ライフサイエンスコーパス: transgenic mice

1 ed complement system (FH/C4b-binding protein transgenic mice).

2 nd by erythrocyte-derived microvesicles from transgenic mice.

3 on ancestor (UCA) of the human VRC26 bnAb in transgenic mice.

4 lomerulosclerotic lesions in the anti-Thy1.1 transgenic mice.

5 a oligomers and plaques to monomers in 5XFAD transgenic mice.

6 against Toxoplasma gondii in HLA supermotif, transgenic mice.

7 ing the Tjp1 floxed mice and Myh6(Cre/Esr1*) transgenic mice.

8 urons from newborn male and female 4E-BP1-OE transgenic mice.

9 ues synaptic plasticity defects in tau P301S transgenic mice.

10 se (FASN) from OL progenitor cells (OPCs) in transgenic mice.

11 stemic anaphylaxis in human FcepsilonRIalpha transgenic mice.

12 on led to a partial rescue of cells in Duxbl transgenic mice.

13 thrombus formation in vivo in humanised PXR transgenic mice.

14 amyloid-dependent calcium dyshomeostasis in transgenic mice.

15 nd SMAD4 was observable in prostates of ETV1 transgenic mice.

16 ntrol, hAChE-S, hAPPswe, and hAChE-S/hAPPswe transgenic mice.

17 ntroducing the dystrophin mutation into IL-5 transgenic mice.

18 ioral and neuropathological phenotypes in HD transgenic mice.

19 ecomes detectable in Abeta precursor protein-transgenic mice.

20 analysis of data generated using the pLckCre transgenic mice.

21 he capacity of AS to propagate in bovine PrP transgenic mice.

22 molecular identifiers for the generation of transgenic mice.

23 pressing wild-type (WT) or mutant tau in non-transgenic mice.

24 their use compared to the bevy of available transgenic mice.

25 n may underlie the cognitive deficits in FUS transgenic mice.

26 xb8 myeloid progenitors from Cas9-expressing transgenic mice.

27 both primary human erythroid precursors and transgenic mice.

28 type labeled in adult pigmented Cdh3-GFP BAC transgenic mice.

29 a, reduced ovarian size, and subfertility in transgenic mice.

30 ene, an inducer of urothelial hyperplasia in transgenic mice.

31 ere prominent in skin lesions of human IL-26 transgenic mice.

32 erebellum, as was shown in Jdp2-promoter-Cre transgenic mice.

33 ed in brains of FTLD-TDP patients and TDP-43 transgenic mice.

34 FH, and CD74 in the KCNH2-3.1 overexpression transgenic mice.

35 tes using the Zona pellucida 3-Cre (Zp3-Cre) transgenic mice.

36 6 weeks) and old (57-60 weeks) wild-type and transgenic mice.

37 uction of proliferation in both CV- and R47H-transgenic mice.

38 supported by results in human (h) GRK4gamma transgenic mice.

39 ged adipocytes and increased body weights in transgenic mice.

40 2) in vivo in HSV-1-infected SYMP HLA-A*0201 transgenic mice.

41 ion against lethal EV71 challenge in hSCARB2-transgenic mice.

42 alidated in cultured cells, and used to make transgenic mice.

43 onsive element modulator isoform IbDeltaC-X) transgenic mice, a mouse model of extensive atrial remod

44 The hearts of mutant VCP transgenic mice also exhibit profound defects in cardiom

45 neuron and astrocyte cultures, as well as in transgenic mice and a non-transgenic mouse model of PD.

46 rein, we examined this activity in RARE-LacZ transgenic mice and by RARE-Luciferase reporter assays i

47 question, we generated 4E-BP1-overexpressing transgenic mice and confirmed marked reductions in prote

48 that RAN proteins drive C9-ALS/FTD in C9-BAC transgenic mice and establish a novel therapeutic approa

49 Cardiomyocyte-specific MCUb overexpressing transgenic mice and Mcub gene-deleted (Mcub(-)(/-)) mice

50 sion in muscle progenitor cells using double-transgenic mice and myoblastic cell lines.

