ライフサイエンスコーパス: KO mice

1 ich Otop1 was genetically inactivated (Otop1-KO mice).

2 na1c from D1R-expressing neurons (D1-cacna1c(KO) mice).

3 ed in the cortices of betaOHB-treated aralar-KO mice.

4 sconnection between both structures in adult KO mice.

5 ty, and attenuate neuronal damage in FBN-ARO-KO mice.

6 y in acute hippocampal slices from the Mecp2 KO mice.

7 e in insulin release was also present in FXR-KO mice.

8 ficacy and rescued memory recall in the Fmr1 KO mice.

9 ne: P = 0.0002) which was abolished in Orai1 KO mice.

10 us (P = 0.04) which failed to occur in Orai1 KO mice.

11 -IFNAR1 antibody and in immunodeficient Rag1 KO mice.

12 ues of wild-type (WT), Nlrp3-KO and Caspase1-KO mice.

13 nflammation, and oxidative stress in FBN-ARO-KO mice.

14 whereas MCP-1 and IL-6 predominated in IRF3-KO mice.

15 tom score and extended lifespan in the Mecp2 KO mice.

16 crobial analysis showed gut dysbiosis in DRA-KO mice.

17 d with Ins2 (Akita) to generate Ins2 (Akita)/KO mice.

18 d short-term plasticity were normal in Doc2b KO mice.

19 of WT mice and was not detected at the uPAR KO mice.

20 tion responses to TCP were enhanced in TAAR1-KO mice.

21 x and social interaction in vivo of the Fmr1-KO mice.

22 failed to reduce bacterial burden in MHC-II KO mice.

23 taneous remyelination, phenocopying OSMRbeta KO mice.

24 sistance, the magnitude being lower in ALR-H-KO mice.

25 ikely aggravates status epilepticus in Orai1 KO mice.

26 henotype similar to that of constitutive p11 KO mice.

27 glucose tolerance were further aggravated in KO mice.

28 hich resemble neurodevelopmental deficits in KO mice.

29 fiber synaptic function onto PCs in Cacna2d2 KO mice.

30 g compared to single Hfe or endothelial Bmp2 KO mice.

31 bstantia nigra in wild-type but not in TAAR1-KO mice.

32 ds to altered short term-depression in GluA3 KO mice.

33 cardiac dysfunction was attenuated in these KO mice.

34 rea parameters could be observed in GABA-CB1-KO mice.

35 ession were similar to those of WT and Nlrp3-KO mice.

36 transfer between wild-type (WT) and Il-18bp KO mice.

37 istant to glucose challenge than WT or ALR-H-KO mice.

38 in renal proximal tubules isolated from P2X4 KO mice.

39 GLT-1 in the cerebral cortex in the synGLT-1 KO mice.

40 cells, and an increase in apoptotic cells in KO mice.

41 sease between PIV-vaccinated Tbet KO and CD4 KO mice.

42 improved survival of high-lysine/low PN fed KO mice.

43 ng PAK2 specifically in muscle, but not PAK1 KO mice.

44 t of LGMD2H pathology, are present in TRIM32 KO mice.

45 ed to vigorous seizures and a quick death in KO mice.

46 icantly reduced in Casp1-KO but not in Nlrp3-KO mice.

47 ated inflammatory programs in WT versus IRF3-KO mice.

48 1, similar to was has been observed in TRPA1 KO mice.

49 and likely contribute to ataxia in Cacna2d2 KO mice.

50 albumin (PV) GABAergic interneurons of Ahnak KO mice.

51 creased in liver and skeletal muscle of CysC KO mice.

52 pulmonary vaso-occlusions in End.TGFbetaRII-KO mice.

53 nd tissue iron overload compared with single KO mice.

54 lung tumorigenesis and metastasis in Gprc5a-ko mice.

55 e SE was nearly abolished in EP2 conditional KO mice.

56 These changes were not seen in MIOX-KO mice.

57 nd marked accumulation of progesterone in XX-KO mice.

58 erone levels were observed in both XY and XX KO mice.

