ライフサイエンスコーパス: mutant mouse

1 ance of CEACAM16, we created a Ceacam16-null mutant mouse.

2 ously proposed for the NMNAT2-deficient Blad mutant mouse.

3 vitro and in vivo in peripheral axons of the mutant mouse.

4 teoblast differentiation was impaired in the mutant mouse.

5 pansion, is down-regulated in the triallelic mutant mouse.

6 the colobomatous phenotype of the Foxg1(-/-) mutant mouse.

7 f severe forms of RASopathies, the KRAS(12V) mutant mouse.

8 n was lower in the Snell dwarf, a long-lived mutant mouse.

9 utation in cell cultures and in the CNS of a mutant mouse.

10 P380), while denervation was frequent in the mutant mouse.

11 ities that are not observed in either single mutant mouse.

12 as almost completely abolished in the GluN2B mutant mouse.

13 , and improved kidney function in the Arl13b mutant mouse.

14 of the cadherins is preserved in the reeler mutant mouse.

15 e we studied the survival of RGCs in the rd1 mutant mouse, a known model of early onset, autosomic re

16 d a preneoplastic stage in the patched (ptc) mutant mouse, a model for the brain tumor medulloblastom

17 In this study, we utilized a targeted mutant mouse (Abcc6(-/-)) as a model system for PXE.

18 TFK0 binding to both the wild-type and H447I mutant mouse acetylcholinesterase (mAChE) have been inve

19 we describe an N-ethyl-N-nitrosourea-induced mutant mouse, alien (aln), which has abnormal primary ci

20 The Traf3ip1 mutant mouse and cell lines will provide valuable resour

21 combination of neutralizing antibody (nAb), mutant mouse and pharmacological approaches to test the

22 Anti-hypoallergenic Cyp c 1 mutant mouse and rabbit sera were tested for their abili

23 isease by generating a novel knock-in CaV1.1 mutant mouse and use this model to investigate the cellu

24 Using the c-Cbl RING finger mutant mouse as a model of a myeloproliferative disease

25 We previously characterized the Enpp1(asj) mutant mouse as a model of generalized arterial calcific

26 Therefore we used this mutant mouse as a model to study possible developmental

27 We deep sequenced wildtype and Tbx5-mutant mouse atria, identifying 2600 novel Tbx5-depende

28 ts as visual dysfunction in the heterozygous mutant mouse, B6;C3-Opa1(Q285STOP).

29 ogenous imprinted genes in Dnmt1o and Dnmt3L mutant mouse backgrounds.

30 In addition, mGluR8 null mutant mouse behavioral phenotyping revealed an anxiety-

31 Homozygous Hpse2 mutant mouse bladders contained urine more often than di

32 evated 20-carbon (C20) LCB production in the mutant mouse brain and eye, resulting in surprising neur

33 nd turnover of Dab1 occurred normally in the mutant mouse brain and in primary cortical neurons treat

34 an autophagy marker, were also increased in mutant mouse brain as compared to wild-type mouse brain.

35 wild-type levels in the Cers2-rescued Cers1 mutant mouse brains.

36 migration was examined in a hypopmorphic C3G mutant mouse (C3G(gt)(/gt)) by using retrograde Dil labe

37 The first mutant mouse carries a single amino acid point mutation

38 otein, we have generated a novel ENU-induced mutant mouse carrying a missense mutation in the OPA3 ge

39 We have generated a novel ENU-induced mutant mouse carrying a protein-truncating nonsense muta

40 Using a Cre-LoxP approach, we generated a mutant mouse carrying a targeted deletion of Smad4 in th

41 nt, a bispecific fusion protein comprising a mutant mouse CD80 (CD80w88a) and lymphocyte activation a

42 Lineage tracing experiments in Foxc1 mutant mouse cerebella indicate that aberrant migration

43 In fact, every genetically modifiedCbp mutant mouse characterized thus far exhibits impaired lo

44 induced mutagenesis, the identification of a mutant mouse (chompB) with a block in early B cell devel

45 xpression profiling in Apc-mutant and Ctnnb1-mutant mouse colon adenomas identified candidate genes f

46 of FEN1 (Fen1(E160D/E160D)), and the second mutant mouse contains two amino acid substitutions in th

47 synthesis and secretion of various SLRPs in mutant mouse corneas.

