ライフサイエンスコーパス: mutant mice

1 ration and myogenic differentiation in these mutant mice.

2 ative role in repetitive behavior of Shank3B mutant mice.

3 e to repetitive grooming behavior in Shank3B mutant mice.

4 on of the muscle atrophy and weakness in Gne mutant mice.

5 he cochlear USH2 complex assembly using USH1 mutant mice.

6 in prostate tumors of Pten/Trp53 double-null mutant mice.

7 ts as well as in muscle and liver tissues of mutant mice.

8 h is the output of the FEO, in single Period mutant mice.

9 ndritic spines in extinction-resistant S831A mutant mice.

10 kely contributing to reduced stamina of Abl2 mutant mice.

11 ntrols, which was severely attenuated in the mutant mice.

12 32 reduced vessel constriction and PH in Pbx-mutant mice.

13 including TSC2 or TSC1, in developing SCs of mutant mice.

14 ed behavior as well as autonomic function in mutant mice.

15 investigated neuroinflammation in our CHMP2B mutant mice.

16 was extended in Atg7 cKO; SOD1(G93A) double-mutant mice.

17 t in slices from GABAA receptor alpha1(H101R)mutant mice.

18 ts in the septal extracellular matrix of the mutant mice.

19 ied phenotypes, especially obesity, in these mutant mice.

20 nd epithelial proliferation in the uterus of mutant mice.

21 boosted in tumor tissues of Apc Olfm4 double-mutant mice.

22 and shortened the lifespan of the SOD1(G85R) mutant mice.

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

24 knockout and ovalbumin-sensitized filaggrin mutant mice.

25 tion stress in vivo, we used Hus1/Atm double mutant mice.

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

27 to IL-10 restored protective immunity to the mutant mice.

28 velopment of disease, when transplanted into mutant mice.

29 ay improves neurological phenotypes in Mecp2 mutant mice.

30 of Oxtr in Oxtr(-/-):Avpr1alpha(-/-) double-mutant mice.

31 e DNA to alter virtually any gene and create mutant mice.

32 ation of renal cysts and tumors in Vhl/Trp53 mutant mice.

33 greatly delayed the motor impairment in the mutant mice.

34 ifferentiation and restores these defects in mutant mice.

35 and osteoblast differentiation in Spop-null mutant mice.

36 is in neurons of the CNS using gene-targeted mutant mice.

37 ally rescued abnormal brain structure in Dvl mutant mice.

38 tion ameliorates abnormal behaviors in adult mutant mice.

39 o evidence of overt immune deficiency in HED mutant mice.

40 evel was elevated in the hippocampus of Lrp4 mutant mice.

41 led to reduced fitness in both wild-type and mutant mice.

42 ave shown severe dental defects in DSPP-null mutant mice.

43 duced CYFIP2 expression in heterozygous null mutant mice.

44 a reason for the osteopenic phenotype in the mutant mice.

45 in the renal tubules of Tsc1 and rpS6 double-mutant mice.

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

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

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

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

50 racteristics of the glomerulopathy in Col4a3 mutant mice.

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

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

53 d by the need to generate and cross germline mutant mice.

54 ior, an effect not observed in S831A phospho-mutant mice.

55 ber of dental mesenchymal stem cells in Evc2 mutant mice.

56 yonic stem cells and in Emx1-cre conditional mutant mice.

57 reduced excessive repetitive grooming in the mutant mice.

58 detect genotype differences in female Mecp2 mutant mice.

59 aled that, in vivo, the half-life of GFAP in mutant mice (15.4 +/- 0.5 days) was much shorter than th

60 pontaneous malignant tumors in 54 of 93 Bap1-mutant mice (58%) versus 4 of 43 (9%) wild-type litterma

61 t different disease stages from desmoglein 2-mutant mice, a well characterized AC model.

62 ng result was observed in male Pdx1(DeltaIV) mutant mice after 3 weeks of birth (i.e., the onset of w

63 ir bundles show morphological defects as the mutant mice age and while mechanotransduction currents c

64 that mechanontransduction is affected as the mutant mice age.

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

66 Notably, mutant mice also exhibited reduced expression of V-type

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

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

69 pharmacological beta3 inhibition in elastin mutant mice and explants attenuates aortic hypermuscular

70 itis occur at high frequency in Eda and Edar mutant mice and explore the pathogenic mechanisms relate

71 annels in Cav1.2 dihydropyridine insensitive mutant mice and found that ventral tegmental area (VTA)

72 o our knowledge, the first isolation of HLHS mutant mice and identification of genes causing HLHS.

73 n in a phosphatase and tensin homolog (Pten) mutant mice and identified 12 candidate trunk drivers an

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

75 of altered immunological tolerance unfold in mutant mice and in immunodeficient mice that received p5

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

77 ardiac vascularization was increased in some mutant mice and reduced cardiac injury in these animals.

