ライフサイエンスコーパス: KO mouse

1 ects of innate immune challenge in the PC1/3 KO mouse.

2 subtypes retained homologous coupling in the KO mouse.

3 red in the embryonic heart of the global CAR-KO mouse.

4 on by generating and characterizing a PSD-95 KO mouse.

5 analysis or immunohistochemistry in the Rs1h-KO mouse.

6 e fibrosis similar to that seen in the Bmal1 KO mouse.

7 underlies the hyperconnectivity in the Fmr1 KO mouse.

8 age-related pathologies in the Gsk3a global KO mouse.

9 underlie the behavioral deficit in the fmr1 KO mouse.

10 ed pathologies in the striated muscle of the KO mouse.

11 IFN-gamma production by T cells in the IL-2-KO mouse.

12 (FXS), the Fmr1 (tm1Cgr) or Fmr1 "knockout" (KO) mouse.

13 transport of B12 in a TCblR/CD320-knockout (KO) mouse.

14 ient phenotype similar to the IRF8 knockout (KO) mouse.

15 rmation parameters using the IGF-I knockout (KO) mouse.

16 s synaptic correlates in the fmr1 knock-out (KO) mouse.

17 The Fmr1 KO mouse, a model of FXS, exhibits elevated translation

18 cific Na(+) /Ca(2+) exchange (NCX) knockout (KO) mouse, a model of cellular Ca(2+) overload.

19 The Fmr1 knockout (Fmr1-KO) mouse, a mouse model for FXS, has been shown to repl

20 The multidrug resistance 2 (Mdr2)-knockout (KO) mouse (adenosine triphosphate-binding cassette b4(-/

21 This COX10 KO mouse allowed us to correlate the muscle function wit

22 Moreover, given that this conditional Fktn-KO mouse allows the generation of tissue- and timing-spe

23 ss this issue, we used the miR-155 knockout (KO) mouse and diffuse large B-cell lymphoma (DLBCL) cell

24 stemically inactivated in adult mouse (alpha-KO mouse), and the role of PDGFRalpha was examined in th

25 m potentiation (LTP) is impaired in the fmr1 KO mouse, and motor skill training does not occlude LTP

26 increased in these regions in WT but not in KO mouse aorta in response to Ang II.

27 eostasis and establish the liver-specific GS KO mouse as a model with which to study effects of chron

28 We used DAT-KO mouse as model for DTDS to explore the potential util

29 The ERG of the Rs1h-KO mouse at early ages reflects disruption of photorecep

30 Furthermore, PancMet KO mouse beta-cells were more sensitive to dexamethasone

31 inhibitory neurotransmission deficits in the KO mouse BLA.

32 We transplanted SMS2 KO mouse bone marrow into low-density lipoprotein (LDL)

33 dependent increase in LPC levels in the PPT1-KO mouse brain positively correlates with elevated expre

34 e phagocytic cells are recruited in the PPT1-KO mouse brain remains poorly understood.

35 nduced by ROS, in human INCL as well as PPT1-KO mouse brain tissues are markedly elevated.

36 lic phospholipase A(2) (cPLA(2)) in the PPT1-KO mouse brain, is a 'lipid signal' for phagocyte recrui

37 xpression remained unaltered in adult WT and KO mouse brain, SC, and kidneys.

38 -KO mice, as well as in transgenic alpha-Syn-KO mouse brains in vivo.

39 ptide precursor VGF was also affected in PC1 KO mouse brains with a decrease in the level of an endog

40 cessing of proenkephalin was impaired in PC1 KO mouse brains with a decrease in the level of Met-Enke

41 des in the lipid-associated fraction of HEXB KO mouse brains, and intraneuronal accumulation of gangl

42 g of proSAAS into PEN was not altered in PC1 KO mouse brains.

43 is study, we generated a TSHR knockout (TSHR-KO) mouse by homologous recombination for use as a model

44 We generated a Chga knock-out (KO) mouse by the targeted deletion of the Chga gene in n

45 The PEDF-knockout (KO) mouse captures crucial elements of the human disease

46 Our technique revealed that Top1mt KO mouse cells process the mitochondrial transcripts nor

47 In the Fmr1 KO mouse, chronic treatment with mGluR5-negative alloste

48 AO A/B double knock-out (KO) mice in a MAO B KO mouse colony.

49 tic transmission in a TARP gamma-4 knockout (KO) mouse corroborates our expression data and demonstra

50 vers, or spleens of MyD88 KO mice, the first KO mouse described with this phenotype to our knowledge.

