ライフサイエンスコーパス: knock-in mice

1 sponsible for the myopathy in the Fhl1 W122S knock-in mice.

2 235fs patient lymphoblasts, and TREX1-V235fs knock-in mice.

3 77605, crizotinib, and DN30 Fab in human HGF knock-in mice.

4 oblasts derived from pathogenic LRRK2-R1441G knock-in mice.

5 ination and subsequent Htt aggregation in HD knock-in mice.

6 sion of papillomas of TPA-treated Hras(G12V) knock-in mice.

7 (LVH), which is reproduced in Raf1(L613V/+) knock-in mice.

8 fected cells, transgenic Xenopus laevis, and knock-in mice.

9 in vivo was normal in TTT/AAA beta2 integrin knock-in mice.

10 cells derived from mice and patients, and in knock-in mice.

11 ral and neuropathological phenotypes in SCA1 knock-in mice.

12 expanded in immunoglobulin heavy chain Vh11 knock-in mice.

13 pDCs from IRAK1[D359A] x IRAK2[E525A] double knock-in mice.

14 ygous (Het) and homozygous (Hom) T4826I-RYR1 knock-in mice.

15 oid lineages in kinase-dead IKKalpha (KA/KA) knock-in mice.

16 gtin striatal cells derived from the HdhQ111 knock-in mice.

17 progenitor cell (HSPC) phenotypes of Mll-PTD knock-in mice.

18 2 throughout development using Emx1-Cre(+/+) knock-in mice.

19 by crossing APPPS1-21 mice with APOE isoform knock-in mice.

20 We have created Ptpn11(E76K) conditional knock-in mice.

21 tions on hematopoiesis and leukemogenesis in knock-in mice.

22 analyses of GluA1 S831D/S845D phosphomimetic knock-in mice.

23 ured in B cells from heterozygous TACI A144E knock-in mice.

24 ing platelets from c-Cbl KO and c-Cbl(YF/YF) knock-in mice.

25 s and in mammary glands and tumors from mp53 knock-in mice.

26 ession was monitored using Pdx1(tm1Cvw) lacZ knock-in mice.

27 uced OVA-specific B cells only in human IL-6 knock-in mice.

28 ation was significantly compromised in these knock-in mice.

29 eactive astrocytes in the striatum of HD140Q knock-in mice.

30 t increased the platelet counts in Jak2V617F knock-in mice.

31 tion with CX3CR1(GFP/WT);CCR2(RFP/WT) double knock-in mice.

32 mislocalization and cone degeneration in the knock-in mice.

33 ls, and gene-targeting for the generation of knock-in mice.

34 This effect is lost in S1928A knock-in mice.

35 cal neurons in wild-type and parvalbumin-Cre knock-in mice.

36 d ALDH2-deficient, ALDH2*1/*2, heterozygotic knock-in mice.

37 In mutp53 knock-in mice, a MDM2 isoform similar to human MDM2-B is

38 ing a Western-type diet to apolipoprotein E2 knock-in mice, a model of metabolic syndrome, produced 3

39 In Foxp3DTR knock-in mice, about 99% Treg depletion was achieved, re

40 Using IkappaBbeta knock-in mice (AKBI), in which the IkappaBalpha gene is

41 ts and melanocytes and generated a series of knock-in mice allowing forced incorporation of either al

42 s completely abolished in G6P-insensitive GS knock-in mice, although AICAR-stimulated AMPK activation

43 ML/RARalpha oncogene in cells and transgenic knock-in mice, an observation confirmed and extended by

44 nd GluN2B (also known as Grin2b) CTDs in two knock-in mice and analyzed the mice's biochemistry, syna

45 RASSF1A levels were reduced in PML/RARalpha knock-in mice and APL patient samples.

46 activity in PHTS-derived lymphoblasts, Pten knock-in mice and cell lines expressing missense and non

47 Using Vgat- and Vglut2-ires-Cre knock-in mice and ESR1 immunohistochemistry, we demonstr

48 evelopment, we generated and analyzed mutant knock-in mice and found that mice expressing a kinase-de

