ライフサイエンスコーパス: knock-in mice

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

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

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

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

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

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

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

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

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

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

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

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

13 liorates Purkinje cell degeneration in SCA17 knock-in mice.

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

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

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

17 235fs patient lymphoblasts, and TREX1-V235fs knock-in mice.

18 ent increased survival relative to wild-type knock-in mice.

19 77605, crizotinib, and DN30 Fab in human HGF knock-in mice.

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

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

22 tor dysfunction in UQCRC1 p.Tyr314Ser mutant knock-in mice.

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

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

25 lation and elicit behavioral changes in SOUL knock-in mice.

26 bility of the expanded CAG repeat in Htt CAG knock-in mice.

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

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

29 Ddr2 during tooth formation using Ddr2-LacZ knock-in mice.

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

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

32 peared to be reduced during periodontitis in knock-in mice.

33 variants and in cells derived from P387-TSP4 knock-in mice.

34 he NSC's physiological role in corresponding knock-in mice.

35 ailure, all of which were inhibited in SERCA knock-in mice.

36 , we generated phospho-deficient GluA2 Y876F knock-in mice.

37 d serum ceramide levels in Cln3 (Deltaex7/8) knock-in mice.

38 ing human fecal transfers into ATG16L1 T300A knock-in mice.

39 CRF(2)(-/-), and MC-deficient Kit(W-sh/W-sh) knock-in mice.

40 ased Th17 cells selectively in ATG16L1 T300A knock-in mice.

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

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

43 In Npm1c/Dnmt3a mutant knock-in mice, a model of AML development, leukemia is p

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

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

46 of genetic cooperativity in the brain of HD knock-in mice (allelic series of Hdh mice).

47 Osteoclasts from the knock-in mice also showed reduced Src activity.

48 er validate these results, we also used Q175 knock-in mice, an animal model of Huntington's disease i

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

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

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

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

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

54 llenged wild-type mice but not in Nlrp3L351P knock-in mice and ex vivo-stimulated mutant macrophages.

55 Moreover, we generated cks2(cks1/cks1) knock-in mice and found that CKS1 can compensate for CKS

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

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

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

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

60 ated from "redox dead" (Cys17Ser) PKARIalpha knock-in mice and their wild-type littermates.

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

62 ing HIV-1 antibodies in human bnAb precursor knock-in mice and wild-type macaques vaccinated with imm

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

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

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

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

67 igher (+)-PHNO binding in both humans and in knock-in mice, and this effect was restricted to D3 sele

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

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

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

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

72 hodopsin level in the retinae of Rho(P23H/+) knock-in mice at 1 month of age.

73 In myocytes from SERCA knock-in mice, basal SERCA activity and SR calcium conte

74 Knock-in mice bearing a mutation of MET caspase cleavage

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

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

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

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

79 CHIP-S20E knock-in mice better clear ubiquitinated proteins and ar

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

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

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

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

84 To test this, we generated knock in mice carrying a mutation (Bmp7(R-GFlag)) that p

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

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

87 We showed that knock-in mice carrying N88K, a prevalent CMS mutation of

88 we generated and characterized heterozygous knock-in mice carrying the human R100W-mutated allele (N

89 To assess the function of CCN1 in vivo, knock-in mice carrying the integrin alpha6beta1-binding-

90 Knock-In mice carrying the SJ1 patient mutation (SJ1(RQ)

91 sed in lesions of ApoE(-) (/) (-) /P387-TSP4 knock-in mice compared to ApoE(-) (/) (-) mice.

92 oclast number were significantly elevated in knock-in mice compared with wild-type mice.

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

94 1 inhibits the development of AML in Mll-Af9 knock-in mice; conversely, further reducing Runx1/Cbfbet

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

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

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

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

99 Heterozygous and homozygous R405W-desmin knock-in mice develop both a myopathy and a cardiomyopat

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

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

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

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

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

105 Female TDP-43(Q331K) knock-in mice displayed increased weight relative to wil

106 Adult heterozygous knock-in mice displayed smaller neuromuscular endplates

107 expression, either by siRNA or from the R47H knock-in mice, displayed a similar phenotype.

108 lts indicate that while female TDP-43(Q331K) knock-in mice do display progressive behavioural phenoty

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

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

111 Here, R1441C and G2019S knock-in mice enabled thorough evaluation of dendritic s

112 y sequences elicited in human bnAb precursor knock-in mice encoded functional improbable mutations cr

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

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

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

116 Y. pestis-infected Mefv(M680I/M680I) FMF knock-in mice exhibited IL-1-dependent increased surviva

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

118 Compared with Raptor(+/+) mice, Raptor(D/D) knock-in mice exhibited smaller livers and hearts, and a

119 The knock-in mice express low levels of the resulting trunca

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

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

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

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

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

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

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

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

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

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

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

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

132 Mice with myeloid-specific Ccn1 deletion and knock-in mice expressing CCN1 unable to bind alpha(v)bet

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

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

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

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

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

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

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

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

141 We further show that knock-in mice expressing pV1 sensed heat normally but su

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

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

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

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

146 avage by hydroxylamine, and macrophages from knock-in mice expressing the E3 ligase-inactive HOIL-1[C

