exhibit a significant decrease in inf

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

135 Transgenic animals exhibited higher and inheritable resi

136 harbor" locus in ferret zygotes and created transgenic animals expressing a dual-fluorescent Cre-rep

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

138 Transgenic animals expressing both human proteins exhibi

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

140 Finally, transgenic animals expressing constitutively active Akt

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

142 Transgenic animals expressing Drosophila Fig4 missense m

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

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

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

146 Transgenic animals expressing GFP regulated by the glial

147 Transgenic animals expressing mutations that disrupt Ca(

148 t was validated using immunofluorescence and transgenic animals expressing NF-kappaB inducible imagin

149 Indeed, transgenic animals expressing vGPCR manifest vascular tu

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

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

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

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

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

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

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

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

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

159 Transgenic animals have become a widely used model to id

160 Dsp transgenic animals have been engineered with superior en

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

162 n, but findings from studies of various AMPK transgenic animals have not reached consensus on this ma

163 Transgenic animals heterozygous for the germline Stat5 n

164 Tau transgenic animals homozygous for loss of these enhancer

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 Using non-transgenic animal model of Abeta oligomer injection as w

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

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

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

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

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

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

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

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

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

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

192 microgliosis are consistently observed in AD transgenic animal models devoid of such pathologies, bri

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

194 r across species, our data also suggest that transgenic animal models expressing human ACE2, such as

195 Transgenic animal models expressing rhodopsin glycosylat

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

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

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

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

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

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

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

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

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

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

206 Transgenic animal models of Pompe disease mirroring the

207 Most transgenic animal models of retinal degeneration caused

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

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

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

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

212 Fluorescent proteins are used extensively in transgenic animal models to label and study specific cel

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

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

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

216 agy has therapeutic benefits in cellular and transgenic animal models.

217 evaluation of conventional cell culture and transgenic animal models.

218 research is performed using cell culture and transgenic animal models.

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

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

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

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

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

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

225 3-kinase activity in the skeletal muscle of transgenic animals overexpressing human placental growth

226 82, P<0.05) and were significantly higher in transgenic animals (P<0.01).

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

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

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

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

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

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

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

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

235 substantia nigra pars compacta of aged LRRK2 transgenic animals revealed alterations in autophagosome

236 Unexpectedly, transgenic animals revealed an additional series of phot

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

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

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

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

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

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

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

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

245 Transgenic animals showed varied degrees of phenotype ma

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

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

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

249 Our pharmacological and transgenic animal studies find that reducing polyamines

250 Transgenic animal studies have demonstrated that hepatic

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

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

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

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

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

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

257 Transgenic animals that cannot form new myelin exhibit d

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

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

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

261 Transgenic animals that were homozygous rather than hemi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Transgenic animals were then bred with animals lacking m

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

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

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

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

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

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

295 ly human antibodies as biotherapeutics using transgenic animals with a notion that such mAbs bypass h

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).