59 corresponding reduction in ethanol intake in KO mice.

60 as absent in both platelet- and global-COX-1-ko mice.

61 enal IR was significantly attenuated in P2X4 KO mice.

62 ent in more severely injured Grp78 knockout (KO) mice.

63 ed from wild-type, Kv3.1 and Kv3.3 knockout (KO) mice.

64 ction in male and female Cacna2d2 knock-out (KO) mice.

65 ls from C57BL/6N wild-type and FXR-knockout (KO) mice.

66 , effects similar to those observed in Itm2b(KO) mice.

67 a mouse model of autism, Shank3b knock-out (KO) mice.

68 icient (B2m KO) and MHC-II-deficient (MHC-II KO) mice.

69 omoted B-cell hyperproliferation in Nlrc5(mo-KO) mice.

70 abolished in beta-cells from SUR1-knockout (KO) mice.

71 transgenic (MIOX-TG) and MIOX knockout (MIOX-KO) mice.

72 ages using intestinal tissues from Lkb1(Lgr5-KO) mice.

73 impaired in CB(1) receptor knockout (CB (1) -KO) mice.

74 with MAOIs in wild-type and TAAR1-knockout (KO) mice.

75 enescent hepatocytes than livers of Nemo(LPC-KO) mice.

76 ing Tnfaip3(fl/fl) xCd207(+/cre) (Tnfaip3(Lg-KO) ) mice.

77 ALR-L-KO mice (1-, 2-, and 4 wk old) and Adeno-Cre-transfected

78 In contrast, after GCI, GFAP-ARO-KO mice: (1) lacked the normal elevation of astrocyte ar

79 gile X Mental Retardation 1 (Fmr1) knockout (KO) mice, a model of Fragile X Syndrome (FXS) with abrog

80 B member 4 (Abcb4(-/-); Mdr2(-/-)) knockout (KO) mice, a sclerosing cholangitis model.

81 Results showed that KO mice accumulated high concentrations of upstream lysi

82 tion was reduced in the facial nerve of CD38 KO mice after axotomy.

83 ge and microglial activation in the GFAP-ARO-KO mice after GCI, suggesting that the defects in the KO

84 expression in microglia/macrophages of STAT6 KO mice after ICH.

85 rophage inflammatory protein-1alpha in GPR37-KO mice after ischemia.

86 f the excitatory/inhibitory balance in Orai1 KO mice aggravates chemoconvulsant-mediated seizures.

87 PS2APP;Trem2(ko) mice also exhibited more dendritic spine loss around

88 Notably, D1-cacna1c(KO) mice also show the same exaggerated remote contextua

89 and hepcidin in double Bmp6/endothelial Bmp2 KO mice, although no other BMP ligand mRNAs were increas

90 e preclinical research using Fmr1 knock out (KO) mice, an effective treatment for FXS has yet to be d

91 ls are increased in FXR-knockout (KO) or SHP-KO mice and are decreased by activation of FXR in a SHP-

92 Clamps also were performed in ghrelin-KO mice and C57BL/6N mice administered the growth hormon

93 e, we report the characterizations of Mfsd7c-KO mice and compare these characterizations to phenotypi

94 obtained from striated muscle-specific Speg-KO mice and compared them with wild-type (WT) controls.

95 Psen1 KO mice and knock-in (KI) mice with homozygous FAD-assoc

96 vealed a complete lack of testosterone in XY-KO mice and marked accumulation of progesterone in XX-KO

97 Here, we generated fat-specific Chrna2 KO mice and observed thermogenic defects in cold and met

98 sient receptor potential vanilloid 1 (TRPV1) KO mice and prevented by the TRPV1 antagonist, capsazepi

99 n was observed in colonoids derived from DRA-KO mice and short hairpin RNA-mediated DRA knockdown in

100 y, we studied Kirrel3 loss of function using KO mice and showed that Kirrel3 is a synaptic adhesion m

101 fibroblasts, and thymocytes from WT and MCU KO mice and the isolated working rat heart.