51 t complementary tools for cell labeling with transgenic mice and organic dyes that allow high-resolut

52 We experimentally investigated transgenic mice and performed genetic studies in a UK-ba

53 Using transgenic mice and pharmacologic studies, we found that

54 kin lesions of imiquimod-treated human IL-26 transgenic mice and psoriasis patients.

55 human angiotensin-converting enzyme 2 (ACE2) transgenic mice and Syrian hamsters with both viruses re

56 pleted in SIRS, HSCs were spared in CHRFAM7A-transgenic mice and that these mice also had increased i

57 l by crossing RGS12(fl/fl) mice with CMV-Cre transgenic mice and then further induced the mice to dev

58 57BL/6 mice, Foxp3-diphtheria toxin receptor transgenic mice, and tumor necrosis factor (TNF) alpha r

59 loped negative allosteric modulators (NAMs), transgenic mice, and viral-assisted optogenetics to test

60 ivo, in SYMP individuals and SYMP HLA-A*0201 transgenic mice; and 2) in vivo in HSV-1-infected SYMP H

61 nts of atrial remodeling that are present in transgenic mice, animal AF models, and human AF.

62 uorescent histone 2B fusion protein (H2B-FP) transgenic mice are important tools for tracking the mit

63 K18 hACE2 transgenic mice are, therefore, highly susceptible to SA

64 lung and spleen of ESAT-6(1-20)-specific TCR transgenic mice at 2 wk postinfection with M. tuberculos

65 te-specific genetic inactivation of HDAC2 in transgenic mice attenuated the ultrastructural disorgani

66 Human papillomavirus transgenic mice bearing CIN lesions were treated with MP

67 Plasma transfusion from Apom transgenic mice but not Apom knockout mice blocked fibro

68 tment had only marginal effects on tumors in transgenic mice, but PEG-[SN22](4) treatment caused comp

69 learance was enhanced in vivo in CD68.hMcl-1 transgenic mice by reconstitution of apoptosis with BH3

70 otics in farm animal production, we produced transgenic mice carrying a bovine tracheal AMP gene prom

71 The i.p. administration of LPS to transgenic mice carrying a human SE-coding HLA-DRB1 alle

72 Transgenic mice carrying the intronic multimerized enhan

73 g native human IL-37 (IL-37Tg) with those of transgenic mice carrying the mutation of aspartic acid (

74 ion and increased CatA activity in the LV of transgenic mice (CatA-TG) reduced EC-SOD protein levels

75 We observed that in the lineage-tracing transgenic mice Cdh5-CreER(T2)::R26R-EYFP, endothelial-d

76 Within sessions, the response bias of transgenic mice changed with respect to lick behavior bu

77 e, from vaccinated ESAT-6(1-20)-specific TCR transgenic mice, conferred equivalent protection against

78 d changes in PKA signaling are attenuated in transgenic mice constitutively expressing adropin and in

79 Next, we generated C57BL/6 transgenic mice constitutively expressing the caspase-1

80 esistance to bacterial infection in the PG-1 transgenic mice could be resulted from the direct bacter

81 We generated a strain of transgenic mice, cU2, overexpressing human microRNA 34c,

82 Loss of stathmin in MMTV-Delta16HER2 transgenic mice decreased the incidence and increased th

83 Transgenic mice (Def(++)) expressing human alpha-Def-1 d

84 Anti-Thy1.1 transgenic mice develop glomerular lesions that mimic co

85 Transgenic mice develop interstitial myocardial and peri

86 Cdx2-transgenic mice develop myelodysplastic syndrome with pr

87 Transgenic mice developed a lethal immune dysregulation

88 Remarkably, 100% of the NP23-NHD13 double transgenic mice developed acute myeloid leukemia (AML) w

89 F4 (interferon regulatory factor 4) in Tcl-1 transgenic mice developing a murine CLL highly similar t

90 despite harboring highly dysfunctional fat, transgenic mice display massive beta-cell hyperplasia, r