78 derived SMCs and the aortic media of elastin mutant mice and SVAS patients have enhanced integrin bet

79 ertility based on phenotypic defects of Rhox-mutant mice and the finding that aberrant RHOX promoter

80 auditory tube glands fail to develop in HED mutant mice and the functional implications include loss

81 Ezh2 was found in CRPC tumors of Pten/Trp53 mutant mice, and expression levels of SKP2 and EZH2 were

82 -delivered fluorescent proteins, analysis of mutant mice, and two-photon microscopy, we follow long-r

83 xigenic agouti-related peptide fibers in the mutant mice appeared identical to that in control mice.

84 after peripheral nerve injury and that Celf2 mutant mice are defective in axon regeneration.

85 Primary osteoblasts from mutant mice are defective in supporting B lymphopoiesis

86 Expression data from both wild-type and mutant mice are included.

87 Aneuploid cells in these mutant mice are likely eliminated early in development t

88 Mutant mice are resistant to age- and diet-induced weigh

89 Importantly, phenotypes of OGT-SCKO and Prx mutant mice are very similar, implying that compromised

90 These mutant mice are viable and fertile and do not show any s

91 Gas2 homozygous mutant mice are viable but have severely impaired fertil

92 ropic malformations resembling those in Pbx1 mutant mice, arguing for strong conservation of gene fun

93 asal airway, and furthermore establish Rdh10 mutant mice as an important model system to study CA.

94 ng a bacteremia-derived meningitis model and mutant mice, as well as antibodies against the two recep

95 The mutant mice became persistently ketotic and tolerated th

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

97 al potential for GABA is more depolarized in mutant mice, but is restored by application of the NKCC1

98 observed malignant mesotheliomas in two Bap1-mutant mice, but not in any wild-type animals.

99 early-life (pre-puberty, CRHOEdev) in double-mutant mice (Camk2a-rtta2 x tetO-Crh) and tested their b

100 depressive-like phenotypes of GABAA receptor mutant mice can be reversed by treatment with convention

101 In desmoglein 2-mutant mice, cardiomyocyte diameters are normal during t

102 We screened mutant mice carrying hemizygous deletions of 22q11DS gen

103 ined the renal phenotype of newborn compound mutant mice carrying only one allele of Par1a or Par1b.

104 Homozygous mutant mice carrying this mutation developed renal TMA a

105 tly increased in organoids created from Cftr mutant mice compared with wild-type controls, suggesting

106 e nuclei of CA1 neurons in wild type but not mutant mice, consistent with nBMP2 playing a role in the

107 MYPT1(SM+/+) , MYPT1(SM-/-) and the knock-in mutant mice containing nonphosphorylatable MYPT1 T853A w

108 nd functional analysis of ovaries from these mutant mice (Ctnnb1(ex3)cko) showed no defects in ovaria

109 Using mutant mice deficient in the ZIP14 metal transporter, we

110 Scx-mutant mice demonstrated disrupted callus healing and as

111 Indeed, the mutant mice demonstrated increased glucose effectiveness

112 ive basket cell terminals were unaffected in mutant mice, demonstrating interneuron subtype-specific

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

114 However, Fmn2 mutant mice develop accelerated age-associated memory de

115 Female mutant mice develop endometrial hyperplasia due to aberr

116 We confirmed that TDP-43 mutant mice develop impaired motor performance, accompan

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

118 Mutant mice developed a Bartter syndrome phenotype, char

119 The adult mutant mice developed dilated hearts and showed signific

120 Mutant mice developed greater locomotor deficits in open

121 A few mutant mice developed hydrocephalus.

122 wed minor increase in bone mass, 6-month-old mutant mice developed osteoporosis, associated with an i

123 Our study confirmed that p53 mutant mice developed osteosarcomas with increased metas

124 pressor gene in the intestinal tract as Cftr mutant mice developed significantly more tumors in the c

125 However, mutant mice did have a large midline cavity originating

126 In the present study, we show that Wdr34 mutant mice die in midgestation and exhibit open brain a

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

128 On a high protein diet, mutant mice display disease exacerbation, including elev

129 Moreover, mutant mice display impaired brain-derived neurotrophic

130 In addition, mutant mice displayed defective insulin secretion and GL

131 utation (Notch2HCS), and heterozygous global mutant mice displayed gain-of-Notch2 function.