102 The KO mice and their matched wild-type mice were challenged

103 nges were remarkably reduced in Ins2 (Akita)/KO mice and, likewise, in vitro experiments with XBP1 si

104 ress this issue, we used Ca(V)3.3 knock-out (KO) mice and a panselective T-channel blocker 3,5-dichlo

105 Wild-type and DRA-knockout (KO) mice and crypt-derived colonoids were used as models

106 We generated Rab39b knockout (KO) mice and found that they exhibited cortical neurogen

107 Bmp2 and Hfe compared with single knockout (KO) mice and littermate controls.

108 eukin-1 (IL-1) using IL-1alphabeta knockout (KO) mice and perioperative IL-1 receptor type 1 (IL-1R1)

109 For that, AnxA1, Fpr2/3 knockout (KO) mice and wild-type (WT) controls were infected intra

110 Ghrelin knockout (KO) mice and wild-type (WT) littermates underwent an ins

111 ice using Lgr5-regulated CRE-ERT2 (Lkb1(Lgr5-KO) mice) and the traced lineages by using a CRE-depende

112 5 expression were detected in End.TGFbetaRII-KO mice, and activated TGFbeta signaling was present in

113 ) and aortic rings ( P=0.0060) from End.LepR-KO mice, and murine and human endothelial sprouting angi

114 mRNAs were increased in the livers of double KO mice, and only Bmp6 and Bmp2 mRNA were induced by die

115 sitive cells in the ischemic cortex of GPR37 KO mice, and RT-PCR identified an enrichment of M1-type

116 eding did not increase their number in ALR-H-KO mice, and the increase in ALR-H-HET was greater than

117 fter GCI, suggesting that the defects in the KO mice are because of a loss of E2 rather than an incre

118 alpha, suggesting that BMSCs from Col6alpha2-KO mice are highly sensitive to TNFalpha signaling.

119 Lung tumor suppressor gene Gprc5a-knockout (ko) mice are susceptible to lung inflammation, tumorigen

120 er 3 (GAT3), in the hippocampus of the Mecp2 KO mice, as well as a corresponding increase of GAT3 cur

121 Primary cultures of GCPs from Jdp2-KO mice at postnatal day 5 were more resistant to apopto

122 tructure of wild-type and p38gamma knockout (KO) mice at baseline and after abdominal aortic banding

123 lar bone formation between WT and Col6alpha2-KO mice based on the mineral appositional rate, bone for

124 In aralar-knock-out (KO) mice, betaOHB recovers from the drastic drop in spec

125 The KI/KI and KI/KO mice both have significantly smaller muscle fiber cro

126 d disease severity in wild-type (WT) and B2m KO mice but failed to reduce bacterial burden in MHC-II

127 pocyte-specific tuberous sclerosis complex 1 KO mice by crossing floxed mice with Adipoq-Cre.

128 tantly, targeting PGE(2) signaling in Gprc5a-ko mice by PTGES inhibitor suppressed MDSC recruitment,

129 While Lrrk2 KO mice can control Mycobacterium tuberculosis (Mtb) rep

130 oton pumps at the apical surface of A-ICs in KO mice compared to controls.

131 wed axon loss in the cochlear nerves of Nhe6 KO mice compared to WT mice.

132 l volume and trabecular number in Col6alpha2-KO mice compared with WT.

133 ere significantly elevated in the SG of Nhe6 KO mice, compared to WT littermates.

134 sive biochemical characterization of Aldh7a1-KO mice consuming a low lysine/high PN diet.

135 However, most crypts from Lkb1(Lgr5-KO) mice contained functional ISCs that expressed increa

136 Cerebellum of Jdp2-knockout (KO) mice contains lower number of Atoh-1 positive GCPs t

137 In addition, TLR4 and TLR2/4 KO mice demonstrated a significant increase in the numbe

138 ccinated WT mice to naive CD4-deficient (CD4 KO) mice demonstrated that antigen-experienced CD4(+) T

139 ngs mimicked the constitutive Cfl2-knockout (KO) mice described previously, including sarcomeric disr

140 We recently reported that Kiss1r KO mice develop obesity, along with reduced metabolism a

141 r abdominal aortic banding demonstrated that KO mice developed less ventricular hypertrophy and that

142 We further demonstrated that Gal2-KO mice developed significantly larger tumors than WT mi

143 3 months of infection with H felis, Nlrc5(mo-KO) mice developed gastric hyperplasia (P < .0001), sple

144 terestingly, the phenotype of KO->WT and WT->KO mice did not differ from that of WT->WT mice.