91 GLK transgenic mice displayed enhanced distant metastasis.

92 In triple transgenic mice, downregulation of IKK2 (Sftpc-cRaf-IKK2

93 In human papillomavirus transgenic mice engineered to express human papillomavir

94 Physiological analysis revealed that the transgenic mice exhibit impaired diastolic function, wit

95 These PG-1 transgenic mice exhibited enhanced resistance to nasal b

96 In vivo, msuPAR2 transgenic mice exhibited signs of severe renal disease

97 In somatic transgenic mice expressing 66 GGGGCC repeats, inactivati

98 , we crossed OVE26 type 1 diabetic mice with transgenic mice expressing a constitutively active mTOR

99 Studies with transgenic mice expressing a G(q)-linked designer GPCR s

100 models of T2DM: (1) obesity-independent MKR transgenic mice expressing a mutated form of the human i

101 We have shown that transgenic mice expressing a picornavirus RNA-dependent

102 Male and female transgenic mice expressing a point mutation of mGlu5 tha

103 al nuclei (LDT/SubLDT) using male and female transgenic mice expressing channelrhodopsin-(ChR2)-EYFP

104 Using transgenic mice expressing Channelrhodopsin2 specificall

105 ral afferent nerve fibers in head-restrained transgenic mice expressing ChR2 in TRPV1 containing neur

106 Male and female transgenic mice expressing Cre recombinase in FSIs allow

107 tics of CWD prions passaged through deer and transgenic mice expressing different cervid PrP(C) polym

108 d photoablation of single synapses in mature transgenic mice expressing fluorescent labels in neurons

109 Here, we show that transgenic mice expressing human angiotensin-converting

110 To test this possibility, transgenic mice expressing human BDNF in skeletal muscle

111 ted with cognitive dysfunction using APPSwDI transgenic mice expressing human beta-amyloid precursor

112 observed in the brain extracellular space of transgenic mice expressing human CysC as compared to lit

113 coagulability induced by 5B9 with heparin in transgenic mice expressing human PF4 and FcgammaRIIA rec

114 1P) knock-in mice were generated by crossing transgenic mice expressing lecithin retinol acyltransfer

115 sensitive to the effects of heat stress, and transgenic mice expressing Mgat4d were partially protect

116 mpared suppression of innate inflammation in transgenic mice expressing native human IL-37 (IL-37Tg)

117 We inoculated transgenic mice expressing normal human PrP with amplifi

118 of CD8 T cells on gastrointestinal motility, transgenic mice expressing ovalbumin on enteric neurons

119 tolerance mechanisms has relied primarily on transgenic mice expressing TCRs targeting well-character

120 vivo real-time dual-recording in conditional transgenic mice expressing the calcium indicator protein

121 eceptors to activate the targeted B cells in transgenic mice expressing the germline VH of the VRC01

122 Here, we evaluate transgenic mice expressing the human angiotensin I-conve

123 ur subsequent studies using cardiac-specific transgenic mice expressing the transcriptionally active

124 on of C/EBPbeta in human wild-type alpha-Syn transgenic mice facilitates PD pathologies and elicits m

125 ogenic skeletal muscle biology, we generated transgenic mice for doxycycline-inducible and skeletal m

126 ic mouse variants (WT, R15L, & S59L), TDP-43 transgenic mice, FTLD-TDP patient brains, and transfecte

127 from the compound mice and controls into HGF-transgenic mice further uncovered that HGF induces prost

128 Last, aged male and female APP/PS1 transgenic mice, genetically null for the beta2 nAChR su

129 Splenocytes from HLA-DQ8 transgenic mice given TIMP-GLIA nanoparticles, but not c

130 othelial cell (EC) migration and global Glrx transgenic mice had impaired ischemic vascularization, t

131 recent study by Liu and colleagues described transgenic mice harboring a large repeat expansion (C9-5