49 We generated CUGBP1-S302A knock-in mice and found that the reduction of translatio

50 We confirmed this finding in Mll-Af9 knock-in mice and human M4/M5 acute myeloid leukemia (AM

51 ta-enhanced green fluorescent protein (EGFP) knock-in mice and Langerin-EGFP-diphtheria toxin recepto

52 Heterozygous knock-in mice and littermate controls underwent microPET

53 We had previously generated point mutant knock-in mice and now report novel findings as a result

54 -liposome vaccine in 2F5 bnAb VHDJH and VLJL knock-in mice and rhesus macaques modified KYNU activity

55 gy deficit, we have investigated, in Hdh CAG knock-in mice and striatal cells, the hypothesis that de

56 Here we investigated astrocytes from HD140Q knock-in mice and uncovered evidence that mHtt decreases

57 H activity in striatal cells derived from HD knock-in mice and YAC128 mice.

58 Here, we constructed Pol beta R137Q knock-in mice, and found that homozygous knock-in mouse

59 e findings in vivo, we engineered DAT Val559 knock-in mice, and here we demonstrate in this model the

60 he myeloproliferative phenotypes in FLT3-ITD knock-in mice, and significantly prolonged the survival

61 Triple-mutant TNF knock-in mice are more prone than wild-type mice to deve

62 We generated heterozygous STING N153S knock-in mice as a model of SAVI.

63 Here, we establishRnaseh2b(A174T/A174T)knock-in mice as a subclinical model of disease, identif

64 ioblastoma multiforme (GBM)-prone H-Ras(12V) knock-in mice as well as in glioma cell lines and patien

65 Here, we demonstrate that, in M172 knock-in mice, basal SERT protein levels, 5-HT transport

66 alizing antibody (ficlatuzumab) in human HGF knock-in mice bearing c-MET-amplified tumors.

67 n of EPRS phosphorylation, we generated Eprs knock-in mice bearing phospho-deficient Ser999-to-Ala (S

68 In knock-in mice bearing the common human RTT missense muta

69 d by oxidation-resistant Cys42Ser PKG Ialpha knock-in mice being markedly protected from these clinic

70 GSK-3beta in constitutively active GSK-3beta knock-in mice (betaKI) significantly decreased, myocardi

71 In GAD67-GFP knock-in mice, BF cholinergic (choline acetyltransferase

72 havioral differences were accompanied in the knock-in mice by changes in medium spiny neuron intrinsi

73 ed phospholamban (PLN)-deficient S2814D(+/+) knock-in mice by crossing two colonies, S2814D(+/+) and

74 ed phospholamban (PLN)-deficient/S2814D(+/+) knock-in mice by crossing two colonies, S2814D(+/+) and

75 We generated knock-in mice carrying a single nucleotide change in exo

76 ning this approach with an allelic series of knock-in mice carrying frequent RTT-associated mutations

77 rstand the pathogenesis of BVMD we generated knock-in mice carrying the BVMD-causing mutation W93C in

78 raction in bone homeostasis, we examined the knock-in mice (Cbl(YF/YF)) in which the PI3K binding sit

79 d markedly reduced splenomegaly in Jak2V617F knock-in mice compared with placebo treatment.

80 verexpressed in BM and spleen of Jak2(V617F) knock-in mice compared with wild-type littermates.

81 is reduced in multiple cell types from T300A knock-in mice compared with WT mice.

82 1 inhibits the development of AML in Mll-Af9 knock-in mice; conversely, further reducing Runx1/Cbfbet

83 The P56S Vapb knock-in mice could be a valuable tool to gain a better

84 Dystroglycan knock-in mice (Dag1(Y890F/Y890F)) had no overt phenotype

85 Disruption of Sall1-NuRD in vivo in knock-in mice (DeltaSRM) resulted in accelerated differe

86 Significantly, the knock-in mice demonstrate accumulation of P56S VAPB prot

87 Examination of homozygous knock-in mice demonstrates significant increases in proi

88 Unlike b12 knock-in mice, described in the companion article, 4E10H

89 These knock-in mice develop aggressive tumors compared with p5

90 Here, we show that Rag2(R229Q) knock-in mice developed an inflammatory bowel disease af

91 of all Langerin(+) skin DCs in Langerin-DTR knock-in mice did not affect such responses independentl