145 ever, the gross levels of H3R17me2a in CARM1 KO mice did not significantly decrease, indicating that

146 Knockout (KO) of IL-6 in muscle lamin A/C-KO mice diminishes the deficits in trabecular bone mass

147 rebrain glutamatergic neuron-selective Ahnak KO mice display a depression-like behavioral phenotype s

148 In contrast, PV interneuron-selective Ahnak KO mice display an antidepressant-like behavioral phenot

149 CD11c(+) cells from Sema3E KO mice displayed increased expression of costimulatory

150 In contrast, IFN-beta-KO mice displayed minimal differences in viral burdens w

151 s ineffective to afford protection in Fpr2/3 KO mice during infection.

152 n, which reduced the GIR required by ghrelin-KO mice during the clamps, increased plasma corticostero

153 f naive CD4(+) T cells to PIV-vaccinated CD4 KO mice exacerbates disease.

154 CD4SP T cells from TCF1 KO mice exhibit downregulation of P2 transcript variant

155 Particularly, ALX/FPR2 KO mice exhibit exacerbated inflammation in their saliva

156 We also show that D1-cacna1c(KO) mice exhibit elevated death of young hippocampal neu

157 At basal steady state Zip14 KO mice exhibited a phenotype that included muscle wasti

158 Eight-week-old double endothelial Bmp6/Bmp2 KO mice exhibited a similar degree of hepcidin deficienc

159 DRA-KO mice exhibited an increased colonic paracellular perm

160 In addition, CFs in KO mice exhibited increased multivesicular transmission,

161 When given cerulein, Ctrl-KO mice exhibited lower intrapancreatic chymotrypsin act

162 In contrast, double Hfe/endothelial Bmp2 KO mice exhibited reduced hepcidin and increased extrahe

163 onstrated that ovariectomized female FBN-ARO-KO mice exhibited significantly attenuated astrocyte act

164 The GFAP-ARO-KO mice exhibited significantly attenuated reactive astr

165 pocyte-specific tuberous sclerosis complex 1 KO mice exhibited similar detrimental effects.

166 Brain-specific Orai1 and STIM1 knockout (KO) mice exhibited significantly stronger seizures (P =

167 In contrast, STAT6 knockout (KO) mice exhibited worse outcomes than WT mice in both I

168 Adipocyte-specific Raptor KO mice experienced exacerbated alcohol-induced steatosi

169 Homozygous Ctrl-KO mice expressed no detectable CTRL protein in the panc

170 In the KO mice, expression of pERK was strongly reduced indicat

171 ating the protection, as IFN-gamma knockout (KO) mice failed to acquire protection when infected with

172 KO mice fed GC-1 diet for 2 and 4 weeks had decreased se

173 Our data showed that YAP( KO) mice fed an HFD exhibited lower serum alanine aminot

174 le-neuron genetic approach in SR conditional KO mice from both sexes, we demonstrate a cell-autonomou

175 ged metabolically with the HF/HC diet; ALR-H-KO mice gained the least weight and had the least steato

176 Conversely, in vivo, platelet-COX-1-ko mice had a distinctly different profile from global-C

177 Consistently, the KO mice had a significant increase in hepatic mRNAs for

178 ymorphonuclear neutrophils (PMNs) from these KO mice had defective innate immune responses, including