132 Here, using cell-based assays and tau transgenic mice harboring an acetylation-mimic mutation

133 Transgenic mice harboring an inactivating mutation in th

134 basis to the HSAN V phenotype, we generated transgenic mice harboring the human 661C>T mutation in t

135 ies of bacterial artificial chromosome (BAC) transgenic mice harboring this expansion described an ab

136 l dystrophy type1 (LCD1) and generated novel transgenic mice harbouring a single amino acid substitut

137 Tracking genetically labelled cells in transgenic mice has given insight into cell behavior, bu

138 Several Bmpr2 transgenic mice have been reported to develop mild spont

139 Hepatocyte-specific glypican-3 transgenic mice have decreased levels of phosphorylated

140 Transgenic mice (HBUS) that express the epidermal growth

141 the present work, hepatocyte-specific COX-2 transgenic mice (hCOX-2-Tg) and their wild-type (Wt) lit

142 and murine colon cancer cell lines, and FXR transgenic mice, here we identified an additional, poten

143 In the older transgenic mice, however, LTP was impaired in a way that

144 from leukocyte Ig-like receptor B1 (LILRB1) transgenic mice, humanized mice, and genetically enginee

145 oteins in hearts from Parkin(-/-) and Parkin transgenic mice identified the transcription factor estr

146 2 signaling on oligodendroglia, we generated transgenic mice in which Cxcr2 is selectively ablated in

147 ct of MPA was absent in human papillomavirus transgenic mice in which the expression of progesterone

148 sease-relevant Ags, without the need for BCR transgenic mice, in settings where tolerance pathways ar

149 s, we used dental pulp cells from a panel of transgenic mice, in which fluorescent protein expression

150 expression of constitutively active FoxO1 in transgenic mice induced an increase in hepatic serpinB1

151 ns and a similar demyelinating neuropathy in transgenic mice, is instead retained the ER where it act

152 though control LTP was impaired in the young transgenic mice, it was not TNFalpha-dependent.

153 Here, we show that Vav1-hJAK2V617F transgenic mice (JAK2V617F+) have high BM FN content ass

154 oth GDE3 and CB2 in the spleen, spleens from transgenic mice lacking GDE3 displayed doubling of LPI c

155 Tau transgenic mice lacking HDAC6 show reduced survival char

156 Although transgenic mice lacking the mitochondrial complex I acce

157 Transgenic mice lacking the N-terminal region of the WWP

158 c c-fms promoter to generate c-fms-eGFP-L10a transgenic mice (Mac(TRAP)).

159 We assessed this possibility using transgenic mice (MIP-TF mice) whose B-cells express enha

160 fter a stroke or sham operation in DCX/DsRed transgenic mice of either sex.

161 Using transgenic mice, optogenetics, and pharmacogenetics, we

162 survival or motor phenotypes in C9orf72 BAC transgenic mice originally described by Liu et al.

163 Although transgenic mice overexpressing asyn have previously been

164 bit DYRK1A function only during gestation of transgenic mice overexpressing Dyrk1a (mBACtgDyrk1a).

165 In transgenic mice overexpressing human Abeta, the brain-to

166 pathology have been observed in the brain of transgenic mice overexpressing human tau with aggregatio

167 DN and its underlying mechanism, we crossed transgenic mice overexpressing kallistatin with OVE26 mi

168 We previously reported that, in young transgenic mice overexpressing mutated amyloid precursor

169 on and differentiation of fat cells, whereas transgenic mice overexpressing Tagln2 using the adipocyt

170 We generated transgenic mice overexpressing TMEM43 in either its wild

171 In addition, transgenic mice overexpressing VDR in beta-cells were pr

172 Transgenic mice overexpressing WT VCP exhibit normal car

173 Here we generated heart-specific transgenic mice overexpressing WT VCP or a VCP(K524A) mu

174 K18 ACE2 transgenic mice produced a modest TH1/2/17 cytokine stor

175 ssion of heart failure (HF) and CaMKIIdeltaC transgenic mice rapidly develop HF and arrhythmias.

