ライフサイエンスコーパス: double knockout mice

1 uc1 and T-cell receptor alpha chain (Muc/TCR double knockout mice).

2 with mice with disruptions in Vil1 and Gsn (double-knockout mice).

3 y to account for the attenuated phenotype in double knockout mice.

4 0(-/-) IL-6(-/-) or IL-10(-/-) STAT3(Hep-/-) double knockout mice.

5 nfections in wild-type BALB/c and IL-4/IL-13 double knockout mice.

6 ced in both S6K2 knockout mice and S6K1/S6K2 double knockout mice.

7 ed in the brain, we also generated Pak5/Pak6 double knockout mice.

8 everse the observed heart dysfunction in the double knockout mice.

9 findings were seen in the lungs of ADA/A(3) double knockout mice.

10 ficantly delayed in L-selectin-deficient and double knockout mice.

11 as mostly blocked in CD40-Act1 and BAFF-Act1 double knockout mice.

12 early progression were delayed in RAG1/LDL-R double knockout mice.

13 tion of cocaine place preference in DAT/SERT double knockout mice.

14 persists in suprabasal cells in Skn-1/Tst-1 double knockout mice.

15 severe desmoglein 3 mutant phenotype in the double knockout mice.

16 ly reduced in the synaptophysin/synaptogyrin double knockout mice.

17 te for the loss of synapsins I and II in the double knockout mice.

18 and their numbers are unaffected in K(b)D(b) double knockout mice.

19 d neuron-specific Bcl7a and Bcl7b single and double knockout mice.

20 tion in lungs, we generated Ifit2/IFNAR(-/-) double knockout mice.

21 ts, wild-type and melatonin receptor MT1/MT2 double knockout mice.

22 ne secretion that are exacerbated in Itk/Txk double-knockout mice.

23 ficiency, we generated Cited2 and HIF-1alpha double-knockout mice.

24 sence of particular muscles in the Msc;Tcf21 double-knockout mice.

25 ology and therefore created STAT1/STAT6(-/-) double-knockout mice.

26 hemolysis was exclusively manifested in the double-knockout mice.

27 s observed in forebrain-specific Lmnb1/Lmnb2 double-knockout mice.

28 gulated CCL3, we generated CCL3(-/-)TTP(-/-) double-knockout mice.

29 n over 3 days; hgd40 reduced colitis in TNFR double-knockout mice.

30 e histopathological features observed in the double-knockout mice.

31 aling in this model by generating ADA/A(2B)R double-knockout mice.

32 generations to generate Mstn(-/-)/Ldlr(-/-) double-knockout mice.

33 on that was also absent in CRF1 + 2 receptor double-knockout mice.

34 oprotein (Apo)E-deficient mice and ApoE-GaL3 double-knockout mice.

35 s in thymocyte maturation in Deltex1/Deltex2 double-knockout mice.

36 n the latter case in both wild-type and TNFR double-knockout mice.

37 -/- mice is corrected in [Akp2-/-; Enpp1-/-] double-knockout mice.

38 reduction in the expression of Arx in Dlx1/2 double-knockout mice.

39 ice and Ldlr(-/-)/apoA-I null (apoA-I(-/-)), double-knockout mice.

40 ne regulation were absent in the CAR-null or double-knockout mice.

41 and developmental phenotypes of Rb and K-ras double-knockout mice.

42 (apoA-I(-/-)) gene, LDLr(-/-)/apoA-I(-/-) or double-knockout mice.

43 reviously derived PKIalpha mutants to obtain double-knockout mice.

44 generate H1c/H1(0), H1d/H1(0), or H1e/H1(0) double-knockout mice.

45 initiation was significantly delayed in the double-knockout mice.

46 further reduced by 2- to 3-fold in AQP1/AQP5 double-knockout mice.

47 ells from the colon crypts of Msh2-/- p53-/- double-knockout mice.

48 g order) by WT, STC1 knockout, and STC1/STC2 double-knockout mice.

49 d Apoa1 knockout mice to generate Apoe/Apoa1 double-knockout mice.

50 as shown by megakaryocyte-specific (Pf4-Cre) double-knockout mice.

