ライフサイエンスコーパス: mutant mice

1 onsible for this rescue of plasticity in the mutant mice.

2 y and mortality from aortic rupture in young mutant mice.

3 ffected or only minimally affected in Cep290 mutant mice.

4 , learning, and memory are impaired in these mutant mice.

5 ted normal Ig isotype secretion in the Duox1 mutant mice.

6 njury in control and conditional Ift88 cilia mutant mice.

7 modulator improved social behavior in Shank3 mutant mice.

8 mutant DSPP in the odontoblasts of the DSPP-mutant mice.

9 xpression is able to rescue deficits of Nae1 mutant mice.

10 duced in inducible, ECCre+;FAK(Y397F/Y397F) -mutant mice.

11 avoiding defects observed in germline Ikaros mutant mice.

12 nderlying cause for SOAE enhancement in some mutant mice.

13 severity of vascular malformations in Cdc42 mutant mice.

14 ere isolated from wild type and nBmp2NLS(tm) mutant mice.

15 n of the skin and lung were unaltered in the mutant mice.

16 yngeal endoderm and is downregulated in Tbx1 mutant mice.

17 and Tlr4 KO mice but failed to do so in Tlr9 mutant mice.

18 urinary excretion of Na(+) and urea in both mutant mice.

19 nd western blot experiments in wild-type and mutant mice.

20 rming odontoblasts in the wild-type mice and mutant mice.

21 altered T cell numbers in the spleens of A20 mutant mice.

22 n is inhibited in locus coeruleus neurons of mutant mice.

23 cyte phenotype from emerging in unchallenged mutant mice.

24 ved functional pancreas, in apancreatic Pdx1 mutant mice.

25 ucing ends, which is present at birth in the mutant mice.

26 Wnt6 mRNA level was found in MeCP2K412R sumo-mutant mice.

27 e to repetitive grooming behavior in Shank3B mutant mice.

28 nd epithelial proliferation in the uterus of mutant mice.

29 enes are significantly down-regulated in the mutant mice.

30 processes, the upper lip remained intact in mutant mice.

31 l cyst growth in postnatal kidneys from Pkd1 mutant mice.

32 initial segments of betaIV-spectrin and AnkG mutant mice.

33 r growth was observed in kinase-inactive GK5 mutant mice.

34 racteristics of the glomerulopathy in Col4a3 mutant mice.

35 pheral myelinated fibers in Schip1 knock-out mutant mice.

36 nly evident in homozygous, not heterozygous, mutant mice.

37 ate this, we generated a series of nesprin 1 mutant mice.

38 min-positive GABAergic interneurons in Grin1 mutant mice.

39 e also observed in cystic kidneys from Hnf1b mutant mice.

40 ic severity observed in young congenital BBS mutant mice.

41 nt to recapitulate the phenotype observed in mutant mice.

42 blood-brain barrier was maintained in Flvcr2 mutant mice.

43 ble behaviors, respectively, in male PC-Tsc1 mutant mice.

44 ffects of RSPO1 overexpression in Apc(Min/+) mutant mice.

45 po-T) is upregulated in podocytes from Synpo mutant mice.

46 y contribute to altered neurotransmission in mutant mice.

47 n2-linked ALS and also generated Ubqln2 null mutant mice.

48 nhibition (PPI) of acoustic startle in Grin1 mutant mice.

49 loss of mature PT cells, lethal to the Hnf4a mutant mice.

50 5 (ATF5)-mediated stress response pathway in mutant mice.

51 The resultant double-mutant mice 5xF:pGB mice displayed a full rescue of hipp

52 The adipose SNS degenerates progressively in mutant mice after 8 weeks of age.

53 ficient in splenic macrophages isolated from mutant mice after secondary systemic infection with Stap

54 Nisch-mutant mice also exhibited increased rates of glucose ox

55 Mutant mice also failed to develop corpora lutea, as evi

56 we show that in Fgfr3;Fgfr4 (Fgfr3;4) global mutant mice, alveolar simplification is first observed a

57 were discovered by the circling behavior of mutant mice, an indicator of balance dysfunction.

58 ch, here we generated Nisch loss-of-function mutant mice and analyzed their metabolic phenotype.