176 RdRP-transgenic mice (RdRP mice) resist infection and disease

177 (B6xA/J)F1 and (B6xNOD)F1 HER2 transgenic mice received Ad/E2TM after NK cell depletion

178 strategy to attenuate acute kidney injury in transgenic mice receiving contrast material.

179 igher (p < 0.05) brain signal enhancement in transgenic mice relative to wild type mice at all dose l

180 EZH2(T416D) in mammary epithelia of HER2/Neu transgenic mice reprograms HER2-driven luminal tumors in

181 meleon-Nano15 (fluorescent calcium reporter) transgenic mice, respectively.

182 ate-specific overexpression of Myc in Hi-Myc transgenic mice resulted in overexpression of ACLY, ACC1

183 The lack of this mechanism in transgenic mice results in aberrant GH secretion and bod

184 In OT-II CD4(+) anti-OVA TCR transgenic mice sensitized to ovalbumin antigen, B cell

185 in the early-stage obese adipose tissue, the transgenic mice showed a healthier metabolic profile, in

186 sistance to nasal bacterial infection as the transgenic mice showed a higher survival rate (79.17% VS

187 TIMP3 transgenic mice showed compromised bone integrity as opp

188 /c mice and native virus in hACE2-expressing transgenic mice showing activity at the lowest tested do

189 -old humanized regulatory light chain mutant transgenic mice silenced the mutated allele (RLC-47K) wi

190 In K5.TGFbeta1/K5.Smad7 bigenic (double transgenic) mice, Smad7 transgene expression reversed tr

191 vivo studies, we developed humanized RNase 7 transgenic mice, subjected them to experimental UTI, and

192 K18 hACE2 transgenic mice succumbed to SARS-CoV-2 infection by day

193 While hACE2 transgenic mice support infection and pathogenesis, thes

194 Following injection to AD transgenic mice, TDP-43 induced inflammation, interacted

195 ive deletion of HIF-1alpha in CNS neurons in transgenic mice tended to blunt the increase in HVR that

196 Transgenic mice (Tg) mice specifically overexpressing hu

197 nd increased marrow adipocytes; in contrast, transgenic mice (Tg) with osteoblastic-specific deletion

198 of skin samples from hamsters and humanized transgenic mice (Tg40h) at different time points after i

199 reatly improved in pregnant Lm-infected GNLY-transgenic mice than in wild-type mice that lack GNLY.

200 his issue by using HBV replication-competent transgenic mice that are depleted of circulating HBsAg,

201 ins of uninjured and olfactory bulbectomized transgenic mice that correspond to distinct stages in th

202 njecting a uracil analog, 4-thiouracil, into transgenic mice that express cell-type-specific uracil p

203 Transgenic mice that express either a NUP98-PHF23 (NP23)

204 Here, we report findings from transgenic mice that express human PrP 117V on a mouse P

205 trackable populations of B cells in B1-8i Ig transgenic mice that express the VH186.2 H chain and rec

206 We have developed transgenic mice that overexpress [(25, 28, 29) triprolyl

207 We generated transgenic mice that overexpress fluorescence-tagged IDO

208 Next, we used transgenic mice that overexpress galanin in noradrenergi

209 regulating NF-kappaB activation by studying transgenic mice that overexpress mitochondrial-targeted

210 Transgenic mice that overexpress mutant SOD1 develop par

211 performed histologic analyses of livers from transgenic mice that overexpress the AATD-associated Pi*

212 urodegeneration in vivo, we generated triple transgenic mice that overexpressed alpha-syn A53T mutati

213 We generated transgenic mice that overexpressed TIMP3 or [-1A]TIMP3 d

214 Accordingly, transgenic mice that prostate-specifically overexpress E

215 ssion in lung, blood and bone marrow of Cas9 transgenic mice that receive systemic injection of adeno