51 The connexin43 knockout (Cx43alpha1 KO) mouse dies at birth from outflow obstruction associa

52 The Fmr1 KO mouse displays phenotypes similar to symptoms in the

53 Compared to wild type mice, the LIF KO mouse displays reduced astrocyte and microglial activ

54 Consistent with this, FIP200 KO mouse embryo fibroblasts and liver cells showed incre

55 Reconstitution of KO mouse embryo fibroblasts showed that both the pleckst

56 Using SV40- and K-Ras-transformed caspase-2 KO mouse embryonic fibroblast cells reconstituted with e

57 In response to adipogenic stimuli, PP5-KO mouse embryonic fibroblast cells showed almost no lip

58 r disease (FAD) PS1 mutants expressed in PS1-KO mouse embryonic fibroblasts inhibited both the EphB2-

59 d MIP-1alpha was reduced in IL-18 knock-out (ko) mouse embryonic fibroblast (MEF)-like cells.

60 Wild-type and PP5-deficient (KO) mouse embryonic fibroblast cells were used to show b

61 wild-type (WT) and Bcl-xL knock-out (Bcl-xL-KO) mouse embryonic fibroblast cells.

62 We show that lysates from Nedd4-1 knockout (KO) mouse embryonic fibroblasts (MEFs) have significantl

63 e (WT) and p21-activated kinase 1-null (PAK1-KO) mouse embryonic fibroblasts (MEFs), we found TF and

64 n in both wild-type (WT) and RSK2 knock-out (KO) mouse embryonic fibroblasts (MEFs).

65 We found that in PAI-1 knock-out (KO) mouse embryonic fibroblasts), alphavbeta3 endocytosi

66 ockdown or Parp1 heterozygosity of Brca2(cko/ko) mouse embryonic stem cells (mESCs), carrying a null

67 Analysis of miR-34/449 knockout (KO) mouse embryos demonstrates significant spindle misor

68 In Oga KO mouse ES cells, we observed pronounced changes in exp

69 Conditional KO mouse experiments indicate that the effect of KLF2 on

70 The size and weight of IRBP KO mouse eyes were greater than those of the WT mouse, e

71 Micro-computed tomography of A(2A)KO mouse femurs showed a significantly decreased bone vo

72 The IL-13 KO mouse had a separate phenotype to that of the IL-4 KO

73 ll homing to the gut and as a result the VDR KO mouse has reduced numbers of CD8alphaalpha IEL with l

74 The Mtm1 knockout (KO) mouse has a severe phenotype and its short lifespan

75 A fragile X knockout (fmr1 KO) mouse has been described that has some of the charac

76 eneration of the connexin-36 knock-out (Cx36 KO) mouse has offered a unique opportunity to examine th

77 odel of ApoE deficiency, the ApoE knock-out (KO) mouse, has reduced synapses and cognitive impairment

78 we have now employed a genetic HRI-knockout (KO) mouse hepatocyte model.

79 c cardiac contractile performance of the PLN-KO mouse in the long term.

80 We generated an AKAP7 KO mouse in which all isoforms were deleted and tested w

81 tion in vivo, we generated a conditional RB1-KO mouse in which pRb expression is efficiently extingui

82 Studies in the insulin receptor FOXO1 KO mouse indicate that insulin is a key signaling molecu

83 w that the rate of cone cell loss in the GC1 KO mouse is comparable to that previously described in t

84 The Rs1h-KO mouse is consistent with human clinical X-linked juve

85 that the faster Vus of smooth muscle of the KO mouse is consistent with, but does not prove without

86 dy provides the first evidence that the Fmrl KO mouse is impaired in inhibitory control, attention, a