59 Our analysis of mutant mice and cultured endothelial cells shows that Ep

60 Wnt signaling in central pathfinding in Fzd3 mutant mice and Fzd3 morpholino treated frogs and found

61 Analyses of PCP-mutant mice and genetic interaction studies show that th

62 By creating mutant mice and human cerebral organoids, here we found

63 mphoproliferation and autoimmunity in scurfy mutant mice and immunodysregulation polyendocrinopathy e

64 These processes can be perturbed in mutant mice and in explant culture, mimicking the defect

65 turnover of dendritic spines is impaired in mutant mice and is accompanied by an increase in neurona

66 We further examined R579W mutant mice and mice with pan-cellular Tcf4 heterozygosi

67 Supplementing gut-sterilized p53-mutant mice and p53-mutant organoids with gallic acid re

68 enile-like R2b resident macrophages in cilia mutant mice and restores rapid cystogenesis.

69 alysis and immunoblot studies revealed P497S mutant mice and UBQLN2 knockout HeLa and NSC34 cells hav

70 solated from naive (uninfected) nBmp2NLS(tm) mutant mice and wild type mice, but are deficient in spl

71 ha-actin switch was delayed in systemic CAP2 mutant mice, and myofibrils remained in an undifferentia

72 his study, we generated Camk2a/Camk2b double-mutant mice, and observed that loss of CAMK2, as well as

73 nent delta and theta EEG oscillations in the mutant mice, and reached burst-suppression pattern earli

74 By contrast, SBI-425 treatment of Enpp1 mutant mice, another model of ectopic mineralization ass

75 We report that when female Ppp1r15a mutant mice are fed a high fat diet they gain less weigh

76 associated with human infertility, the point mutant mice are fertile despite meiotic defects.

77 Constitutive Lpar1 null mutant mice are protected from partial sciatic nerve lig

78 ZFP708 mutant mice are viable and fertile, yet embryos fail to

79 fficient to promote sociability in monogenic mutant mice as well as in MIA offspring.

80 ns likewise distinguished phenotypes of Lyst-mutant mice, as well as background differences between w

81 with failure in periderm formation in Grhl3 mutant mice associated with premature closure of the can

82 nical properties of the TMs of wild-type and mutant mice at audio frequencies is required to elucidat

83 f-administration in wild-type (WT) and Npas2 mutant mice at different times of day.

84 d reinstatement) in wild-type (WT) and Npas2 mutant mice at different times of day.

85 The mutant mice became persistently ketotic and tolerated th

86 found identical results in both control and mutant mice before E17.5 when the temporal muscle makes

87 rment of macrophage function in nBmp2NLS(tm) mutant mice, bone marrow derived (BMD) macrophages and s

88 teoblast differentiation, is reduced in Pkd1 mutant mice but the mechanism governing PC1 activation o

89 ferlin distribution were unaffected in these mutant mice, but auditory brainstem response wave-I ampl

90 aging we assessed axon/myelin-units in Anln-mutant mice by focused ion beam-scanning electron micros

91 n also be induced in conditional adult cilia mutant mice by introducing renal injury.

92 nesis of these disorders, we generated Disc1 mutant mice by introducing the 129S6/SvEv 25-bp deletion

93 essed the hearts of adult Handlr and Atcayos mutant mice by transverse aortic banding and found that

94 xiety-like behaviors in Hdh(+/Q111) knock-in mutant mice by using a battery of behavioral tests.

95 EGFR-mutant glioma evolution in conditional mutant mice by whole-exome sequencing, transposon mutage

96 involved in the occurrence of ICH in Col4a1 mutant mice, by raising the intravascular pressure in th

97 to the presently held view, we find that Mci mutant mice can specify MCC precursors.

98 Here, we report generation of mutant mice carrying a mutation only at the E'-box cis-e

99 osoglutathione concentrations were higher in mutant mice compared to WT.

100 n the corneal keratocytes of the Dox-induced mutant mice, compared to the littermate controls.

101 Skeletal muscles from mutant mice contained 'cores' characterized by severe my

102 In Nell2 mutant mice, contralateral RGC axons abnormally invaded

103 Mutant mice demonstrate a twofold increase in T-regulato

104 ences human AF risk, and adult-specific Tbx5-mutant mice demonstrate spontaneous AF.