51 inding lectin-A and mannose-binding lectin-C double-knockout mice.

52 and an overall delay in ossification in the double-knockout mice.

53 he brain and viscera in all genotypes except double-knockout mice.

54 res was significantly ameliorated in TRPC1/4 double-knockout mice.

55 (-/-), IRF-8(-/-), and IRF-4(-/-)IRF-8(-/-) (double-knockout) mice.

56 Daily urine output in AQP1/AQP3 double knockout mice (15 ml) was 9-fold greater than in

57 nesoid X receptor; Small Heterodimer Partner double knockout mice, a model for bile acid overload, di

58 e roles of HA in cutaneous injury responses, double-knockout mice (abbreviated as Has1/3 null) that l

59 In NEP/NEP2 double-knockout mice, Abeta levels were marginally incre

60 However, Nfil3/Rag1 double-knockout mice adoptively transferred with wild-ty

61 The Id1-Id3 double knockout mice also display vascular malformations

62 The double knockout mice also exhibited gene- and tissue-spe

63 Double knockout mice also had normal ERG responses in da

64 mice lacking RPE65, but they are reduced in double knockout mice also lacking opsin, suggesting a co

65 s have lower rate of neuritogenesis in vitro Double-knockout mice also have reduced levels of GM1 gan

66 n cell development, we generated Brn3b/Brn3c double knockout mice and analyzed their retinas and opti

67 oduced Slc39a14 single and Slc30a10/Slc39a14 double knockout mice and compared their phenotypes with

68 duced galactosylceramide in the brain of the double knockout mice and the significantly higher psycho

69 olipoproteins worsened behaviour deficits of double knockout mice and their performance was undisting

70 s further enhanced in ApoE(-/-)LXRalpha(-/-) double knockout mice and was accompanied by higher serum

71 However, using B cell-specific c-/N-myc double-knockout mice and E(mu)-myc transgenic mice bred

72 We also generated RIG-I(-/-) x MDA5(-/-) double-knockout mice and found that a lack of both RLRs

73 s illustrated by their presence in K(b)/D(b) double-knockout mice and in mice lacking a nonclassical

74 axis, MI was induced in Cd36(-/-) Mertk(-/-) double-knockout mice and led to increases in myocardial

75 uTAC were near completely lost in M2/M4(-/-) double-knockout mice and potency of BuTAC was right-shif

76 G4 mice, cultures from heterozygous Il13-Il4 double knockout mice, and a highly selected set of BABL/

77 models-wild-type C57BL/6 mice, LDLR/apobec-1 double knockout mice, and human apolipoprotein (apo)B/ch

78 a and total urinary iron was observed in the double knockout mice, and this was associated with compr

79 eedback response was severely blunted in the double-knockout mice, and synthesis of cholesterol and f

80 ypically characterize ADAMTS-4- and ADAMTS-5-double-knockout mice, and to determine the effect of del

81 neurons was completely abolished in TRPC1/4 double-knockout mice, and was abolished in 74% of latera

82 levated out of proportion to the mRNA in the double-knockout mice, apparently owing to the failure of

83 The double knockout mice appear healthy, reproduce well and

84 KLF1(-/-) KLF2(-/-) double knockout mice are anemic at embryonic day 10.5 (E

85 /-) mice and the brains of PS1/2 conditional double knockout mice are inversely correlated.

86 Nova1/Nova2 double knockout mice are paralyzed and fail to cluster A

87 Tet1/Tet2 double-knockout mice are characterized by developmental

88 STAT3, since T lymphocytes from STAT1-STAT3 double-knockout mice are growth stimulated by IFN-alpha/

89 In addition, CD8-/-CD28-/- double-knockout mice are susceptible to EAE.

90 FGF1-FGF2 double-knockout mice are viable and fertile and do not d

91 Surprisingly, double-knockout mice are viable, with subtle alterations

92 tion that the enhanced flu susceptibility of double-knockout mice arises from an intrinsic impairment

93 et-fed apoE and apoE/endothelial NO synthase double knockout mice as models of atherosclerosis, we sh