87 The Ndufs4 knockout (Ndufs4 KO) mouse is a mitochondrial complex 1-deficient model t

88 The dopamine transporter knockout (DAT KO) mouse is a model of chronic hyperdopaminergia used t

89 The Fmr1 knock-out (KO) mouse is a useful model for studying FXS.

90 DAT-Knockout (DAT-KO) mouse is currently the best animal model for this sy

91 While a CPEB knockout (KO) mouse is sterile but overtly normal, embryo fibrobla

92 PancMet KO mouse islets failed to upregulate GLUT2 and pancreati

93 Perifusion of neurexin-1alpha KO mouse islets revealed a significant increase in secon

94 ntly, glucose cycling was abolished in G6pc2 KO mouse islets, confirming that G6pc2 opposes the actio

95 nd cardiac function in CaMKIIdelta knockout (KO) mouse left ventricle (LV).

96 The GAL3-KO mouse line exhibited normal breeding and physical dev

97 Thus, we use a conditional GluN2B KO mouse line to assess both basal and ethanol-dependent

98 lementary mouse models, an alpha4 knock-out (KO) mouse line and a knock-in line (Leu9'Ala) expressing

99 used conditional and conventional knock-out (KO) mouse lines, with viral expression of Cre-recombinas

100 that compared with wild type littermates, UG-KO mouse lungs express markedly elevated levels of SCCA-

101 notably, the metastasized B16F10 cells in UG-KO mouse lungs express MMP-2, MMP-9, and MMP-14 as well

102 Remarkably, UG-KO mouse lungs overexpress two calcium-binding proteins,

103 The increased chemotaxis of Fpr2-KO mouse macrophages in response to LLC Sup was due to t

104 The RS-KO mouse mimics structural features of human X-linked ju

105 vel skeletal muscle-specific GRK2 knock-out (KO) mouse (MLC-Cre:GRK2(fl/fl)) to gain a better underst

106 ole of Abi1, we generated a conditional Abi1-KO mouse model and MEFs lacking Abi1 expression.

107 Here we present the first report of a Tcap KO mouse model for LGMD2G and the results of an investig

108 use of our Pdx1-Cre-driven conditional PAK4 KO mouse model for testing in vivo potential functions o

109 Obliteration of CHGA expression in a KO mouse model led to decreased size and number of chrom

110 nd more severe cardiac injury, making the MT-KO mouse model of alcohol-induced cardiac fibrosis a use

111 Thus, in the Ndufs4 KO mouse model of mitochondrial optic neuropathy, papave

112 We are the first to establish a viable KO mouse model of Tcap deficiency and our model mice dem

113 Using a conditional KO mouse model where Atg7, a critical gene for macroauto

114 When using an AMPK-beta1 KO mouse model, the protective effects of metformin stil

115 Using the Aire KO mouse model, we demonstrated an essential role for CC

116 atory T(h)1 pathway is dominant in the PC1/3 KO mouse model.

117 g a Th17 response in the hyperlipidemic apoE KO mouse model.

118 ne 2,3-dioxygenase, and was confirmed in IDO-KO mouse model.

119 mparing tumor formation in an Mdr2-knockout (KO) mouse model (n = 15) and tumor growth in a remote BN

120 story of a retinoschisin gene knockout (Rs1h-KO) mouse model and evaluated the long-term effects of r

121 A knockout (KO) mouse model exhibits behavioral and adult neurogenes

122 The PC1/3 knock-out (KO) mouse model has allowed us to elucidate its physiolo

123 dence for this problem in the Fmr1-knockout (KO) mouse model of Fragile X syndrome and describe poten

124 ala synaptic function in the Fmr1 knock-out (KO) mouse model of FXS, however, remain largely unexplor

125 hippocampal synapses in the Fmr1-knock-out (KO) mouse model of FXS.

126 thyl-CpG-binding protein 2 (Mecp2) knockout (KO) mouse model of Rett syndrome, we show that naive exc

127 The knockout (KO) mouse model showed the absence of endosialin/TEM1 ex

128 in Ras activation, using a RasGRP1 knockout (KO) mouse model to examine the response of keratinocytes

129 A conditional betaENaC MG knockout (KO) mouse model was generated to elucidate the pathogene

130 he underlying mechanism by using a knockout (KO) mouse model with a genetic ablation of Splunc1.