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

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

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

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

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

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

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

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

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

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

157 lication of a similar strategy to Nl3(R451C) knock-in mice (genetic cue) also caused successful recov

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

159 Here we report that knock-in mice harboring a cysteine-to-alanine substituti

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

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

162 further generated and analyzed R405W-desmin knock-in mice harboring the orthologous form of the huma

163 Knock-in mice harbouring the T316A variant showed defect

164 Moreover, whereas heterozygous knock-in mice have a normal life span, homozygous animal

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

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

167 rease Trem2 expression, and in parallel from knock-in mice heterozygous or homozygous for the Trem2 R

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

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

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

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

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

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

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

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

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

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

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

179 sess learning and memory in homozygous Kv7.2 knock-in mice, Kv7.2(S559A), which show reduced M-curren

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

181 Knock-in mice lacking critical oxidation sites in CaMKII

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

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

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

185 g mutant presenilin 1 (PS1) or PS1(M146V/+) "knock-in" mice leads to a complete rescue of deficits in

186 In ApoE(-) (/-) /P387-TSP4 knock-in mice, lesions size measured by Oil Red O did no

187 nes (ISGs), we hypothesized that STING N153S knock-in mice may develop more severe autoinflammatory d

188 her studies of male and female TDP-43(Q331K) knock-in mice may help to unravel the mechanisms underly

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 In knock-in mice, Msx2 gene was replaced by n-LacZ gene enc

192 In SCA17 knock-in mice, mutant TBP inhibits SP1-mediated gene tra

193 Wild-type (WT) and mutated TrkB knock-in mice (Ntrk2tm1Ddg/J) with impaired BDNF signali

194 ecapitulated in the hearts from R405W-desmin knock-in mice of both genotypes.

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

196 teraction in bone remodeling, we created OPG knock-in mice (opg (AAA) ).

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

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

199 In mouse studies, phospholemman knock-in mice (PLM(3SA); phospholemman [FXYD1] in which

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

201 Foxf1(WT/S52F) knock-in mice recapitulated histopathologic findings in

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

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

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

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

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

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

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

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

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

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

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

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

214 For example, S180A knock-in mice showed markedly reduced spontaneous tumori

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

216 ed and survival of heterozygote Tsc2(S1365A) knock-in mice subjected to the same stress is improved b

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

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

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

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

221 nsive wild-type mice, but not C42S PKG1alpha knock-in mice that are resistant to disulfide activation

222 elicited antibody responses in macaques and knock-in mice that exhibited the mutational patterns, st

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

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

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

226 Homozygous knock-in mice that express a phosphorylation-silencing m

227 Here we show that knock-in mice that express catalytically inactive caspas

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

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

230 ruses, we generated heterozygous STAT1 R274W knock-in mice that have a frequently reported STAT1 muta

231 We previously generated STING N153S knock-in mice that have a human disease-associated gain-

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

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

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

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

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

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

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

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

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

241 Here, we use Cbfb-MYH11 knock-in mice to show that IL1RL1 is expressed by cell p

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

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

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

245 The blood pressure of wild-type and C42S knock-in mice was assessed using implanted telemetry pro

246 The prevailing phenotype of Trem2 R47H knock-in mice was decreased expression levels of Trem2 i

247 Using knock-in mice, we also find that induced expression of D

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

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

250 Using sorted B cells from V(H)B1-8 knock-in mice, we evaluated B-1b, marginal zone, and fol

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

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

253 In bnAb precursor knock-in mice, we isolated a vaccine-elicited monoclonal

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

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

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

261 HSC-specific Nlrp3(L351P) knock-in mice were generated by crossing transgenic mice

262 ed in a child with this disorder, and Grin2a knock-in mice were generated to model and extend underst

263 ivo, new phosphorylation-deficient p53-S180A knock-in mice were generated.

264 f C674 oxidation on apoptosis in vivo, SERCA knock-in mice were subjected to chronic ascending aortic

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

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

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

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

269 ed in tumors grown in the Ifnar1(S526A) (SA) knock-in mice, which are deficient in IFNAR1 downregulat

270 ed glutamatergic transmission in FDD and FBD knock-in mice, which carry pathogenic FDD and FBD mutati

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

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

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

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

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

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

277 In humans and knock-in mice with a loss of function BDNF SNP (Val66Met

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

279 confirmed cognitive deficits in Atxn1154Q/2Q knock-in mice with brain-wide expression of mutant ATXN1

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

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

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

283 To this end, we generated knock-in mice with Cre-conditional expression of a cytid

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

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

286 Using knock-in mice with disrupted ZBP1 nucleic acid-binding a

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

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

289 e the dramatically different manifestations, knock-in mice with human HD-AIP missense mutations c.500

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

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

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

293 ouse model obtained by crossing JAK2V617F/WT knock-in mice with PF4iCre transgenic mice.

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

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

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

297 ecific S-35 riboprobe were carried out in 30 knock-in mice with the FAAH C385A polymorphism (20/30 AC

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

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.