94 D), lesion development was reduced by 54% in double knockout mice, as compared with matched LDLR(-/-)

95 Deletion of LOX-1 (LDLR/LOX-1 double knockout mice) attenuated autophagy, TLR9 express

96 ogical changes usually occurred in untreated double knockout mice between approximately 3 (weaning) a

97 Both Smug1-knockout and Smug1/Ung-double knockout mice breed normally and remain apparentl

98 o began to occur between P4 and P9 in e,nNOS double knockout mice, but labeling was more extensive in

99 ssure and baroreflex function was reduced in double knockout mice, but no more than single knockout o

100 Compared with LDLR(-/-) mice, double-knockout mice (CatS(-/-)LDLR(-/-)) developed sign

101 b(-p50NF-kappaB-/-) and db(-)/db(-PARP-1-/-) double knockout mice compared with db(-)/db(-) mice.

102 acic aorta was reduced by 59% in CX3CR1/apoE double knockout mice compared with their CX3CR1(+/+)/apo

103 ion of tumor growth and metastasis in NOX1/2 double knockout mice compared with WT mice.

104 e reductions also were observed in Rag1/IDO1 double-knockout mice compared with Rag1-/- mice (which l

105 was significantly less severe in ADAMTS-4/5-double-knockout mice compared with WT mice.

106 from palm oil) consumption, LDLr-/- LCAT-/- double knockout mice, compared with LDLr-/- mice, had si

107 rs grow 2-fold faster in the tumstatin/TSP-1 double-knockout mice, compared with either the tumstatin

108 In double-knockout mice, constitutive phosphorylation of EI

109 However, only double-knockout mice continued to exhibit low liver Hamp

110 Moreover, the double-knockout mice could potentially serve as models i

111 xpressed in the adult myocardium, we created double-knockout mice (CRbL/L p130-/-) to determine it th

112 lar myocytes isolated from beta(1)beta(2)-AR double knockout mice, creating pure beta(1)-AR and beta(

113 against the Sprn 3' UTR, we established that double-knockout mice deficient in both Sho and PrP(C) ar

114 efense to flu by analyzing Argonaute 1 and 3 double-knockout mice deficient in components of the RNA-

115 decreased CD4 or MHC class II expression and double-knockout mice deficient in MHC class I- and II-re

116 us model of oral staphylococcal infection in double knockout mice, deficient in the receptors for IL-

117 n, we generated delta-sarcoglycan/dystrophin double knockout mice (delta-Dko) in which residual sarco

118 These double knockout mice demonstrate a complete loss of D1 p

119 nd both IL-1beta knockout and IL-1beta/IL-18 double knockout mice demonstrated significant splenic B

120 one marrow cells obtained from TLR2 and TLR4 double-knockout mice, demonstrating that P. gingivalis L

121 In addition, the Wwox;p53(Deltaosx1) double knockout mice developed poorly differentiated ost

122 When placed on a high-fat diet, these double-knockout mice developed atherosclerosis at a much

123 By contrast ApoE/GaL3 double-knockout mice did not show an increase in patholo

124 ith Ku80, Lig4, and Atm deficiency, Paxx/Xlf double-knockout mice display embryonic lethality associa

125 D88 is dominant over TRIF because TRIF/MyD88 double knockout mice displayed a more pronounced phenoty

126 Infection of the double-knockout mice displayed a lack of lung disease an

127 with this possibility, Fmr1(-/y); Cpeb1(-/-) double-knockout mice displayed amelioration of biochemic

128 Using Sr-bI/Abcg5 double knockout mice (dko), the present study investigat

129 f either the AC1 or AC8 genes or both genes [double knockout mice (DKO)].