131 Here we compare a liver-specific knockout (KO) mouse model with total KO mice.

132 f nNOS was provided by an nNOS knockout (NOS-KO) mouse model, B6-129S4-Nos1(tm1Plh)/J.

133 Here we report the first NIS knockout (KO) mouse model, obtained by targeting exons 6 and 7 of

134 In a vimentin knockout (Vim KO) mouse model, we note that Vim KO mice challenged wit

135 loid cell-specific SIRT1 knockout (Mac-SIRT1 KO) mouse model, we show that ablation of SIRT1 in macro

136 Using the Jak3 knock-out (KO) mouse model, we show that Jak3 is expressed in colon

137 fiber bundles from a nebulin knock-out (NEB KO) mouse model.

138 n using a tamoxifen-inducible Lkb1 knockout (KO) mouse model: Rosa26-Cre(ER): Lkb1(flox/flox) (abbrev

139 novel B6.Cg-Pla2g6(DeltaEx2-VB) (PLA2g6 ex2(KO)) mouse model.

140 ted global as well as cardiac-specific HSPB7 KO mouse models and found that loss of HSPB7 globally or

141 vention studies using DBA2/J and Nos3 (eNos) KO mouse models of diabetes, TEPP-46 treatment reversed

142 sis, as demonstrated using single and double KO mouse models.

143 ypes have not been delineated in conditional KO mouse models.

144 By comparing relevant previous knockout (KO) mouse models (3'RR KO and hs3b-4 KO) to a novel muta

145 aches of COX-2 transgenic (Tg) and knockout (KO) mouse models to evaluate the mechanism of COX-2 in F

146 1-, STIM2-, and double STIM1/STIM2-knockout (KO) mouse models, which reveal the essential role of STI

147 To date, four separate alsin knockout (Alsin(KO)) mouse models have been generated, and despite hopes

148 n quantifiable or qualitative changes in DAT KO mouse MSNs relative to wild-type (WT) littermates.

149 g corresponding double- and triple-knockout (KO) mouse mutants.

150 ineralization of vibrissae, whereas grafting KO mouse muzzle skin onto WT mice did not.

151 verity to that in WT mice, but the iPLA2beta-KO mouse myocardium contained more parasite pseudocysts.

152 bound stimulation of ICa in both WT and NOS3-KO mouse myocytes.

153 naline (Iso) was studied in both WT and NOS3-KO mouse myocytes.

154 in permeabilized phospholamban knockout (PLN-KO) mouse myocytes phosphorylates ryanodine receptors (R

155 tants of SynIII in primary SynIII knock-out (KO) mouse neurons at early stages of in vitro developmen

156 We generated a conditional KO mouse of the Bit1 gene by using the Cre-LoxP recombin

157 sing a megakaryocyte-specific Mkl2 knockout (KO) mouse on the conventional Mkl1 KO background to prod

158 s a sarcomeric protein that when absent (NEB KO mouse) or present at low levels (nemaline myopathy (N

159 in A and B dramatically decreased in the PC1 KO mouse pituitaries, while the levels of peptides deriv

160 stimulation was significantly higher in CSE-KO mouse preparations compared to the amplitude of S-IJP

161 inine (l-NNA, 200 mum) and in nNOS-knockout (KO) mouse preparations, PAG shifted the transwall gradie

162 We generated a germline CETN2 knock-out (KO) mouse presenting with syndromic ciliopathy including

163 ulation of Abcg2 in some tissues of the Mrp4 KO mouse prompted us to evaluate the possibility that Ab

164 ing heart-brain stem preparation of the Cx36-KO mouse, respiratory-coupled sympathetic nerve discharg

165 enting normal Rs1h protein in the adult Rs1h-KO mouse restored the normal ERG configuration.

166 ious electrophysiological studies of the GC1 KO mouse retina, provide evidence that GC1-GCAP1 interac

167 n early age, the retinoschisin knockout (Rs1-KO) mouse retina has progressive photoreceptor degenerat

168 unaltered in the connexin36 (Cx36) knockout (KO) mouse retina, indicating that it is not dependent on

169 P levels and polymerized F-actin in the Rpgr(ko) mouse retina.

170 In the Rs1-KO mouse, retinal layer formation and synaptic protein e

171 ubtypes in wild-type (WT) and Cx36 knockout (KO) mouse retinas.