48 We evaluated two independent nsp15 mutant mouse coronaviruses, designated N15m1 and N15m3,

49 We generated a novel mutant mouse (Dclre1c(leaky)) that develops a LS phenoty

50 Here we report on a complex A mutant mouse, defective for the Ift122 gene.

51 knockout are rescued by generating a double mutant mouse deficient for both PAP synthesis and hydrol

52 The Ttll5 mutant mouse develops slow photoreceptor degeneration wi

53 r-deficient phenotype observed in one Dfnb31 mutant mouse (Dfnb31(wi/wi)) suggest that DFNB31 may als

54 In the quakingviable (qk(v)) hypomyelination mutant mouse, diminished expression of isoforms of the s

55 Consistent with this, a Ttll5 mutant mouse displays a complete loss of RPGR glutamylat

56 However, the Ntn1 gene trap mutant mouse does not display all the phenotypes predict

57 and C) remain unknown, we generated a novel mutant mouse, dys-1A(-/-), with selective loss of dysbin

58 t for invasive tumor formation in Rb1 family mutant mouse embryo fibroblasts (MEFs).

59 Homozygous eIF2alpha mutant mouse embryo fibroblasts were resistant to the ap

60 e cullin3-based ubiquitin E3 ligase) in Sufu mutant mouse embryonic fibroblasts (MEFs) can restore th

61 Mechanistically, Tmem30a-mutant mouse embryonic fibroblasts (MEFs) exhibited dimi

62 Spry1(-/-) and Spry2(-/-) double mutant mouse embryonic fibroblasts exhibited decreased c

63 Consistent with this, a mutant mouse embryonic stem cell line with a deletion in

64 In this study, using mutant mouse embryonic stem cells completely lacking in

65 mination of Wnt pathway activities in Sestd1 mutant mouse embryonic tissue reveals disrupted PCP path

66 ded in the tooth bud mesenchyme in Osr2(-/-) mutant mouse embryos and is partially restored in the to

67 E12.5) and E13.5 Osr2(RFP/+) and Osr2(RFP/-) mutant mouse embryos and performed whole transcriptome R

68 function is confirmed by the fact that Brg1 mutant mouse embryos and RNAi knockdown cells exhibit a

69 Finally, we showed that Apaf1 mutant mouse embryos are able to complete palate fusion

70 s in tendon development were detected in the mutant mouse embryos as early as embryonic day 16.5 (E16

71 Surprisingly, Katnb1 null mutant mouse embryos display hallmarks of aberrant Sonic

72 vation-80% of Pax9(del/del);Wise(-/-) double-mutant mouse embryos exhibit rescued palatal shelf eleva

73 Hectd1 mutant mouse embryos exhibit the neural tube defect exen

74 studies showed that Robo1(-/-);2(-/-) double mutant mouse embryos have disruptions in both ventral an

75 Mutant mouse embryos lack primary cilia and, like talpid

76 Mutant mouse embryos lacking the heparan sulfotransferas

77 es invaded the floor plate of Robo1/2 double mutant mouse embryos or Slit1/2/3 triple mutants.

78 In Osr1 mutant mouse embryos, expression of Sox9 persisted in th

79 both sonic hedgehog(-/-) and in Zic2(kd/kd) mutant mouse embryos, providing further evidence that th

80 In Six3 conditional-mutant mouse embryos, specification of the neuroretina w

81 Neural derivatives of NC were lost in Foxd3 mutant mouse embryos, whereas abnormally fated NC-derive

82 ube and cardiac neural crest defects in Pax3-mutant mouse embryos.

83 y uncharacterized AVSD phenotype of Shh(-/-) mutant mouse embryos.