130 We generated double-knockout mice (DKO) lacking the 2 cardiac CaMKII

131 Homozygous double-knockout mice (Egr-1-/-/apoE-/-) in the C57BL/6 b

132 treatment to modulate pathophysiology in the double knockout mice enhances the potential of this muri

133 In addition, double knockout mice exhibit an impaired cardiac respons

134 notypically normal while SV2A- and SV2A/SV2B double knockout mice exhibit severe seizures and die pos

135 pted in combination with RIP1, the resulting double knockout mice exhibit slightly prolonged survival

136 Lhx1; Lhx5 double-knockout mice exhibit a downregulation of Gad1 an

137 phane, and (c) MEFs derived from Bax and Bak double knockout mice exhibited even greater protection a

138 Unexpectedly, ADA/A(2B)R double-knockout mice exhibited enhanced pulmonary inflam

139 ompared to littermate controls, flu-infected double-knockout mice exhibited increased mortality, cons

140 In the periphery, Apoe/Apoa1 double-knockout mice exhibited substantial atheroscleros

141 s from other donors ex vivo and H-2Db beta2m double knockout mice expressing a chimeric HLA-A*0201/H2

142 uced asthma, we generated double-transgenic, double-knockout mice expressing human HLA-DQ8, HLA-DQ6,

143 Administration of wild-type human LDLR to double knockout mice, expressing hPCSK9, led to diminish

144 Because alpha(1)A/B double knockout mice fail to develop hypertrophy in resp

145 lyn(-/-) triple-knockout or hck(-/-)fgr(-/-) double-knockout mice failed to undergo respiratory burst

146 To answer this question, we produced double knockout mice for Bmp6 and beta2-microglobulin (a

147 Using single and double knockout mice for MMP-2 and MMP-9, we show that M

148 Analyses of double knockout mice further revealed that IL-36alpha an

149 B/c background TGF-beta1(-/-)/IFN-gamma(-/-) double knockout mice, generated by cross-breeding, did n

150 injected into the vitreous of "knockout" or "double knockout" mice genetically deficient in IL-1 rece

151 In neuraminidase 3 and 4 double-knockout mice, GM3 ganglioside is stored in micro

152 beta knockout mice (TCR-beta(0)) to generate double-knockout mice (GT(0)/TCR-beta(0)).

153 ic low-density lipoprotein receptor/apobec-1 double knockout mice had a similar cytokine response as

154 ssion in tissue culture models, and miR-133a double knockout mice had elevated levels of Hand2 mRNA a

155 cently found that macrophages from RhoA/RhoB double knockout mice had increased motility of the cell

156 Double knockout mice had increased p53 and H2AX phosphor

157 Both apoE knockout and double knockout mice had low HDL cholesterol levels when

158 The double knockout mice had reduced survival and impaired g

159 e, with the exception that female ADAMTS-4/5-double-knockout mice had a lower mean terminal body weig

160 The double-knockout mice had greater impairment of urinary-c

161 ts from syntaxin-2 and syntaxin-4 single- or double-knockout mice had no secretion defect.

162 We also found that slit1, -2 or -3 single or double knockout mice have impaired development of the tr

163 oth muscle cells and CX3CR1/apolipoprotein E double knockout mice have significantly reduced atherosc

164 NOS1/3-/- double knockout mice have suppressed beta-adrenergic res

165 ) binding protein null mice (Mttp-LKO, i.e., double knockout mice) hepatic steatosis was greatly dimi

166 TPCs in endolysosomes from wild-type and TPC double-knockout mice, here we show that, in contrast to

167 Reprogramming of SSC from Tet1 and Tet2 double knockout mice however lacked demethylation of H19

168 Using Dnmt3a and Tet2 double-knockout mice in which the development of maligna

169 presenilin in the adult brain, we generated double knockout mice, in which both presenilins were del

170 ine deaminase (AID)/secretory mu-chain (mus) double-knockout mice, in which a normally diverse repert

171 this thesis, we developed three colonies of double-knockout mice including IL-2Ralpha(-/-) CD4(-/-),

172 Analysis of RORgamma/RORalpha double knockout mice indicated that in certain tissues R

173 Analysis of RON and IFN-gamma receptor double-knockout mice indicates that the enhanced suscept

174 -reactive thymocytes was normal in B7-1/B7-2 double-knockout mice, indicating that CD40-CD40L-depende

175 ack beta2-microglobulin, but not in K(b)D(b)-double-knockout mice, indicating that these CD8 T cells

176 genetic deletion of P2X2 and P2X3 receptors (double knockout mice) lack responses to all taste stimul

177 ephosphorylation defects were rescued in the double knockout mice lacking both calpain-1 and PTP1B.