132 At 3 m of age, mutant mice displayed increased sensorimotor gating, anx

133 Furthermore, mutant mice displayed none of the behavioral alterations

134 Mutant mice displayed reduced wound angiogenesis, which

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

136 to the accepted concept that p53 homozygous mutant mice do not accumulate mutant p53 in normal cells

137 of a nonphosphorylatable rpS6 in these Tsc1-mutant mice exacerbated cystogenesis and caused drastic

138 Trim28(+/D9) mutant mice exhibit a bi-modal body-weight distribution,

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

140 The mutant mice exhibit augmented spontaneous infiltration o

141 Furthermore, Mili mutant mice exhibit behavioral deficits such as hyperact

142 Hoxb8 mutant mice exhibit compulsive grooming and hair removal

143 Pnldc1 mutant mice exhibit disrupted LINE1 retrotransposon sile

144 ch other, Bmp4(ncko/ncko)Inhba(-/-) compound mutant mice exhibit early developmental arrest of all to

145 itro, whereas hematopoietic progenitors from mutant mice exhibit normal differentiation.

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

147 Finally, we confirmed that Kir6.2 mutant mice exhibit severe memory deficits and impaired

148 In addition, betaCys93 mutant mice exhibited adaptive collateralization of card

149 Mutant mice exhibited fewer suppressive Tregs in the inj

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

151 ine cell content was extremely poor, and the mutant mice exhibited impaired glucose homeostasis.

152 DSS-challenged mutant mice exhibited increased recruitment of myeloid-d

153 significant renal structural abnormalities, mutant mice exhibited low urine osmolality at baseline a

154 Newly generated Gata3 hypomorphic mutant mice exhibited neonatal lethality associated with

155 mpared with wild-type littermates, HNF-1beta mutant mice exhibited polyuria and polydipsia.

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

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

158 Male and female mutant mice exhibited spontaneous cardiac rhythm abnorma

159 Mutant mice expressed far less Ae1 in A-ICs, but basolat

160 In familial hemiplegic migraine type 1 mutant mice expressing human mutations (R192Q and S218L)

161 Homozygous mutant mice failed to produce enamel.

162 Mutant mice had a decreased density of parvalbumin- and

163 Mutant mice had left atrial enlargement and Micu2(-/-) c

164 On postnatal day 30 (P30) mutant mice had lower SGN density compared to their wild

165 NLS mutant mice had no gross changes in immunophenotype or i

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

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

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

169 oms in human patients, we observed that Evc2 mutant mice had smaller incisors with enamel hypoplasia.

170 in muscle development in vivo by generating mutant mice harboring a skeletal muscle-specific deletio

171 Nevertheless, to date, none of the mutant mice has survived beyond weaning stage.

172 Mutant mice have alkaline urine but do not exhibit overt

173 Mutant mice have altered hematopoietic stem and progenit

174 siological and behavioral phenotypes of NRG1 mutant mice have been investigated extensively, practica

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

176 The mutant mice have gross defects in chorioallantoic branch

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

178 Foxg1(-/-) mutant mice have microphthalmic eyes with a large ventra

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

180 rthermore, in cancer-prone, heterozygous APC mutant mice, homozygous deletion of the Rad52 gene suppr

181 RNA-seq in Wiz mutant mice identified genes differentially regulated in

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

183 ell recording of synaptic responses in MeCP2 mutant mice in vivo, we show that visually driven excita

184 zure, and sudden death were detected in RQ/+ mutant mice in vivo; however, when provoked, cortical se

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

186 res of connectivity are maintained in reeler mutant mice, in which neural positioning is scrambled.

187 In this study, we generated mutant mice, in which the exocrine tissue is hypoplastic

188 ty, while deregulated MYC expression in KRAS mutant mice increases this phenotype.

189 ce of early microglial changes in our CHMP2B mutant mice indicates neuroinflammation may be a contrib

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

191 e find that the key defect in Fat4 and Dchs1 mutant mice is decreased proliferation in the early scle

192 that the strong erythroid phenotype in Ex12 mutant mice is favored by changes in iron metabolism tha

193 otype observed in the dorsal columns of Nrg1 mutant mice is related to conduction failure.

194 cess fluid after inflammation; however, Nrp2-mutant mice lacked superficial lymphatic capillaries, le

195 Moreover, mutant mice lacking both ACVR2A and ACVR2B demonstrated

196 Mutant mice lacking either protein showed a major decrea

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

198 n, we found that two different lines of Per2 mutant mice (ldc and Brdm1) anticipated restricted food

199 mE7M-B6 mutant mice lost morphine-induced receptor desensitizati

200 miR-29 expression was 2-fold higher in Bmpr2 mutant mice lungs at baseline compared with controls and

201 PlexA1 mutant mice maintain CM connections into adulthood and e

202 r in juvenile and adult mice, and that Foxp2 mutant mice may provide a tractable model system for the

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

204 NA binding and effects on gene expression in mutant mice, mouse isolated stem cells and engineered mo

205 o-olfactogram (EOG) recordings on the double-mutant mice, NCKX4(-/-);CNGB1(DeltaCaM), which are simul

206 In the gut of Ascl1(-/-) mutant mice, neurogenesis is delayed and reduced, and po

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

208 3A)variant in hearing studies of B6 mice and mutant mice on the B6 background.