84 notype of Foxa1 and Foxa2 single- and double-mutant mouse embryos.

85 , we examined the location of SPN in various mutant mouse embryos.

86 , we crossed Emu-myc mice with the p53(515C) mutant mouse, encoding the mutant p53R172P protein that

87 vessel networks favor interactions with Flt1 mutant mouse endothelial cells.

88 We constructed a homozygous mutant mouse ES cell line in the Traf2 gene that is know

89 Our strategy to generate null mutant mouse ES cells is applicable to thousands of gene

90 The HeCo mutant mouse exhibits subcortical band heterotopia (SBH)

91 Remarkably, the Pals1 mutant mouse exhibits the critical features of LCA such

92 Electroretinography showed mutant mouse eyes had a selective loss of the b-wave ind

93 Histological analysis of mutant mouse eyes showed protein extravasation from dila

94 ing the dominant-negative MyoVa neurological mutant mouse Flailer, we find that MyoVa plays an essent

95 eration of an analog-sensitive kinase allele mutant mouse for GSK3beta, we show that the beta isoform

96 use lines expressing wildtype (WT) and L151F mutant mouse GCAP1 with or without a C-terminal GFP fusi

97 We previously created a knock-in mutant mouse harboring a dominantly negative mutant thyr

98 This mutant mouse harbors a dominant-negative mutated thyroid

99 Importantly, each mutant mouse has a distinct phenotype, suggesting divers

100 The Jimpy mutant mouse has a point mutation in the proteolipid pro

101 Increased glucose entry in the gamma2 mutant mouse hearts was directed through the remodeled m

102 Analysis of a heterozygous mutant mouse in which the NF-kappaB-dependent IkappaB al

103 r 2 (eEF2), we generated an eEF2 Gly(717)Arg mutant mouse, in which the first step of diphthamide bio

104 trast, phenotypes in the retina of the DSCAM mutant mouse indicate that DSCAM functions in both self-

105 ury, protamine sulfate perfusion of the Cfl1 mutant mouse induced a broadened and flattened foot proc

106 The Purkinje cell degeneration (pcd) mutant mouse is characterized by mutations in Nna1, a ge

107 ar development by generating a conditionally mutant mouse lacking endothelial p120 and determining th

108 Using a loss-of-function mutant mouse lacking the guanylate kinase domain of PSD-

109 A complementary mutant mouse lacking the transactivation function AF-2 o

110 A new mutant mouse (lamb1t) exhibits intermittent dystonic hin

111 on in humans and in retinal degeneration rd7 mutant mouse leads to increased S-cones accompanied by r

112 We screened an ethyl nitrosourea mutant mouse library for IMPase gene (Impa) mutations an

113 Like talpid(3) chicken limbs, the mutant mouse limbs are syndactylous with uneven digit sp

114 In this report, we describe the mutant mouse line 20884, generated by N-ethyl-N-nitrosou

115 racterized the in vivo roles of Rex1 using a mutant mouse line disrupting its transcription.

116 ing carcinogenesis in vivo, we subjected the mutant mouse line Dsk5, in which the intrinsic activatio

117 The flatiron (ffe) mutant mouse line harbors a hypomorphic mutation in Fpn1

118 nt study, this prediction was tested using a mutant mouse line lacking this potential imprinting cont

119 servations indicate that our novel profilin1 mutant mouse line may provide a new ALS model with the o

120 mice from the N-ethyl-N-nitrosourea-induced mutant mouse line nur5 display tremor and an abnormal ga

121 To evaluate this possibility, a Traf3ip1 mutant mouse line was generated.

122 Here, we studied a novel mutant mouse line, in which the projections from the bra

123 hat co-segregated with cleft palate in a new mutant mouse line.

124 either DAT- or D1R-expressing neurons in our mutant mouse lines by colocalization studies.