216 Here, using K18-hACE2 transgenic mice that were originally developed for SARS

217 work we show, in freely behaving SUDEP-prone transgenic mice, that apnea is induced when spontaneous

218 However, in hGRK4gamma 142V transgenic mice, the renal ETBR was hyperphosphorylated

219 The exposure of LRRK2 transgenic mice to a sub-toxic dose of MPTP resulted in

220 uximab was given to human CD20(+) (hCD20(+)) transgenic mice to continuously deplete hCD20(+)-express

221 Using transgenic mice to fate map and to selectively kill SVZ-

222 e an astroglia-specific promoter fragment in transgenic mice to identify an anatomically defined subs

223 se widefield and 2-photon calcium imaging of transgenic mice to measure mesoscale and cellular respon

224 Here, we have generated compound transgenic mice to overexpress Wnt family member 7B (Wnt

225 Using transgenic mice to perturb expression of either GluN2A o

226 address causality, we used chemogenetics in transgenic mice to selectively manipulate activity of ne

227 We crossed DO mice with syngeneic HER2 transgenic mice to study the genetics of an anti-self HE

228 We used Fos(CreERT2/+)/Ai14 transgenic mice to tag cells activated by and potentiall

229 o improve microvascular blood flow in sickle transgenic mice undergoing I/R, and we suggest how such

230 In neonatal transgenic mice, up to postnatal day 14, a similar incre

231 ically expressed in the respiratory tract of transgenic mice upon induction by bacterial infection.

232 se brains, and inhibiting PKR in C9orf72 BAC transgenic mice using AAV-PKR-K296R or the Food and Drug

233 odel of beta-amyloidosis, we compared PS2APP transgenic mice versus PS2APP mice lacking Trem2 (PS2APP

234 The phenotype of CRISPRi transgenic mice was compared to mice with germline delet

235 The response of DO F1 HER2 transgenic mice was remarkably variable.

236 Ex vivo electrophysiology in double-transgenic mice was used to assess intrinsic excitabilit

237 to neurovirulence, assessed as paralysis of transgenic mice, was low in isolates from those vaccinat

238 Here, using AXIN2 lineage tracing in BAC-transgenic mice, we confirm the regenerative potential o

239 n. Using a vaccine-challenge model in HLA-DR transgenic mice, we demonstrated significant alterations

240 In the transgenic mice, we detected RNase 7 expression in the k

241 Using a selective viral tracing method and transgenic mice, we examined the connectivity of four co

242 Using transgenic mice, we have demonstrated that expression of

243 ers that were experimentally validated using transgenic mice, we identified a 2.9-kb regulatory eleme

244 maging of mammary cell ensembles from GCaMP6 transgenic mice, we reveal how stimulus evoked Ca(2+) os

245 Using transgenic mice, we show that increased or decreased OPC

246 ombined with optogenetics in male and female transgenic mice, we show that VP(VGluT2) neurons prefere

247 Finally, TH-MYCN transgenic mice were administered cyclophosphamide alone

248 CD11b-cre transgenic mice were also used to delete Lpar1 in microg

249 NP23-NHD13 double transgenic mice were generated by interbreeding NP23 and

250 o test this hypothesis, Lck-Dlx5;Lck-MyrAkt2 transgenic mice were generated.

251 groups of myosin regulatory light chain N47K transgenic mice were injected with M7.8L packaged in ade

252 cin aminoglycoside nephropathy model of INF2 transgenic mice were used to demonstrate altered dynein-

253 e role of PKCbetaII in B cells by generating transgenic mice where expression of the transgene is dir

254 itionally and selectively ablated in mature, transgenic mice where the human diphtheria toxin (DT) re

255 this question, we generated male and female transgenic mice wherein a disrupted cGMP-gated channel (

256 eparation isolated from Pirt-Cre;R26-GCaMP6s transgenic mice, which allows for simultaneous monitorin