179 Furthermore, FBN-ARO-KO mice had exacerbated neuronal damage and worse cognit

180 Furthermore, H. pylori-infected Neil2-KO mice had greater inflammation and more epithelial cel

181 Adipocyte-specific Atg5 KO mice had increased circulating levels of fibroblast g

182 Casp1-KO mice had increased in osteoclast numbers, whereas the

183 We found that ischemic AKI in NGAL knockout (KO) mice had worse renal outcomes compared with wild-typ

184 In addition, Tnfaip3(Lg-KO) mice harbored increased numbers of IL-12-expressing

185 nalyses reveal islets from HFD-fed Galpha(z) KO mice have a dramatically altered gene expression patt

186 The KI/KO mice have a significant decrease in voluntary movemen

187 However, only the KI/KO mice have clear skeletal muscle histologic changes in

188 Adult Dock3 KO mice have impaired muscle function and Dock3 KO myobl

189 We first determined that global Kiss1r KO mice have significant alterations in body temperature

190 Skeletal muscle-targeted Lrrc8a KO mice have smaller myofibers, generate less force ex v

191 that striated muscle-specific Speg-knockout (KO) mice have defective triad formation, abnormal excita

192 Platelets from Slc44a2(KO) mice have impaired activation in response to thrombi

193 R activity, and the germline Grb14-knockout (KO) mice have improved insulin signaling in liver and sk

194 rotein (Gsalpha) in osteocytes (Dmp1-Gsalpha(KO) mice) have abnormal myelopoiesis, osteopenia, and re

195 ET than WT mice and further reduced in ALR-H-KO mice; HF/HC reduced regulatory T-cell frequency only

196 Administration of purified OPN to the OPN KO mice, however, restored the TRALI response and pulmon

197 gh)) were accumulated in the lungs of Raptor KO mice in the LLC lung metastasis model, leading to dec

198 ere delayed in only the PVPV-Akt1 knock out (KO) mice in association with increased apoptosis with no

199 r of NGAL-deficient CD4(+) T cells from NGAL KO mice into CD4 KO or WT mice led to worse renal functi

200 We show that the auditory synapse of GLAST KO mice is more vulnerable to cisplatin administration d

201 KO mice lacked epileptic seizures when fed a low lysine/

202 Increased atherosclerosis in CYP17A1 XY KO mice lacking testosterone was associated with altered

203 oliferation or Wnt/beta-catenin signaling in KO mice, likely a result of decreased thyroid hormone re

204 Some intestinal crypts from Lkb1(Lgr5-KO) mice lost ISCs compared with crypts from control mic

205 pancreas-specific disruption of Prkd1 (PRKD1(KO) mice), mice that express oncogenic KRAS (KC mice), a

206 lurane induction of hypnosis in the Ca(V)3.3 KO mice more robustly than in the WT mice.

207 ed from 6 to 7 months onward in PS2APP;Trem2(ko) mice, notwithstanding the reduced plaque load at lat

208 investigated conditional/conventional double KO mice of BMP-receptor 1a (BMPR1a; targeted to PV-INs)

209 Here, we compared WT and GluA3 KO mice of both sexes and identified several important r

210 euron-specific Drp1 activator in vivo Bbeta2 KO mice of both sexes display elongated mitochondria in

211 KO mice on GC-1 also had higher levels of total liver BA

212 Constitutive Ahnak KO mice or forebrain glutamatergic neuron-selective Ahna

213 s completely abrogated in OSMRbeta knockout (KO) mice, OSM overexpression in the chronically demyelin

214 In EC-AGO1-KO mice, overexpression of TSP1 substantially attenuated

215 ampal engram reactivation is reduced in Fmr1 KO mice performing contextual fear memory recall.

216 ed Na(v) availability in Fhf2 knockout (Fhf2(KO)) mice predisposes to abnormal excitability at the ti

217 B signalling was disrupted in the OC of Nhe6 KO mice, probably due to TrkB reduction, caused by over

218 since both PIV-vaccinated B2m KO and MHC-II KO mice produced less Coxiella-specific IgG than PIV-vac

219 The heterozygous PME-1 KO mice produced normal levels of endogenous Abeta and e

220 lood from platelet-COX-1-ko and global-COX-1-ko mice produced similar eicosanoid profiles in vitro: f

221 t not WT, mice developed fibrosis; and ALR-H-KO mice progressed to cirrhosis.