105 agnetic resonance imaging we identified that mutant mice demonstrated abnormalities within the medull

106 Scx-mutant mice demonstrated disrupted callus healing and as

107 We screened 36,530 third-generation germline mutant mice derived from N-ethyl-N-nitrosourea-mutageniz

108 triguingly, however, under prolonged stress, mutant mice develop larger tumors and have a higher tumo

109 Homozygous mutant mice develop lethal postnatal inflammation of the

110 d in many healthy tissues and, because Ipo11 mutant mice develop lung tumors, also implicates Importi

111 We report that Col4a1 mutant mice develop progressive neuromuscular pathology

112 Mutant mice developed a Bartter syndrome phenotype, char

113 Homozygous Nppb mutant mice developed acute and lethal heart failure aft

114 The adult mutant mice developed dilated hearts and showed signific

115 Mutant mice developed high levels of intracellular and s

116 Furthermore, the STING mutant mice developed lung fibrosis similar to that of p

117 antigen 4 (CTLA-4) immunoglobulin (Ig), Qa-1 mutant mice developed robust donor-specific antibody res

118 LPS treatment in monogenic mutant mice did not induce amounts of interleukin-17a (I

119 Interestingly, VE-cadDEE/DEE mutant mice did not require endothelial p120, demonstrat

120 osine-2A receptor (A2AR) in culture and Lrp4 mutant mice diminishes the osteoclastogenic deficit and

121 addition, neuromuscular synapses in vezatin mutant mice display premature signs of deterioration, no

122 Consistently, the mutant mice displayed hippocampal-dependent learning and

123 Ilea of mutant mice displayed increased expression of enterocyte

124 These mutant mice displayed myofiber necrosis, weaker muscle s

125 Furthermore, mutant mice displayed none of the behavioral alterations

126 Here we report that these mutant mice displayed significantly impaired glucose tol

127 Approximately 30% of mutant mice displayed symptoms of stroke and ischemic re

128 We studied dysbindin-1 null mutant mice (Dys(-/-)) to shed light on retinal neurodev

129 Adult Bax/Bak mutant mice exhibit aberrant co-activation of antagonist

130 th Has2(f/f);Wnt1-Cre and Has2(f/f);Osr2-Cre mutant mice exhibit cleft palate at complete penetrance,

131 Pnldc1 mutant mice exhibit disrupted LINE1 retrotransposon sile

132 Notably, the brains of the mutant mice exhibit impaired global neuronal activity-de

133 Lyst-mutant mice exhibit neurologic phenotypes that are sensi

134 J-, but not on the C57BL/6J-background, Lyst-mutant mice exhibit overt tremor phenotypes associated w

135 (B6) strain background, MRL-Atp6v1b1vtx/vtx mutant mice exhibit profound hearing impairment, which i

136 onse to running exercise, however, the Fndc5 mutant mice exhibit reduced glucose tolerance and insuli

137 h2(tm1.1Ecan) Heterozygous Notch2(tm1.1Ecan) mutant mice exhibit severe cancellous and cortical bone

138 Pten mutant mice exhibit social behavior deficits, elevated s

139 B cells from mutant mice exhibited a diminished concentration of cyto

140 Homozygous and heterozygous mutant mice exhibited altered hippocampal morphology at

141 We found that Hdh(+/Q111) mutant mice exhibited depressive-like, but not anxiety-l

142 Mutant mice exhibited fewer suppressive Tregs in the inj

143 voluted tubules (DCTs): Ksp-cre;Pth1r(fl/fl) Mutant mice exhibited hypercalciuria and had lower serum

144 Myeloid cells from immunized Stat3 mutant mice exhibited impaired antigen-presenting functi

145 Although the mutant mice exhibited jaw structures and occlusion compa

146 The Zpld1 mutant mice exhibited normal hearing function as assesse

147 VE-cadGGG/GGG mutant mice exhibited reduced VE-cad-p120 binding, reduc

148 Moreover, these mutant mice exhibited severe cerebellar motor learning d

149 s, striatal synaptosomes isolated from young mutant mice exhibited significantly lower dopamine uptak

150 The mutant mice exhibited vascular defects in pericyte cover

151 Both PRAP1-deficient and E85V knock-in mutant mice fed a chow diet manifested an increase in th

152 creen of N-ethyl-N-nitrosourea (ENU)-induced mutant mice for aberrant immune function, we identified

153 ion activity, whereas those from the caAcvr1-mutant mice formed large osteoclasts and demineralized p

154 stimulating bacteria(10,11) protects C9orf72-mutant mice from premature mortality and significantly a

155 togenic T cells between wild-type and GADD34 mutant mice further indicate that the beneficial effects

156 Mutant mice had a decreased density of parvalbumin- and

157 se-positive osteoclasts, which revealed that mutant mice had more osteoclasts compared with WT mice,