92 RIPK1 kinase-dead knock-in mice did not exhibit any sign of inflammation,

93 myeloid cells from preleukemic PML-RARalpha knock-in mice did not show altered DNA methylation and t

94 The knock-in mice die between E9.5 and 12.5 because of defec

95 The dorsal root ganglia from the TrkAP782S knock-in mice display an increased number of neurons exp

96 Here we show that MeCP2 Ser421Ala knock-in mice display both a reduced threshold for the i

97 onsistent with the human polymorphism, T300A knock-in mice do not develop spontaneous intestinal infl

98 Cxcl12(DsRed) knock-in mice (DsRed-Express2 recombined into the Cxcl12

99 bone marrow mononuclear cells from FLT3/ITD knock-in mice, end-joining of DSBs occurs at microhomolo

100 kinase to inflammation in vivo, we generated knock-in mice endogenously expressing catalytically inac

101 In naive CD4bs, unmutated common ancestor knock-in mice Env(+)B cell clones develop anergy and par

102 Importantly, iNKT cells in hCD1d knock-in mice exert a potent antitumor function in a mel

103 Heterozygous and homozygous knock-in mice exhibited a normal phenotype.

104 The knock-in mice exhibited markedly reduced mitochondrial c

105 Previous studies showed that NL3(R451C) knock-in mice exhibited modestly impaired social behavio

106 Homozygous knock-in mice exhibited reductions in body, organ, and c

107 Livers of Nlrp3(A350V) knock-in mice exhibited severe liver inflammatory change

108 We generated Foxn1 knock-in mice expressing a C-terminal hemagglutinin-tagg

109 n protein's C-terminus in vivo, we generated knock-in mice expressing a C-terminally truncated CBFbet

110 ausal role for DeltaN-Bcl-x(L), we generated knock-in mice expressing a caspase-resistant form of Bcl

111 Knock-in mice expressing a CCN1 mutant that is unable to

112 Using knock-in mice expressing a functional enhanced green flu

113 n of nAChRs containing the alpha4 subunit in knock-in mice expressing a hypersensitive version of the

114 receptor and Galphaq KO mice, as well as in knock-in mice expressing a mutant Ala(286)-CaMKIIalpha t

115 Surprisingly, knock-in mice expressing a mutant isoform of IgSF9 lacki

116 eward properties of morphine were evident in knock-in mice expressing a phosphorylation-deficient S37

117 We found previously that knock-in mice expressing a ubiquitin-binding-defective m

118 myeloid cells and embryonic fibroblasts from knock-in mice expressing an E3 ligase-deficient mutant o

119 ispensable for dystroglycan function because knock-in mice expressing binding-deficient T190M dystrog

120 We generated knock-in mice expressing bNAb 4E10, which recognizes the

121 Here we describe two knock-in mice expressing cancer-associated Aalpha point

122 In contrast, crossing ABIN1[D485N] mice to knock-in mice expressing catalytically inactive mutants

123 Here we used knock-in mice expressing catalytically inactive prostasi

124 Here, we generated knock-in mice expressing Cre recombinase (Cre) under the

125 Knock-in mice expressing Cx50 with a PDZ-binding motif m

126 Here, we report that knock-in mice expressing either of two NS-associated mut

127 and hippocampal axonal sprouting observed in knock-in mice expressing FAD-linked PS1 mutation.