257 We then studied HIV-transgenic mice, which develop HIVAN in the absence of H

258 Using transgenic mice, which enabled endothelium-specific and

259 vant phenotypes than those seen in Hfh4-ACE2 transgenic mice, which express human ACE2 under the cont

260 lastocysts derived from lipodystrophic A-ZIP transgenic mice, which have a genetic block in adipogene

261 nce in cancer etiology, we subjected p16-3MR transgenic mice, which permit the identification and sel

262 Crossing msuPAR2-transgenic mice with 3 different integrin beta3 deficien

263 Transgenic mice with a knock-in mole CYP17A1 enhancer or

264 Furthermore, immunization of HLA-DR transgenic mice with a mixture of the two immunodominant

265 Immunization of HLA-DR transgenic mice with a mixture of these two immunodomina

266 cle defects accompany cardiac dysfunction in transgenic mice with a mutation in the myosin regulatory

267 Rhizolutin treatment of APP/PS1 double transgenic mice with AD significantly dissociated hippoc

268 nd chemerin-overexpressing mice and injected transgenic mice with anti-ChemR23 antibody to block Chem

269 Experiments in transgenic mice with cell-specific overexpression of DEL

270 cells) and in vivo (homozygote/homozygote bi-transgenic mice with CF).

271 induce Tregs in H. polygyrus bakeri-infected transgenic mice with constitutively high T cell-specific

272 ess these issues, we generated a new line of transgenic mice with Cre-driver genes (Foxj1 and Scgb1a1

273 Transgenic mice with desensitized cones (GNAT2 (cpfl3) l

274 Here we demonstrate that inoculation of transgenic mice with different strains of recombinant or

275 To test this hypothesis, transgenic mice with doxycycline-inducible expression of

276 veral antibiotics, we treated male APPPS1-21 transgenic mice with either individual ABX or an ABX coc

277 We generated transgenic mice with expression of Ca(V)1.2 alpha(1C) su

278 lation of neuroinflammation, male and female transgenic mice with forced overexpression of Mfn2 speci

279 targeting Sirt3 expression, we developed new transgenic mice with global Sirt3OX (Sirt3 overexpressio

280 Here, we report the generation of transgenic mice with Gq-coupled designer receptors exclu

281 To test this, we generated transgenic mice with human CDRH3 diversity but simultane

282 Transgenic mice with hypoactive EPO receptor (EPOR) sign

283 voked gamma activity increase is enhanced in transgenic mice with impaired astrocyte calcium signalin

284 Transgenic mice with inducible ablation of Adora2a in en

285 ion in diabetic cardiomyopathy, we generated transgenic mice with inducible cardiomyocyte-specific ex

286 n, HBV infected human liver chimeric mice or transgenic mice with integrated HBV genome.

287 med shotgun proteomics analyses of aortas of transgenic mice with macrophage-specific overexpression

288 rophic lateral sclerosis (ALS), we generated transgenic mice with neuron-specific expression of a sup

289 We have previously reported transgenic mice with neuronal expression of human TDP-43

290 gical tools were used in ex vivo slices from transgenic mice with region-specific Cre recombinase exp

291 We used transgenic mice with resistance to BBB breakdown to inve

292 m and behavior in GluA1 knockout mice and in transgenic mice with selective knockdown of the GluA1 su

293 Transgenic mice with sustained elevation of MG53 in the

294 anced green fluorescent protein (Prox1-EGFP) transgenic mice with telomere dysfunction.

295 togenesis, we generated a GRTH Knock-In (KI) transgenic mice with the R242H mutation.

296 assessed longitudinally and spatially using transgenic mice with ubiquitously expressed Cre/ER and t

297 ined unchanged in HAPOB100 Tg (human APOB100 transgenic) mice with fully functional LDLr, despite inc

298 skin-aging progression, we demonstrate that transgenic mice, with selective expression of CCN1 in de

299 Finally, ATXN1[82Q ] transgenic mice-with cerebellum limited expression of mu

300 Deletion of EC- Notch1 in transgenic mice worsens hypoxia-induced pulmonary hypert