172 Initial studies of a Hyal2 knock-out (KO) mouse revealed a mild phenotype with high serum HA,

173 -C(-/-) sera; however, MBL-null or MASP-1/-3 KO mouse sera demonstrated significantly decreased S2238

174 ubsequent studies in a prosaposin knock-out (KO) (-/-) mouse showed intact but slightly reduced heari

175 volunteers and examined the aged 11beta-HSD1 KO mouse skin phenotype.

176 A comparison of IL-17C+ and IL-17C+KO mouse skin transcriptomes with that of human psoriasi

177 f skin of patients with psoriasis and IL-17C+KO mouse skin, and confirmed an exacerbation of the infl

178 Histological staining of Panx1 knockout (KO) mouse skin revealed a reduction in epidermal and der

179 After dorsal column SCI, miR-155 KO mouse spinal cord has reduced neuroinflammation and i

180 VLP-immunized than in SHIV VLP-immunized CD4 KO mouse splenocytes.

181 The low homeostatic impact of Hcrt(ko/ko) mouse spontaneous waking correlates with decreased c

182 the decrease in AMPAR function in the PSD-95 KO mouse stems from an increase in the proportion of "si

183 was crossed to a conditional Dicer knockout (KO) mouse strain to analyze the role of microRNAs (miRNA

184 tional B cell-specific Kidins220 knockout (B-KO) mouse strain, we show that Kidins220 couples the BCR

185 had a separate phenotype to that of the IL-4 KO mouse, suggesting that both IL-4 and IL-13 play impor

186 after transverse aortic constriction (TAC), KO mouse survival was only 60% of WT, and surviving KO m

187 maffin cells isolated from a PICK1 knockout (KO) mouse the amount of exocytosis was reduced, while re

188 We generated two new strains from the Mdr2-KO mouse, the Mdr2:CCR5 and the Mdr2:CCR1 double knockou

189 eatine kinase conditional frataxin knockout (KO) mouse; this mouse develops a severe cardiac phenotyp

190 We used a 5-HTT knock-out (KO) mouse to examine the effects of genetically driven l

191 the present study, we used an NR2A knockout (KO) mouse to examine the role of this subunit in the exp

192 d a uterine-specific GR knockout (uterine GR KO) mouse using the PR(cre) mouse model.

193 ld type (WT) and phospholamban knockout (PLB-KO) mouse ventricular myocytes to test whether exogenous

194 expression was about the same in both WT and KO mouse visceral yolk sac, brain, and spinal column.

195 This reduction in amyloid plaques in the KO mouse was accompanied by a reduction in Abeta42 level

196 Seizure activity in the KO mouse was only moderately diminished by intraperitone

197 ity in the high-fat diet-fed (HFD-fed) Gpr21 KO mouse was traced to a marked reduction in tissue infl

198 an estrogen receptor beta (ERbeta) knockout (KO) mouse was created by interrupting the gene at the DN

199 ecently, a transglutaminase 3 knockout (TGM3/KO) mouse was generated that showed impaired hair develo

200 In the near term KO mouse, we also observed a profusion of large coronary

201 Hence, by using the TSHR-KO mouse, we provided in vivo evidence, demonstrating th

202 Using a conditional VGLUT3 KO mouse, we show that deletion of the transporter from

203 Using a CD34 knockout (KO) mouse, we tested the hypothesis that CD34 may partic

204 onditioned by osteoblasts derived from IGF-I KO mouse were below those detectable by RIA.

205 Unexpectedly, the silent synapses in the KO mouse were located onto morphologically mature spines

206 X syndrome mouse model, the Fmr1 knock-out (KO) mouse, where pharmacological and genetic reduction o

207 blasts (MEFs) derived from Fam20a knock-out (KO) mouse, while it was detected in the media from WT ME

208 This feature rendered the IL-10 knockout (KO) mouse, whose infiltrating cells are incapable of IL-

209 Cells lacking Abi1 and the conditional Abi1-KO mouse will serve as critical models for defining Abi1

210 ons of the wild-type mouse, but not the Kal7(KO) mouse, with an Abl inhibitor caused an increase in l