158 Moreover, the Nisch-mutant mice had reduced expression of liver markers of g

159 r (IFNLR1) and double IFNAR1/IFNLR1 knockout mutant mice had reduced lung inflammatory pathology comp

160 ouse cortex are involved in myelination, and mutant mice had reduced mature oligodendrocyte cell numb

161 Behaviorally, the mutant mice had reduced voluntary locomotion and explora

162 Single Per1, Per2, and Per3 mutant mice had robust food anticipatory activity during

163 Mutant mice have alkaline urine but do not exhibit overt

164 Mutant mice have altered hematopoietic stem and progenit

165 The obtained hSOD1/rag2 double mutant mice have been characterized.

166 Constitutive Lpar1 null mutant mice have been instrumental in identifying roles

167 We demonstrate that (i) Firre mutant mice have cell-specific hematopoietic phenotypes,

168 We now demonstrate that hypomorphic Foxc1 mutant mice have granule and Purkinje cell abnormalities

169 The mutant mice have gross defects in chorioallantoic branch

170 of Hensen's cells and found that adult Jag1 mutant mice have hearing deficits at the low-frequency r

171 We find that DSCR1 mutant mice have impaired adult hippocampal neurogenesis

172 In conclusion, Notch2HCS mutant mice have increased mature B cells in the MZ of t

173 n menorin homologue, Fam151a, and homozygous mutant mice have no discernible phenotype.

174 Female mdr1a mutant mice have no significant difference in ovarian fo

175 Mutant mice have normal nociceptor populations, which, h

176 The Fndc5 mutant mice have normal skeletal muscle development, gro

177 We found that heterozygote GALC mutant mice have reduced myelin debris clearance and dim

178 Chronic treatment of Mecp2 and Shank3 mutant mice improved body condition, some brain abnormal

179 ratic output of the cerebellar nuclei in the mutant mice improved movement.

180 ional brain-specific Akt1, and double Akt1/3 mutant mice in behaviors relevant to neuropsychiatric di

181 sexes, including wild-type and TrkB(Shc/Shc) mutant mice in which a point mutation (Y515F) of TrkB pr

182 tion in rods and cones in vivo, we generated mutant mice in which Ser21 is substituted with alanine (

183 Using Brn3a and Brn3b mutant mice in which the alkaline phosphatase gene was k

184 f the diencephalon, hypothalamus and eyes in mutant mice in which the Ftm/Rpgrip1l ciliopathy gene is

185 nclusion is further supported by analyses of mutant mice in which we conditionally deleted a floxed a

186 Using conditional Cep290 mutant mice, in which the C-terminal myosin-tail homolog

187 stdc1(-/-) mice and compound Sostdc1 and Lrp mutant mice indicates a strong association between Wnt a

188 the period or phase of the central clock in mutant mice, indicating a defect downstream of the supra

189 ce and were significantly upregulated in the mutant mice, indicating that pre-translational splicing

190 We found that mutant mice injected with the vehicle showed faster indu

191 B cell development in Justy mutant mice is blocked due to a precursor mRNA splicing

192 that the vestibular dysfunction of the Zpld1 mutant mice is caused by loss of sensory input for rotar

193 Also, cochlear afferents of Fzd3 mutant mice lack the orderly topological organization ob

194 Lobular appendages are present in mutant mice lacking BCs, implying that although synchron

195 Moreover, mutant mice lacking both ACVR2A and ACVR2B demonstrated

196 We used mutant mice lacking efficient calcium feedback to boosts

197 We show here that mutant mice lacking otogelin or otogelin-like have a mar

198 ved in these mice have also been observed in mutant mice lacking stereocilin, a model of the DFNB16 g

199 o striatal projection neurons is weakened in mutant mice lacking the SH3 and multiple ankyrin repeat

200 nscriptomic analyses of sensory neurons from mutant mice lacking transcription factors suggest that t

201 ents in vibrotactile touch perception, as do mutant mice lacking USH2A.

202 the vascular basement membrane is reduced in mutant mice, leading to defective endothelial cell-peric

203 in rat PSC-derived kidneys in anephric Sall1 mutant mice, likely due to the poor contribution of rat

204 did not cause a malformed SAN at birth, the mutant mice manifested sinus node dysfunction.