128 Using knock-in mice expressing functional fluorescent delta op

129 to VRC01-class bnAb precursors and immunized knock-in mice expressing germline-reverted VRC01 heavy c

130 Immunization experiments in knock-in mice expressing gl-VRC01 or gl-PGT121 show that

131 To solve these problems, we generated knock-in mice expressing His(6)-HA-SUMO1.

132 Here using striatal neurons derived from knock-in mice expressing mutant huntingtin (STHdhQ cells

133 Here we use knock-in mice expressing NLRC4 with a carboxy-terminal 3

134 farnesylation for B-type lamins, we created knock-in mice expressing nonfarnesylated versions of lam

135 We therefore generated knock-in mice expressing Nrp1 with a mutation of tyrosin

136 s on platelet function in vivo, we generated knock-in mice expressing talin1 mutants with impaired ca

137 s in the mPFC were probed and manipulated in knock-in mice expressing the Cre recombinase under the e

138 Echocardiographic imaging of homozygous knock-in mice expressing the cTnI-R21C mutation shows th

139 eloid cell-specific conditional mutant Nlrp3 knock-in mice expressing the D301N Nlrp3 mutation (ortho

140 pocampal neurotransmission and plasticity in knock-in mice expressing the FHM type 1 (FHM1) R192Q gai

141 ransgenic mice lacking Orai1 or STIM1 and in knock-in mice expressing the loss-of-function Orai1 muta

142 Familial hemiplegic migraine knock-in mice expressing the S218L or R192Q mutation are

143 To address this question we employed Gpx4 knock-in mice expressing the Sec46Ala-Gpx4 mutant, in wh

144 on were investigated using immune cells from knock-in mice expressing the TNFR-associated factor 6 (T

145 several CCBE1 deletion mutants by generating knock-in mice expressing these mutants, by analyzing the

146 Here we use 2 strains of genomic knock-in mice expressing tyrosine to phenylalanine mutat

147 Here, we generated knock-in mice expressing vimentin that have had the seri

148 We investigated this role by injecting "knock-in" mice expressing a phosphorylation-deficient (P

149 tes, we have generated targeted transgenic ("knock-in") mice expressing, in the physiological Ig H an

150 r drugs) technology by creating ROSA26-based knock-in mice for the conditional expression of a Gs-cou

151 ssel growth as 'redox-dead' Cys17Ser RIalpha knock-in mice fully resistant to PKA disulphide-activati

152 keletal abnormalities in NOMID, we generated knock-in mice globally expressing the D301N NLRP3 mutati

153 S436A knock-in mice had disrupted estrous cyclicity and reduce

154 Here we generated and analyzed Pten knock-in mice harboring a C2 domain missense mutation at

155 To address this issue, we created knock-in mice harboring a mutant Lmna allele (LmnanPLAO)

156 Knock-in mice harboring a mutation at the PLC-gamma1 bin

157 Furthermore, in knock-in mice harboring constitutively active eNOS, elev

158 nfection with M. smegmatis, macrophages from knock-in mice harboring R753Q TLR2 expressed lower level

159 Knock-in mice harbouring the T316A variant showed defect

160 P7) wild-type mouse pups and that transgenic knock-in mice have a higher threshold and longer latenci

161 Recent studies analyzing a variety of KO or knock-in mice have indicated that impairments in the T-c

162 These knock-in mice have NOP receptors that function both in v

163 These knock-in mice have NOP receptors that function both in v

164 imary HD neurons prepared from embryos of HD knock-in mice (HD(140Q/140Q)), which have human huntingt

165 We generated Abca4(PV/PV) knock-in mice homozygous for the complex PV allele to in

166 Here we generated knock-in mice in which a known MAPK phosphorylation site

167 ient for sterol-accelerated degradation, and knock-in mice in which endogenous HMGCR harbors mutation

168 We generated Cx43 germline knock-in mice in which serines 325/328/330 were replaced

169 l importance of the CCT domain, we generated knock-in mice in which the critical CCT domain Leu502 re

170 idermal morphogenesis we generated DeltaNp63 knock-in mice in which the DeltaNp63-specific exon is re

171 o address these issues, we engineered triple knock-in mice in which the kinase activity of three neur

172 To address these issues, we have created knock-in mice in which the pH-sensitive green fluorescen

173 forts to refine these models, we constructed knock-in mice in which the second extracellular loops of

174 We recently generated knock-in mice in which wild-type muscle GS was replaced

175 rst reports of Mecp2[R133C] and Mecp2[T158M] knock-in mice, in addition to Mecp2[R306C] mutant mice.