125 Founders of the mutant mouse lines developed DCM with severe heart failu

126 icance of 5-HT(2C)R mRNA editing, we derived mutant mouse lines harboring a knock-in INI or VGV allel

127 b portal provide access to information about mutant mouse lines held as live or cryopreserved stocks

128 We generated four novel mutant mouse lines in which BDNF production from one of

129 li and relapse behavior using four inducible mutant mouse lines lacking the glutamate receptor genes

130 These two mutant mouse lines provide useful animal models for furt

131 Screening of multiple mutant mouse lines revealed that haploinsufficiency of D

132 a subunit expression is perturbed, we used 4 mutant mouse lines that each lack a specific beta subuni

133 We used retinal mutant mouse lines that lack (i) the ipRGCs, (ii) the ph

134 ovide a framework for the development of new mutant mouse lines that mimic human polymorphisms.

135 Here we show the results of screening 810 mutant mouse lines using an in vivo assay to identify mi

136 rformed a forward genetic screen to identify mutant mouse lines with heritable CHD.

137 Analysis of several induced mutant mouse lines with ocular disease phenotypes reveal

138 hyperbilirubinemia in two independent Atp11c mutant mouse lines, and find that it originates from an

139 ight control in vivo, we generated two novel mutant mouse lines, including a constitutive NEGR1-defic

140 Analysis of several Isl1 mutant mouse lines, including animals harboring an SAN-s

141 Here, we have characterized two mutant mouse lines, one lacking calcium and integrin-bin

142 e the prevalence of this mutation in induced mutant mouse lines, vendor C57BL/6 mice and in widely us

143 In analyzing axon regeneration in different mutant mouse lines, we discovered that deletion of suppr

144 mitochondrial transport was affected in both mutant mouse lines.

145 ection (FS) LacZ staining in 313 unique KOMP mutant mouse lines.

146 These mutant mouse lungs display severe hypoplasia, dilation o

147 his present study, we have generated an Mdm2 mutant mouse (Mdm2(Y393F)) to determine whether c-Abl ph

148 In this study, an Mecp2 truncation mutant mouse (Mecp2(308)) with social behavioral defects

149 ase phenotype, we generated an inducible Atm mutant mouse model (Atm(tm1Mmpl/tm1Mmpl), referred to as

150 Using a mutant mouse model (Beethoven) for progressive hearing l

151 We generated a PLN-deficient, RyR2-mutant mouse model (PLN-/-/RyR2-R4496C+/-) by crossbreed

152 Herein we utilized both our Kras/p53 mutant mouse model and human lung cancer cell lines to d

153 imary myoblasts and fibroblasts from an FKRP mutant mouse model and that this enhancement is abrogate

154 particular, astrocytes derived from the SOD1 mutant mouse model of ALS or from human familial or spor

155 tor neurons from cell death in the G93A-SOD1 mutant mouse model of amyotrophic lateral sclerosis (ALS

156 Here, we utilized the Shank3B mutant mouse model of autism to investigate how Shank3 m

157 ng a monoclonal anti-IL6 antibody in a K-ras-mutant mouse model of lung cancer in the absence or pres

158 Here we present a mutant mouse model of OCCC.

159 drug-targeting efficacy in a transgenic p53-mutant mouse model of pancreatic cancer.

160 In a conditional Tp53;Rb1 mutant mouse model of SCLC, we now demonstrate a require

161 In this study we show that in the filaggrin mutant mouse model of spontaneous AD, IL-17RA deficiency

162 Identified was a unique mutant mouse model that develops in utero megabladder, r

163 The I-A(12%) mutant mouse model we describe in the present study is a

164 ors (an mGluR5 NAM and PAM) for TSC, using a mutant mouse model with neuronal loss of Tsc2 that demon

165 t of the target genes are also affected in a mutant mouse model with reduced levels of PEG3 protein.

166 Here we report the first Jbts17 mutant mouse model, Heart Under Glass (Hug), recovered f

167 ome 8, as exemplified by the Fused Toes (Ft) mutant mouse model, results in severely decreased number

168 the NUP98-HOXD13 (NHD13) mouse and the RUNX1 mutant mouse model.