178 of SM-B null mice was studied by generating double knockout mice lacking both h1-calponin and SM-B m

179 Here we demonstrate that conditional double knockout mice lacking both presenilins in the pos

180 Double knockout mice lacking both receptors showed super

181 oretinographic (ERG) responses by generating double knockout mice lacking Lrat or Rpe65 together with

182 ury and mortality in Nrf2(-/-) mice, we used double knockout mice lacking Nrf2 and NADPH oxidase subu

183 l ester accumulation, we generated single or double knockout mice lacking retinoid cycle genes.

184 his report, we demonstrate that T cells from double knockout mice lacking two of the immunosubunits,

185 UT-B-mediated water transport, we generated double knockout mice lacking UT-B and the major erythroc

186 formed bone marrow transplantation in female double-knockout mice lacking both the apoE and apoA-I ge

187 leucine zipper knockout (Nrl(-/-)) mice and double-knockout mice lacking G-protein-coupled receptor

188 Double-knockout mice lacking MCL-1 and cyclophilin D, an

189 T3 cells, (iii) fibroblasts established from double-knockout mice lacking PI3K p85alpha and p85beta c

190 entrainment of circadian activity rhythms in double-knockout mice lacking the inner-retinal photopigm

191 (-/-)/low-density lipoprotein receptor Rag 1 double-knockout mice (lacking the ability to make immuno

192 In RGS7/RGS11 double-knockout mice, light-evoked responses in rod ON b

193 Pkd1 and Smyd2 double-knockout mice lived longer than Pkd1-knockout mic

194 and TLR4 signaling in B6.TLR2(-/-).TLR4(-/-) double-knockout mice markedly reduced the severity of HR

195 In the cardiovascular system, MAGP1;MAGP2 double knockout mice (Mfap2(-/-);Mfap5(-/-)) show age-de

196 In muscle from mdx/utrn(-/-) double knockout mice, MS channels also spend more time a

197 observed in FGF2(-/-) mice and in FGF1-FGF2 double-knockout mice novel impairments in hematopoiesis

198 that of single Ccl2, Cx3cr1 and Ccl2/Cx3cr1 double knockout mice obtained from backcrosses of CCDKO

199 decrease in atherosclerotic disease area in double knockout mice on a regular diet.

200 using wild-type, CD28-, ICOS-, or CD28/ICOS-double knockout mice on C57BL/6 background as T cell sou

201 On a chow diet, these double-knockout mice overaccumulated cholesterol and tri

202 IL-6 knockout in Axl(-/-)Mertk(-/-) double-knockout mice overcomes the inflammatory inhibiti

203 When compared with the double knockout mice, p53-/-NOS2+/+ mice showed a higher

204 )-induced diabetic homozygous PKC-alpha/beta double-knockout mice (PKC-alpha/beta(-/-)).

205 In these Dicer-Pten double-knockout mice, primary fallopian tube tumors spre

206 -alpha and Rev-erb-beta function by creating double-knockout mice profoundly disrupted circadian expr

207 However, in eye-specific COUP-TFI/TFII double-knockout mice, progenitor cells at the dorso-dist

208 dine phosphorylase and uridine phosphorylase double knockout mice recapitulated several features of t

209 yonic fibroblast cells derived from LPA(1&2) double-knockout mice reconstituted with the LPA(2) recep

210 The NaPi2a(-/-)/klotho(-/-) double-knockout mice regained reproductive ability, reco

211 l levels in SR-BI and SR-BI/apolipoprotein E double knockout mice relative to controls.

212 Colitis exacerbation in TLR2/MDR1A double-knockout mice required the unaltered commensal mi

213 nd the expression of PKCbeta in PKCalphabeta double knockout mice rescues PTP.