176 of scopolamine were assessed in BDNF Val/Met knock-in mice, in which BDNF processing and release are

177 Using RyR2(ADA/+) knock-in mice, in which half of the CaM-RyR2 binding is

178 DMBA/TPA treatment of Hras(G12V) knock-in mice induced an even greater incidence of papil

179 a majority of transcript level changes in HD knock-in mice involve alteration of the rate of mRNA pro

180 er primary neurons or striatal cells from HD knock-in mice is sufficient to disrupt the axonal transp

181 "beta3DeltaRGT" knock-in mice lack the 3 C-terminal beta3 tail residues,

182 Knock-in mice lacking critical oxidation sites in CaMKII

183 In anti-thymocyte/Thy-1 autoreactive BCR knock-in mice lacking self-Thy-1 ligand, immunoglobulin

184 We generated TARPgamma-8Delta4 knock-in mice lacking the C-terminal PDZ ligand.

185 regulatory role of this motif, we generated knock-in mice lacking the SIV domain (DeltaSIV).

186 ce, double-mutant Kit(V558Delta;Y567F/Y567F) knock-in mice lacking the SRC family kinase-binding site

187 HGPS knock-in mice (Lmna(HG/+)) develop severe progeria-like

188 rived from the selective breeding of HdhQ150 knock-in mice, manifests an accelerated and more robust

189 stigate this topic, we generated "reciprocal knock-in mice"-mice that make lamin B2 from the Lmnb1 lo

190 The homozygous knock-in mice mimic the clinical phenotypes of RP, inclu

191 hosphorylated in Atoh1's bHLH domain in vivo Knock-in mice of both sexes bearing a GFP-tagged phospho

192 fluorescent proteins in GABAergic (GAD67-GFP knock-in mice) or PV+ neurons (PV-Tomato mice) to study

193 We therefore generated Orai1 knock-in mice (Orai1(KI/KI)) expressing a nonfunctional

194 n in the synaptic vesicle cycle, we produced knock-in mice (Otof(Ala515,Ala517/Ala515,Ala517)) with l

195 atum to those in cerebellum in young Hdh CAG knock-in mice, prior to onset of evident pathological al

196 Our conditional Jak2V617F knock-in mice provide an excellent model that can be use

197 However, GAD67-EGFP knock-in mice reared under hypoxic conditions showed no

198 In PS1M146V knock-in mice, reduced InsP3R1 expression restored norma

199 ce completely lacking FMRP, mGluR-LTD in CGG knock-in mice remains dependent on new protein synthesis

200 appropriate tissues, we have generated Vapb knock-in mice replacing wild-type Vapb gene with P56S mu

201 Sustained GSK3 activity in GSK3(S/A) knock-in mice reportedly accelerates peripheral nerve re

202 We conclude that human IL-6 knock-in mice represent a novel and improved model for h

203 PP and APPsbeta in wild-type and in APPsbeta knock-in mice, respectively.

204 ate that homozygosity for human JAK2V617F in knock-in mice results in a striking phenotypic switch fr

205 photobleaching in slices from VGLUT1(Venus) knock-in mice reveal 75% of VGLUT1-containing vesicles h

206 Heterozygous green fluorescent protein (GFP)-knock-in mice revealed rapid induction of gene expressio

207 ry.In vitroandin vivoanalysis of GSK3 single knock-in mice revealed the unexpected contribution of GS

208 Because homozygous Gpx4 knock-in mice (Sec46Ala-Gpx4(+/+)) are not viable we cre

209 The studies of CBP (S436A) knock-in mice show elevated serum GH levels, a greater r

210 Heterozygous P56S Vapb knock-in mice show mild age-dependent defects in motor b

211 The homozygous P56S Vapb knock-in mice show more severe defects compared with het

212 pheral injection of fluorogold in PTH2R-lacZ knock-in mice showed that most PTH2Rs are on PVN and per

213 The SPAK CCT domain knock-in mice showed typical features of Gitelman Syndro

214 yocytic maturation is not affected in the P1 knock-in mice, suggesting that RUNX1B can regulate endom

215 with FLT3/ITD knock-in mice, the FLT3/D835Y knock-in mice survive significantly longer.