222 Platelet count was normal in Chk knockout (KO) mice, reduced by 92% in Chk;Csk double KO (DKO) mice

223 yperinsulinemic-hypoglycemic clamps, ghrelin-KO mice required a 10-fold higher glucose infusion rate

224 rites and synapses develop normally in Tiam1 KO mice, resembling WT mice at postnatal day 21 (P21), b

225 ired glucose homeostasis of obese male Dusp8-KO mice, respectively.

226 y diminished in female and male PS2APP;Trem2(ko) mice, respectively.

227 cking either IL-12 or IFNgamma in Tnfaip3(Lg-KO) mice restored Th2 responses, whereas administration

228 Subcutaneous adipocytes in KO mice show a size distribution shift toward an increas

229 DG-GluN1 KO mice show CA3 cellular hyperactivity, detected using

230 Moreover, female ALX/FPR2 KO mice show increased autoantibody production and loss

231 Gpr151- knockout (KO) mice show diminished behavioral responses to nicotin

232 Male Shank3b KO mice showed a marked reduction in PVH-OT neuron numbe

233 Phenotypically, Ecm29 KO mice showed increased firing frequency of action pote

234 Atherosclerotic plaques from HFD-treated KO mice showed increased infiltration of M1 type inflamm

235 Macrophages from KO mice showed increased phagocytic activity and elevate

236 hermore, purified CD4(+) T cells from Sema3E KO mice showed increased propensity to differentiate int

237 USP20-KO mice showed normal baseline systolic function but imp

238 In addition, adult male KO mice showed reduced ventral hippocampus-mPFC-evoked p

239 Nhe6 KO mice showed significant reductions in TrkB and Akt ph

240 NanoString analysis of the plaques from KO mice showed upregulation of a number of mRNAs encodin

241 Compared with wild-type mice, CD38 knockout (KO) mice showed reduced microglial activation in the fac

242 Nhe6 knockout (KO) mice showed significant hearing loss compared to WT

243 oxidative stress biomarker, in the brains of KO mice, suggesting that increased oxidative stress may

244 was more pronounced and prolonged in ghrelin-KO mice, supporting previous studies suggesting increase

245 aling that distinguish cohorts of IL-2Ralpha-KO mice that develop early- versus late-stage autoimmune

246 rom quadruple neuroligin-1/2/3/4 conditional KO mice that lacked all neurexins or all neuroligins wer

247 rized beta cells from KATP channel knockout (KO) mice, the researchers revealed a shift in G protein

248 In neurons from Jedi-1 knockout (KO) mice, there was an increase in the fraction of capsa

249 ed on the enhanced memory phenotype of Tiam1 KO mice, Tiam1 may be a potential target for the treatme

250 Here, we used platelet-COX-1-ko mice to define the platelet and non-platelet eicosano

251 vel multiple feature selection tools in Fmr1-KO mice to provide direct evidence that normal functioni

252 t, we use cortical cultures derived from Dcx KO mice to show that the effects of nestin on growth con

253 duced TNF-induced osteoclastogenesis in PAR1 KO mice to WT levels without affecting WT responses.

254 d amyloid precursor protein (APP) knock-out (KO) mice to assess the effects of Abetaos on glutamaterg

255 In USP30 KO mice, TOM subunits have reduced abundance across mult

256 In alpha2delta-1 gene KO mice, treatment with FK506 failed to increase the fre

257 In MAP4K1(KO) mice, tumors grow slower than in wild-type mice and

258 We generated ZO-1 CM-specific knockout (KO) mice using alpha-Myosin Heavy Chain-nuclear Cre (ZO-

259 e cisplatin was also alleviated in PT-DsbA-L-KO mice via the activation of Hsp90 /Smad3 and p53/CTGF

260 mice, rats, and NHPs, but not in M(1) mAChR KO mice, VU0453595 produced dose-related increases in hi

261 compromised astrocyte activation in FBN-ARO-KO mice was associated with robust downregulation of the