169 SCs) isolated from mammary tumors of a Brca1-mutant mouse model.

170 es were made possible by recovery of a Wdpcp mutant mouse model.

171 d survival caused by elevated cGMP in a PDE6 mutant mouse model.

172 he CHD2 in mammals, we have generated a Chd2 mutant mouse model.

173 e was reported for a prostate specific Fgfr2 mutant mouse model.

174 on factor in development of this region in a mutant mouse model.

175 of co-expressed WT-hSOD1 in two established mutant mouse models (L126Z and G37R), and a new model th

176 an extensive morphometric study of two Mecp2-mutant mouse models (Mecp2B and Mecp2J) of RTT.

177 dimensional IHBD structure using a series of mutant mouse models and a resin casting method.

178 As we discuss here, mutant mouse models and clinical evidence indicate that

179 pendent increase in gene expression in MeCP2 mutant mouse models and human RTT brains.

180 ctivity and renal cystic disease in two Pkd1-mutant mouse models at different stages of the disease.

181 -resolution study of normal, transgenic, and mutant mouse models at embryonic and neonatal stages.

182 evious work using viral gene therapy on PDE6-mutant mouse models demonstrated photoreceptors can be r

183 Using mutant mouse models for the most common form of congenit

184 Using mutant mouse models for the most common form of congenit

185 The study of human genetic disorders and mutant mouse models has provided evidence that genome ma

186 Availability of multiple lines of Cx-mutant mouse models has provided some insight into the p

187 Further, we examine how p53 mutant mouse models have been used to test the efficacy

188 Mutant mouse models have identified Fbxo11, Evi1, Tgif1,

189 vivo, and this effect could be replicated in mutant mouse models lacking TNF receptor (TNFRI(-/-)) an

190 ges not observed previously in other genetic mutant mouse models of co-morbid cognitive and autistic-

191 Previous studies in myelin-mutant mouse models of the inherited and incurable nerve

192 Ins2 mutant mouse models provided important insights into the

193 This collection of mutant mouse models provides a resource for further stud

194 As existing JS/MKS mutant mouse models suggest apparently contradictory hyp

195 lyzed KrasG12D;Cyp19-Cre and KrasG12;Pgr-Cre mutant mouse models that express Cre prior to or after t

196 Here, we used Pkd1 mutant mouse models to demonstrate that the nicotinamide

197 rometry was applied to tissues from targeted mutant mouse models to explore the collagen substrate sp

198 Here, we leveraged a cohort of 13 lncRNAnull mutant mouse models to investigate the spatiotemporal ex

199 f fertility, with the production of over 400 mutant mouse models with a reproductive phenotype and wi

200 for CNV formation by generating a series of mutant mouse models with induced conditional deletion of

201 The present study generated 3 mutant mouse models with truncated C termini in 2 differ

202 Our present studies, employing a number of mutant mouse models, identify diacylglycerol acyltransfe

203 ngs in wild type, transgenic and combination mutant mouse models, suggesting either activity-dependen

204 extensive phenotypic overlap with our Foxc1 mutant mouse models, validating our DWM models and demon

205 By targeting molecules in pfGCs with several mutant mouse models, we demonstrate that the somatic pfG

206 h additional Rptor, Rictor, and Rptor/Rictor mutant mouse models, we identify mechanistic target of r

207 Using Col4a1 and Col4a2 mutant mouse models, we investigated the genetic complex

208 uman phenotype can be recapitulated in Cwc27 mutant mouse models, with significant embryonic lethalit

209 nses were defined and verified using various mutant mouse models.

210 lstrom syndrome, as well as in several cilia mutant mouse models.

211 r development in vivo, we generated specific mutant mouse models.

212 t in infertility and predisposes to tumor in mutant mouse models.

213 widely adopted to generate a large number of mutant mouse models.