216 HCV entry factor knock-in mice take up HCV with an efficiency similar to

217 phenylarsonate reactive B cells from Ig V(H) knock-in mice (termed HKIR) were relieved in adoptively

218 recombination to create chimeric TGF-beta1/3 knock-in mice (TGF-beta1(Lbeta3/Lbeta3)).

219 ant p53 gain of function is recapitulated in knock-in mice that carry one null allele and one mutant

220 we report the development of 3 unique c-myc knock-in mice that conditionally express either c-Myc(WT

221 stablished humanized (100% human hemoglobin) knock-in mice that demonstrate a distinct fetal hemoglob

222 e of this inhibitory mechanism, we generated knock-in mice that express a Cdk6 mutant (Cdk6 R31C) ins

223 Here we generate knock-in mice that express a constitutively active form

224 ance in vivo by generating triple-mutant TNF knock-in mice that express a mutant TNF with deficient N

225 In HD knock-in mice that express full-length mutant htt at the

226 igible expression of truncated Pol iota, and knock-in mice that express full-length Pol iota that is

227 Using knock-in mice that express YFP-tagged alpha4 nAChRs subu

228 we show in muscle cells from MH-RyR1(R163C) knock-in mice that increased passive SR Ca(2+) leak caus

229 We generated knock-in mice that lack NAIP of MeCP2 and found that the

230 ells or lungs from Prdx6-null or Prdx6-D140A-knock-in mice that lack the phospholipase A2 activity (P

231 17F mutant, and in platelets from JAK2 V617F knock-in mice that were treated in vivo with JAK2 or pro

232 M cone, or S cone outcome using Nrl(b2/b2) "knock-in" mice that express TRbeta2 instead of NRL from

233 We generated 'knock-in' mice that express non-signalling CD3zeta chain

234 Compared with FLT3/ITD knock-in mice, the FLT3/D835Y knock-in mice survive sign

235 Using human hepcidin knock-in mice, the mechanism of action of the Abs was sh

236 ts role and expression pattern by generating knock-in mice; the enhanced green fluorescence protein (

237 aging in insulinoma cells and beta-cells of knock-in mice through the conditional and unequivocal la

238 We used EGFP-tagged Atoh1 knock-in mice to demonstrate for the first time that Ato

239 Here, we generated AKAP150DeltaPIX knock-in mice to selectively disrupt CaN anchoring in vi

240 Here, we used Nras(LSL-G12D); Cbfb(56M) knock-in mice to show that allelic expression of oncogen

241 uman GX (hGX)-sPLA(2) (i.e. hGX-sPLA(2)(+/+) knock-in mice) to understand more fully the role of GX-s

242 Anti-Id B cells from BCR knock-in mice, together with Id-specific CD4(+) T cells

243 More refined analyses of AKAP150 knock-in mice unable to anchor protein kinase A or prote

244 CD4 alphabeta T cells in LATY136F knock-in mice undergo uncontrolled expansion, resulting

245 tic functions of USP18 in vivo, we generated knock-in mice (USP18(C61A/C61A)) expressing enzymaticall

246 By using human prolactin knock-in mice, we demonstrate that prolactin-Stat5a/b si

247 Using mouse primary PASMCs derived from knock-in mice, we demonstrated that BMPR-II dysfunction

248 Using our newly generated CD11a-mYFP knock-in mice, we discovered that naive CD8(+) T cells r

249 Using Tbx1(Cre) knock-in mice, we found that cells are lost due to apopt

250 Here, using Scf(gfp) knock-in mice, we found that Scf was primarily expressed

251 By generating P23H opsin knock-in mice, we found that the P23H protein was inadeq

252 Using Foxp3(DTR) knock-in mice, we found that Treg-deficient mice had inc

253 Using Gli1(lacZ) knock-in mice, we identified renal interstitial fibrobla

254 In DOR-eGFP knock-in mice, we show a persistent, learning-related pl

255 hose isolated from genome edited mTOR S2159A knock-in mice, we show that mTOR S2159 phosphorylation p

256 By analyzing homozygous Rho(P23H/P23H) knock-in mice, we show that P23H opsin is transported to

257 By using conditional knock-in mice, we show that the HSC defect resulting fro

258 In this study, by using FoxP3/gfp knock-in mice, we showed that TNFR2 signaling did not in

259 is hypothesis, gain-of-function Nlrp3(A350V) knock-in mice were bred onto il17a and Tnf knockout back

260 racterize receptor location and trafficking, knock-in mice were created by inserting the gene encodin

261 A new group of knock-in mice were created that each expresses a single

262 Knock-in mice were generated by gene targeting.

263 specific for hHepc were generated, and hHepc knock-in mice were produced to enable antibody testing.