262 The enhanced resistance of Sema3E KO mice was associated with significantly (p < 0.05) inc

263 , the total chymotrypsinogen content in Ctrl-KO mice was barely reduced indicating that CTRL is a low

264 e response to skeletal muscle injury in Speg-KO mice was compared with that of WT mice, leading to th

265 d at nighttime, a mild hearing loss in GLAST KO mice was found but not at daytime, revealing a potent

266 the caerulein treated miR-216a and miR-216b KO mice was the presence of pancreatic duct glands (PDGs

267 Glucagon resistance in alphaTSC2(KO) mice was associated with improved glucose levels in

268 Liver glucagon resistance in alphaTSC2(KO) mice was characterized by reduced expression of the

269 Using conditional KO mice, we demonstrate that the Lphn2/3 double-deletion

270 flammation and cognitive impairment in NLRP3-KO mice, we transplanted VAT from obese WT or NLRP3-KO d

271 Utilizing Dock3 global knockout (Dock3 KO) mice, we found that the haploinsufficiency of Dock3

272 Using Tbet-deficient (Tbet KO) mice, we showed a partial role for Th1 subset CD4(+)

273 AnxA1 and Fpr2/3 KO mice were highly susceptible to infection, displaying

274 Both male and female homozygous KO mice were infertile, due to abnormal genital organs.

275 Consistently, chow-fed CysC KO mice were more susceptible to lipopolysaccharide-indu

276 The middle and the inner ears of WT and Nhe6 KO mice were not different morphologically.

277 tation of IP-mediated relaxation, iSM-Gprc5b-KO mice were protected from arterial hypertension, and t

278 Moreover, TRPV4 gene-KO mice were protected from Piezo1 agonist- and pressure

279 We found that heterozygous PME-1 KO mice were resistant to Abeta-induced impairments in c

280 When these KO mice were subjected to polymicrobial sepsis, their su

281 stromal cells (BMSCs) from WT and Col6alpha2-KO mice were treated with rmTNFalpha protein, the Col6al

282 GFAP-ARO-KO mice were viable and fertile, with normal gross brain

283 Fhf2(KO) mice were challenged by reducing calcium conductance

284 In this study, we found that IRF3-knockout (KO) mice were greatly protected from sepsis in a clinica

285 pe (WT) C57BL/6 (B6) mice and CD1d knockout (KO) mice were infected ocularly with herpes simplex viru

286 All Cyp17a1 knockout (KO) mice were phenotypically female; however, 58% were Y

287 his study, we found that Opn3-knockout (Opn3-KO) mice were prone to diet-induced obesity and insulin

288 Supporting this, P2X4-deficient (KO) mice were protected against ischemic AKI with signif

289 Sema3E-deficient (Sema3E knockout [KO]) mice were highly resistant to L. major infection, a

290 WT) B6 mice, the symptomatic corneas of CD1d KO mice, which lack iNKT cells, showed (i) decreases in

291 we suppressed beta-catenin in Mdr2 knockout (KO) mice, which develop sclerosing cholangitis due to re

292 Finally, treatment of ALR-L-KO mice with rALR between 1 and 2 wk prevented miR-540 e

293 Nlrc5(mo-KO) mice with chronic H felis infection had increased nu

294 ed, such as in the sera of Il-18bp knockout (KO) mice with CpG-induced macrophage activation syndrome

295 he subcutaneous and brown adipose tissues of KO mice, with greater vascularity and enhanced browning

296 fected WT mice, the symptomatic corneas CD1d KO mice, with iNKT cell deficiency, had increased levels

297 conditions produced conduction block in Fhf2(KO) mice, with Fhf2 wild-type (Fhf2(WT)) mice showing no

298 Microgliosis was impaired in PS2APP;Trem2(ko) mice, with Trem2-deficient microglia showing comprom

299 FD feeding of CysC-deficient (CysC knockout [KO]) mice worsened obesity-associated adipose tissue inf

300 Analysis (IPA) predicted that platelet-COX-1-ko mice would be protected from thrombosis, forming less