205 fespan of most popular high copy number SOD1 mutant mice might be too short to acknowledge benefits o

206 sweat duct luminal cell differentiation, and mutant mice mimic miliaria and provide a possible animal

207 Mutant mice (miR34-KO) and loss-of-function approaches r

208 in CIPN induced by paclitaxel in WT and Tlr9 mutant mice of both sexes.

209 on MRV with the availability of innumerable mutant mice on the B6 background.

210 3A)variant in hearing studies of B6 mice and mutant mice on the B6 background.

211 erexpression of calcineurin Abeta1 in TMEM43 mutant mice or chemical GSK3beta inhibition improves car

212 tion of PU.1 in AML cells from either PU.1lo mutant mice or human patients with AML-inhibited cell gr

213 ponse gain is significantly increased in the mutant mice over littermate controls.

214 As previously reported, Pbx1 homozygous mutant mice (Pbx1-/-) develop malformations and hypoplas

215 Consistent with this possibility, GADD34 mutant mice presented with a similar ameliorated experim

216 We also find that the Ttbk2 conditional mutant mice quickly lose cilia throughout the brain.

217 RyR1 protein content in the muscles of mutant mice reached 38% and 58% of that present in total

218 Collectively, these mutant mice recapitulate many of the disease features se

219 Hyp (Phex mutant) mice recapitulate the XLH phenotype.

220 r pair into the mature cochlea of Otof (-/-) mutant mice reconstituted the otoferlin cDNA coding sequ

221 enotype data from 14,250 wildtype and 40,192 mutant mice (representing 2,186 knockout lines), analyse

222 The concomitant loss of S6K1 in Tsc1-mutant mice restores OCD but does not decrease hyperprol

223 Homozygous deletion of Ets2 in p53 mutant mice resulted in strong down-regulation of snoRNA

224 lineage cells from preclinical wild-type and mutant mice revealed that loss of myeloid STAT3 signalin

225 similar to that observed in betaIV-spectrin mutant mice, revealing that IQCJ-SCHIP1 contributes to n

226 Disruption of CD5 signalosome in mutant mice reveals that it modulates TCR signal outputs

227 by beta-cell M3Rs, since they were absent in mutant mice selectively lacking M3Rs in beta cells.

228 opathy, similarly sized lesions leak less in mutant mice, separating regulation of permeability from

229 Inner hair cells from TMIE mutant mice show altered postsynaptic alpha9alpha10 func

230 Mutant mice show lipid accumulation in the RPE, reduced

231 d as a monogenic cause of autism, and Shank3 mutant mice show repetitive grooming and social interact

232 The Abcc6(-/-)Alpl(+/-) double-mutant mice showed 52% reduction of mineralization in th

233 SCs of mutant mice showed a distorted Golgi morphology and disa

234 sociated domain (TAD(cPcdh)) in neurons from mutant mice showed abnormal accumulation of the transcri

235 Furthermore mutant mice showed alterations in acoustical parameters

236 the conduction velocity of sciatic nerves of mutant mice showed an 80% decrease, the mice displayed o

237 mIgE-ITT-mutant mice showed an impaired memory IgE response subse

238 Mutant mice showed cellular and molecular defects demons

239 Mutant mice showed deficits in the novel object recognit

240 Interestingly, female Zfpm1 mutant mice showed elevated contextual fear memory that

241 Homozygous mutant mice showed hypersusceptibility to infection by m

242 Biochemically mutant mice showed impaired electron transport chain act

243 Consequently, Lyst-mutant mice showed increased susceptibility to bacterial

244 ed that unlike sham controls, ovariectomized mutant mice showed no increase in self-administration.

245 Partial loss-of-function Fech(m1Pas) mutant mice showed reduced retinal neovascularization an

246 ion, and the myopathies in cofilin2 and CAP2 mutant mice showed striking similarities.

247 Hyperactive STAT5 mutant mice showed that the STAT5A homolog had a dominan

248 the PHP.eB-iMecp2 virus in symptomatic Mecp2 mutant mice significantly improved locomotor activity, l

249 as able to rescue the premature death in the mutant mice (Slc25a46-/-).

250 Mutant mice spontaneously developed ILD that mirrors lun

251 tory phenotype in untreated HIF-2alpha S305M mutant mice suggests a function for the HIF-2alpha PAS-B

252 The Nlrp3L351P Il1b-/- Il18-/- mutant mice survived and grew normally until adulthood a

253 As a result, TMs of the mutant mice tend to be significantly more anisotropic wi

254 the role of UVRAG(FS) in vivo, we generated mutant mice that inducibly express UVRAG(FS) (iUVRAG(FS)

255 In contrast, obese mutant mice that lacked both Galpha(q) and Galpha(11) se

256 netic regulation in the brain using H67D HFE-mutant mice that recapitulates the H63D-HFE mutation in

257 ponse to the transgene in treated male Mecp2 mutant mice that was overcome by immunosuppression.