214 Here we report that iRhom1/2(-/-) double knockout mice resemble Adam17(-/-) and Egfr(-/-)

215 Examination of clotting parameters in double-knockout mice revealed that native clotting times

216 The double knockout mice show a massive accumulation of lact

217 % reduction in DTH, and ALCAM(-/-) RAGE(-/-) double-knockout mice show a 27% reduction in DTH reactio

218 As a result, double-knockout mice show markedly altered circadian whe

219 e (PSI) in Cyp1a1(-/-) mice; Cyp1a1/1b1(-/-) double-knockout mice show no PSI cancer but develop squa

220 Electron micrographs of hearts from TPC1/2 double knockout mice showed that cardiomyocytes containe

221 Recent experiments on the double knockout mice showed, however, that their taste b

222 In contrast,Tmprss2(-/-)Tmprss4(-/-)double-knockout mice showed a remarkably reduced virus s

223 eta1(-/-)/recombinase-activating gene 1(-/-) double-knockout mice showed extended survival and did no

224 In addition, double-knockout mice showed misregulation of genes in th

225 Mice lacking both entry receptors (double-knockout mice) showed no evidence of disease afte

226 her FasL or TNF-alpha/lymphotoxin (LT) alpha double knockout mice, showed that therapeutic effects we

227 ere entirely in optic chiasms of Brn3b/Brn3c double knockout mice, suggesting that Brn3c controlled i

228 effect is efficiently blocked in SOCS3-gp130 double-knockout mice, suggesting that SOCS3 deletion pro

229 in immunodeficient RAG-2/common gamma-chain double-knockout mice, suggesting that the changes in exp

230 ion occurred in Treg-deficient NOD.B7-1/B7-2 double-knockout mice, suggesting that the effect of the

231 RelA/TNFR-1 double knockout mice survived embryonic development and

232 (-/-)/low-density lipoprotein receptor Rag 1 double-knockout mice, sustained levels of plasma IK17-sc

233 uc1 and RAG1 were disrupted in mice (Muc/RAG double knockout mice); Th1-mediated colitis was induced

234 AT-6-deficient mice as well as in IL-4/IL-13 double knockout mice that failed to increase SP-D produc

235 s were either partially or fully restored in double knockout mice that lack both caveolin-1 and eNOS.

236 fibrosis was observed in PAI-1(-/-)/uPA(-/-) double knockout mice that was associated with reduced in

237 report rapid lymphoma development in Id2/Id3 double-knockout mice that is caused by unchecked expansi

238 rents revealed that in wild-type and ASIC2/3 double knockout mice the majority of putative low thresh

239 erted in SHIP/Bruton's tyrosine kinase (Btk) double knockout mice, thus identifying the Btk activatin

240 he resistance of TLR9(-/-) as well as TLR2/9 double knockout mice to aerosol infection with Mycobacte

241 LAP2alpha knockout, or emerin and LAP2alpha double knockout mice to be comparable in infectivity to

242 t, L-selectin-deficient, and CD44/L-selectin double knockout mice to determine the requirement for th

243 ice as well as in nrf2 single and keap1-nrf2 double knockout mice to identify those genes regulated b

244 dx/utrn(+/-) heterozygotes and mdx/utrn(-/-) double knockout mice to investigate the role of these cy

245 severe salt-wasting, and generated SPAK/OSR1 double knockout mice to test this.

246 We also generated apoE(-/-)/As3mt(-/-) double knockout mice to test whether As3MT-mediated biot

247 We thus generated double-knockout mice to assess a potential genetic inter

248 n 'rescue' of muscular dystrophy, we created double-knockout mice to test the contributions of utroph

249 The phenotype of Ucp1/Ucp3 double knockout mice was indistinguishable from Ucp1 sin

250 grecanase-mediated degradation in ADAMTS-4/5-double-knockout mice was ablated, to a level comparable

251 Enhanced mortality of double-knockout mice was not associated either with incr

252 In double knockout mice we show that (125)I-amyloid-beta mi

253 In the double-knockout mice we observed defects that were simil

254 By analyzing DUSP5(-/-), SerpinB2(-/-) double knockout mice, we demonstrate that deletion of Se

255 By generating miR-31 and Gprc5a double knockout mice, we show that miR-31 promotes the d

256 Single and double knockout mice were alive and fertile without sign

257 ensity lipoprotein cholesterol levels of the double knockout mice were also greater than those of the