214 Micro-CT analysis of Enpp1 mutant mouse molars revealed 4-fold increased acellular

215 We generated a targeted mutant mouse, nBmp2NLS(tm), in which the nuclear localiz

216 n MHC-II, we established a novel ENU-induced mutant mouse on the C57BL/6 background, named I-A(12%),

217 Loss of full-length RIM2alpha in a RIM2alpha mutant mouse only marginally perturbs photoreceptor syna

218 The Glis3(zf/zf) mutant mouse pancreas shows a dramatic loss of beta and

219 ly restore islet development in Neurog3-null mutant mouse pancreata.

220 scribe mask: a recessive, chemically induced mutant mouse phenotype, characterized by progressive los

221 from analyses of ABL structure-function, ABL mutant mouse phenotypes, and ABL substrates suggest that

222 Pit-1 and increased Lef-1 expression in the mutant mouse pituitary, consistent with the repression o

223 fibroblasts from the long-lived Snell dwarf mutant mouse, previously shown to be resistant to many t

224 Repro22 is a mutant mouse produced via N-ethyl-N-nitrosourea-induced

225 NAC treatment decreased ROS levels in Nkx3.1 mutant mouse prostates, it failed to reduce prostatic ep

226 The Lmna(Dhe/+) mutant mouse provides a novel model of human OM and lami

227 We show that PHD mutant mouse Rag2 proteins that correspond to those foun

228 Using the Cep290 mutant mouse rd16 (retinal degeneration 16), we show tha

229 EGFP reporter mice are available through the Mutant Mouse Regional Resource Center (NINDS/GENSAT coll

230 hrough c-MYC in embryonic and postnatal Pkd1-mutant mouse renal epithelial cells and tissues and coul

231 We found that Brd4 was upregulated in Pkd1 mutant mouse renal epithelial cells and tissues.

232 their therapeutic potential in the FKRPP448L-mutant mouse representing moderate limb-girdle muscular

233 The mutant mouse represents a valuable model to further eluc

234 The Dscam mutant mouse retina also exhibits excess numbers of thes

235 iliary neurotrophic factor (CNTF) in the rds mutant mouse retina.

236 increase in long-chain fatty acids in BMPR2 mutant mouse RVs compared with controls, which correlate

237 e shown that a phosphorylation defective RyR mutant mouse (RyRS2808A) does not respond normally to sy

238 We find that the homozygous nervous (nr) mutant mouse's 10-fold-increased cerebellar tissue plasm

239 sion of Cdk2ap1 or a nonphosphorylatable pRb mutant (mouse Ser(788) --> Ala), suggesting that the CDK

240 The new mutant mouse shaking (shk) differs from other "myelin mu

241 milarities to a previously identified ZAP-70 mutant mouse, SKG, which harbors a distinct hypomorphic

242 About 20%-30% of Hras mutant mouse skin carcinomas induced by chemical initiat

243 A mutant mouse, spasmodic, that has a startle phenotype, h

244 The glycine receptor-deficient mutant mouse spastic carries a full-length long interspe

245 tion, and thus used the serine racemase-null mutant mouse (SR(-/-)), which has less than 10% of norma

246 We generated a mutant mouse strain carrying an F832A mutation in Rb1 th

247 ed a forward genetics approach to identify a mutant mouse strain characterized by the absence of CNS

248 This mutant mouse strain provides a unique model to further e

249 We show that a CRD-BP mutant mouse strain retains expression of the shorter tr

250 er (EOC) in vivo We used the Pten/Kras(G12D)-mutant mouse strain that develops serous EOC with 100% p

251 Surprisingly, our studies of a knock-in mutant mouse strain that expresses a stabilized and tran

252 We generated a mutant mouse strain that lacks exons 13-20 of L3mbtl1.

253 in individual hippocampi from the mast cell mutant mouse strain, C57BL/6 Kit(W-sh/W-sh).