258 In cultured primary podocytes from mutant mice, the absence of Synpo caused loss of stress

259 and proliferation compared with control Pten-mutant mice, the latter of which exhibited increased Erk

260 In mutant mice, the total brain volume was significantly re

261 bal Lamc1 gene deletion in tamoxifen-induced mutant mice, there was minimal change in total cardiac,

262 expansion and sporadic tumour initiation in mutant mice, thereby demonstrating the robust paracrine

263 In Col4a1 mutant mice, this TS was hypermuscularized, with a hyper

264 We further generated Casp2(C320S) mutant mice to demonstrate that caspase-2 catalytic acti

265 We targeted CD73 mutant mice to determine the function of CD73 expressed

266 We crossed diabetic leptin receptor-mutant mice to mice lacking CaMKIIdelta globally.

267 However, crossing the W131A mutant mice to OTII TCR transgenic mice resulted in incr

268 iments reveal how bone marrow from the V154M mutant mice transfer disease to the WT host, whereas the

269 ckout) mice and obese db/db (leptin receptor mutant) mice, two distinct mouse models requiring neithe

270 when upregulated in skeletal muscles of rmd mutant mice using a similar AAV6 vector.

271 h heterozygous and homozygous D252H and null mutant mice using behavioural and motor phenotyping alon

272 In Arx mutant mice, ventral genes, including Olig2, are ectopic

273 ment and gross morphological architecture of mutant mice was indistinguishable from wildtype (WT) lit

274 n via adeno-associated virus (AAV) into FKRP mutant mice was unable to improve dystrophic phenotypes,

275 In the current study, using Evc2/ Limbin mutant mice we recently generated, we analyzed enamel fo

276 strategies affect the phenotype of resulting mutant mice, we characterized Rhbdf1 mouse mutant strain

277 ture system for prostate development and Ret mutant mice, we demonstrate that RET-mediated GDNF signa

278 Here, using both sexes of conditional mutant mice, we discovered that SST(+) interneuron-deriv

279 Using conditional mutant mice, we found that protein prenylation is essent

280 and the spontaneous running distance of the mutant mice were 20% and 50% lower compared to wild-type

281 Purkinje cell dendrites observed within the mutant mice were alleviated.

282 gs suggest that the dental phenotypes of the mutant mice were associated with the intracellular reten

283 We found that Six1 (-/-) Six2 (-/-) double-mutant mice were born with severe craniofacial deformity

284 Clinical findings similar to those in Pbx mutant mice were observed in all patients with varying e

285 total GFAP in astrocytes from wild-type and mutant mice were similar at approximately 3-4 days.

286 opathological alterations observed in TDP-43 mutant mice were similar to some characteristic changes

287 of HFCS in adenomatous polyposis coli (APC) mutant mice, which are predisposed to develop intestinal

288 ed striatal phenotypes in heterozygous Disc1 mutant mice, which could be a promising model of DISC1 h

289 he cross-sectional area of the temporalis in mutant mice, which persisted to the weaning stage.

290 of lung inflammation were altered in Yap/Taz mutant mice, which prevented the development of a proper

291 vascular defects seen in Fgfr1/Fgfr3 double mutant mice, while HK2 overexpression partly rescues the

292 We believe that our studies based on A20 mutant mice will be helpful in understanding the pathoph

293 In Dsk5 mutant mice with a gain-of-function allele that increase

294 Similarly, treatment of TMEM43 mutant mice with a GSK3beta inhibitor improves cardiac f

295 found that reducing the microbial burden in mutant mice with broad spectrum antibiotics-as well as t

296 3G) and non-cleavable Caspase-8(D387A/D387A) mutant mice with defective caspase-8-mediated apoptosis.

297 In mutant mice with increased type I IFN receptor (IFNAR) s

298 ore, sensitization and challenge of mIgE-ITT-mutant mice with ovalbumin resulted in diminished serum

299 rmed a preventative oral treatment of Col4a1 mutant mice with the chemical chaperone phenyl butyric a

300 Treatment of mutant mice with the glucocorticoid receptor antagonist