264 Knock-in mice were susceptible to passive and active ana

265 PERIOD2::LUCIFERASE-knock-in mice were used to report real-time PER2 circadi

266 rylation contributes to platelet function as knock-in mice where GSK3alpha Ser(21) and GSK3beta Ser(9

267 in the peripheral lymph nodes of transgenic knock-in mice, where the IL-15Ralpha intracellular signa

268 om young hetero- and homozygous R349P desmin knock-in mice, which carry the orthologue of the most fr

269 AOC3-knock-in mice, which express a catalytically inactive fo

270 from affected brain regions of Gfap(R236H/+) knock-in mice, which harbor a GFAP mutation homologous t

271 These hCD1d knock-in mice will allow more accurate in vivo modeling

272 E2 had no effect on progenitors from either knock-in mice with 7-aa deletion in helix 12 of ERalpha,

273 n of receptor localization, we have produced knock-in mice with a fluorescent-tagged NOP receptor in

274 n the spleen and in Peyer's patches, whereas knock-in mice with a mutagenic Pol zeta displayed a mark

275 vo and facilitated anemia treatment in hHepc knock-in mice with AI.

276 Knock-in mice with an inactivated S2814 phosphorylation

277 lear inclusion burden was similar between HD knock-in mice with and without the Snell genotype, where

278 Treatment of SBMA knock-in mice with clenbuterol, which was started at dis

279 get the JAK2(V617F) clone in humans by using knock-in mice with conditional expression of JAK2(V617F)

280 this question using conditional JAK2(V617F) knock-in mice with constitutive and inducible expression

281 Knock-in mice with constitutively phosphorylated RyR2 at

282 CE1 S-palmitoylation through the analysis of knock-in mice with cysteine-to-alanine substitution at t

283 tibility in wild-type mice versus transgenic knock-in mice with deficits in GluR1 S831 and S845 phosp

284 Further comparisons of these FLT3/D835Y knock-in mice with FLT3/ITD mice should provide an ideal

285 e (HD), we generated an allelic series of HD knock-in mice with graded levels of phenotypic severity

286 brain and peripheral tissue samples from HD knock-in mice with increasing CAG repeat lengths.

287 ted virus Cre-recombinase in adult, targeted knock-in mice with loxP sites flanking exons 11-22 of th

288 a result, IkappaBalpha(M/M), the homozygous knock-in mice with mutated kappaB enhancers in the Ikapp

289 We generated 3 knock-in mice with mutations introduced into RyR2 that r

290 Using VWF-A1 knock-in mice with mutations that enhance (I1309V) or di

291 mice or in endothelial nitric oxide synthase knock-in mice with phosphomimetic modification of Ser117

292 Adult transgenic GSK3alpha(S/A)/beta(S/A) knock-in mice with sustained GSK3 activity show markedly

293 Knock-in mice with the common human brain-derived neurot

294 We crossed RyR2(R4496C/+) knock-in mice with the newly described Cntn2-EGFP BAC tr

295 iated gene editing was used to produce Reep6 knock-in mice with the p.Leu135Pro RP-associated variant

296 We generated knock-in mice with the P72 and R72 variants and analyzed

297 In fact, compared with straight serine-73 knock-in mice with their relative reduction of 2B+ Mitf,

298 Homozygous mutant knock-in mice with this mutation (Col8a2(Q455K/Q455K)) s

299 We have now generated knock-in mice with two different point mutations in Nefl

300 ors into the hippocampal hilus of aged apoE4 knock-in mice without or with Abeta accumulation.