254 Here we describe a novel mutant mouse strain, Goldenticket (Gt), that fails to pr

255 A conditional mutant mouse strain, in which Pitx2 function is inactiva

256 Mutant mouse strains deficient in RGS7 or -11 were chara

257 Compared with wild-type mice, 2 FHM1 mutant mouse strains developed earlier onset of anoxic d

258 Studies of mutant mouse strains have revealed that each family memb

259 Mutant mouse strains in 60 different GPCRs were generate

260 The fast accumulation of mutant mouse strains in recent years has provided an inv

261 Mutant mouse strains with "autistic-like" phenotypes (Fm

262 e-driven breast tumorigenesis in a series of mutant mouse strains with specific DDR deficiencies to r

263 small intestinal phenotype found in most Apc-mutant mouse strains, this strain has been designated th

264 ked compositional differences between WT and mutant mouse strains.

265 ele of Dscam to use alongside existing Dscam mutant mouse strains.

266 ating glucose metabolism and fat mass in two mutant mouse strains.

267 blood vessel morphogenesis has emerged from mutant mouse studies.

268 On the basis of our mutant mouse study, we suggest that PCP pathway mutation

269 We have also investigated a spontaneous mutant mouse that expresses a truncated MAP7 and found a

270 Here we characterize a Col6a3 mutant mouse that expresses a very low level of a non-fu

271 r, previous genetic studies employed an RGS7 mutant mouse that is hypomorphic, and hence the exact ro

272 Here, we have described a mutant mouse that spontaneously develops pruritic dermat

273 ical development suggest that, in the reeler mutant mouse, the lack of the protein Reelin results in

274 In the nervous (nr) mutant mouse, the majority of PNs die in the fourth to f

275 We generated a Tim-1-mutant mouse (Tim-1(Deltamucin)) in which the mucin doma

276 erapeutic, converted the mild C3 GN of an fH-mutant mouse to a lethal C3 GN with features of human de

277 We used a genetic model of PAH, the Bmpr2 mutant mouse, to study the role of BM-derived circulatin

278 We used a thyroid hormone receptor (TR) beta mutant mouse (TRbetaPV) to establish the relevance of th

279 The histopathologic features of the triple-mutant mouse tumors closely resembled that of human SCLC

280 experiments further showed that Rb/p53/p130-mutant mouse tumors were similar to human SCLC.

281 In 2008, another ERbeta mutant mouse was generated by deleting ERbeta exon 3 whi

282 A mutant mouse was generated in which the arylhydrocarbon

283 Using the ciliopathic Fuz mutant mouse, we find that high arched palate does not,

284 nsgenic gene replacement strategy in a Pitx1 mutant mouse, we have uncoupled two discrete functions o

285 ically older archicortex of the adult reeler mutant mouse, we studied the expression of 11 different

286 RGS11 protein remained unchanged in the RGS7 mutant mouse, where a truncated RGS7 protein was express

287 unit expression were decreased in the Dicer1 mutant mouse, whereas proopiomelanocortin and luteinizin

288 e from a previously reported Orai1 gene-trap mutant mouse which may be a hypomorph rather than a true

289 between the HAS2 knockout mouse and the hdf mutant mouse, which has a mutation in the versican gene,

290 Langton et al. take advantage of the Edaradd mutant mouse, which lacks hair follicles on its tail.

291 Studies of the Wld(s) mutant mouse, which undergoes delayed Wallerian degenera

292 our investigation, we used the Smad1/5(CKO) mutant mouse, whose disorganized growth plate is due to

293 edicts a shift in simple spike activity in a mutant mouse with a brainstem specific mutation.

294 n et al. have identified and characterized a mutant mouse with a dominantly inherited axonal neuropat

295 S) binding protein for pregabalin in vivo, a mutant mouse with an arginine-to-alanine mutation at ami

296 n mu opioid analgesic action, we generated a mutant mouse with brain neuron-specific reductions in P4

297 king a forward genetic screen, we isolated a mutant mouse with defects in interneuron migration.

298 ssess the function of ANKRD26, we prepared a mutant mouse with partial inactivation of the Ankrd26 ge

299 ounds with strong efficacy in a B-Raf(V600E) mutant mouse xenograft model.

300 e scaffolding function, we generated a zap70 mutant mouse (YYAA mouse) with Y315 and Y319 both mutate