258 53 double knockout mice were born out of 756 pups from bree

259 clerosis, hyperglycemic TSP-1(-/-)/ApoE(-/-) double knockout mice were compared with age-matched hype

260 ckout, IL-1beta knockout, and IL-1beta/IL-18 double knockout mice were compared with wild-type mice f

261 Here AQP1/AQP3 double knockout mice were generated and analyzed to inve

262 Fmr1/BKbeta4 double knockout mice were generated to genetically upreg

263 TCRalphaKO mice, IL-12p35-deficient TCRalpha double knockout mice were generated.

264 mice, but the HDL cholesterol levels of the double knockout mice were higher than those of apoE knoc

265 Most double knockout mice were largely protected from lymphom

266 In addition, macrophages from TNFR I/II double knockout mice were LPS tolerizable, and blocking

267 Sperm taken from the cauda epididymides of double knockout mice were microscopically normal and mot

268 Retinal ganglion cell axons from double knockout mice were more severely affected than we

269 Double knockout mice were protected against fasting-indu

270 Importantly, IL-1beta/IL-18 double knockout mice were protected from splenic cell ap

271 Gene expression patterns in keap1-nrf2 double knockout mice were similar to those in nrf2-singl

272 ), IL-12p35(-/-), and IL-12p35(-/-)p40(-/-) (double knockout) mice were infected with the RE strain o

273 ADAMTS-4/5-double-knockout mice were challenged by surgical inducti

274 early in development, and the phenotypes of double-knockout mice were characterized.

275 These effects in the ADAMTS-4/5-double-knockout mice were comparable with those observed

276 icits and dendritic morphology of Apoe/Apoa1 double-knockout mice were compared to APP/Abca1(ko), APP

277 ld and 1-year-old male and female ADAMTS-4/5-double-knockout mice were compared with age- and sex-mat

278 e (control), IDO1-/-, Rag1-/-, and Rag1/IDO1 double-knockout mice were exposed to azoxymethane and de

279 the role of OPN in a model of COPD, Ada(-/-) double-knockout mice were generated, and inflammation an

280 ollecting-duct water channel AQP4, AQP3/AQP4 double-knockout mice were generated.

281 n of cellular immunity, FcgammaR single- and double-knockout mice were immunized with HPV16 L1/L2-E7

282 led that although calvarium and vertebrae of double-knockout mice were normalized with respect to min

283 re necessary for colitis, because Nfil3/Rag1 double-knockout mice were protected from disease.

284 The immunized double-knockout mice were protected from H. pylori chall

285 e embryonic fibroblasts derived from Bax-Bak double-knockout mice were significantly more resistant t

286 single-gene knockouts of RNase L and PKR and double-knockout mice were studied following intratrachea

287 ar cartilage explants from WT and ADAMTS-4/5-double-knockout mice were treated with interleukin-1 (IL

288 s significantly impaired in both single- and double-knockout mice, whereas a more general inhibition

289 nal experiments were performed using mdr1a/b double knockout mice which lack functional P-GP encoded

290 lpha15(-/-) mice, Galpha15(-/-) Galphaq(-/-) double-knockout mice (which express only Galpha11 in mos

291 rogrammed death-ligand 1', whereas in NOD1/2 double knockout mice, which cannot recognize peptidoglyc

292 ed generation of lpa(1)((-/-)) lpa(2)((-/-)) double knockout mice, which displayed no additional phen

293 ch more pronounced in Sdc4(-/-); Pecam1(-/-) double-knockout mice, which develop severe edema.

294 ow that in thymi of alphaGalA(-/-)/Gb3S(-/-) double-knockout mice, which store isoglobosides but no g

295 To test this hypothesis, we examined double knockout mice with deletions of one or both copie

296 ochondrial DNA instability, we have stressed double knockout mice with exogenous thymidine and deoxyu

297 Treatment of these double-knockout mice with phosphoramidon resulted in ele

298 ortic sinus was also markedly altered in the double knockout mice, with 50% reduction in macrophage a

299 depletion, but also in WSX-1/tristetraprolin double knockout mice, with substantial reduction in the

300 We hypothesized that Apoe/Apoa1 double-knockout mice would mimic the phenotype of APP/Ab