209 In Satb1 mutant mice, ooDSGC dendrites lack ON arbors, and the ce

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

211 Using GR K310R mutant mice or mice containing the N-terminal truncated

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

213 These mutant mice presented with severely necrotic liver paren

214 epidermal lipids from wild-type onto Pnpla1-mutant mice promoted rebuilding of the corneocyte-bound

215 d has on the inner ear phenotype of Atp6v1b1 mutant mice provides insight into the hearing loss varia

216 rebral cortex of germ-line heterozygous Pten mutant mice (Pten(+/-)), which model macrocephaly/autism

217 Mecp2 mutant mice recapitulate many of the clinical features o

218 sociated virus 8 to the inner ear of newborn mutant mice reestablishes the expression and targeting o

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

220 3- and 24 m old hetero- and homozygous male mutant mice resulted in lower levels of Drp1 S-palmitoyl

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

222 an clocks are disabled in Period1/2/3 triple mutant mice, resulting in arrhythmic behavior in constan

223 pment, behavioural tests were carried out on mutant mice, revealing an anxiety-like phenotype.

224 hort, survival was reduced in the homozygote mutant mice, revealing strong selection against short-pe

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

226 Functionally, C3H/HeJ (TLR4 mutant) mice reversed M1 macrophage and TH1/TH17 polariz

227 On the other hand, alpha-SNAP-mutant mice show a reduction in alpha-SNAP protein level

228 We found that Hox5-mutant mice show exacerbated pathology compared with wil

229 Furthermore, MeCP2 mutant mice show reduced expression of the cation-chlori

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

231 Consequently, Gipc1 mutant mice show specific defects in axonal projections,

232 Mutant mice showed a reduction of tissue GABA in the hip

233 Adult mutant mice showed a significant reduction in spine dens

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

235 Mutant mice showed deficits in the novel object recognit

236 Biochemically mutant mice showed impaired electron transport chain act

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

238 While young mutant mice showed minor increase in bone mass, 6-month-

239 Mutant mice showed MOR transcript deletion mainly in the

240 Interestingly, the cranial sutures of the mutant mice showed normal anatomical features.

241 hat the chaperone-defective Hsp90alpha-Delta mutant mice showed similar wound closure rate as the wil

242 sheath (HERS) during root development, with mutant mice showing a high incidence of taurodontism: la

243 oreover, IHC exocytosis is also reduced with mutant mice showing lower rates of vesicle release.

244 segmentation clock and somite patterning of mutant mice suggest that LFNG protein may have context-d

245 ng motor symptoms and prolonging survival of mutant mice suggested a potential role of statins in the

246 are stabilized in the presomitic mesoderm of mutant mice, suggesting that both transcriptional and po

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

248 CD-specific HNF-1beta mutant mice survived long term and developed slowly prog

249 We found that mutant mice that cannot elevate cyclin A2 are chromosoma

250 ens stent peritonitis myocytes isolated from mutant mice that have the ryanodine receptor 2 calcium a

251 rtic stenosis (SVAS) patients and/or elastin mutant mice that model SVAS.

252 Furthermore, both male and female mutant mice that specifically lack CFAP69 in OSNs exhibi

253 Mutant mice that were heterozygous for the human allele

254 Although in Apc-Grp78 double mutant mice the Wnt signature was lost, these intestines

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

256 In these mutant mice, the organization of the basal lamina surrou

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

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

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

260 c-fos Deletion or reduction of neuro LSD1 in mutant mice translates into decreased levels of activati

261 as able to override the HF defects in Blimp1 mutant mice, underlining the close reciprocal relationsh

262 lanomas developed simultaneously in Cdk4R24C-mutant mice upon melanocyte-specific conditional activat

263 atory (wheel-running) activity in all Period mutant mice was also robust during food deprivation.

264 The added tumor burden in mutant mice was dependent on tumor necrosis factor-alpha

265 igh caloric diet, although the weight of the mutant mice was indistinguishable from wild-type litterm

266 This low bone mass in the mutant mice was secondary to a decrease in the number of

267 A colony of NLS mutant mice was successfully generated with precise knoc

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

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

270 Furthermore, in the brains of Katnal1 mutant mice we reveal numerous morphological abnormaliti

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

272 Using cardiac-specific conditional targeted mutant mice, we find that endothelial/endocardial deleti

273 Examining wild-type and RIM2 mutant mice, we show here that the sensory photoreceptor

274 Using GSK3beta Ser(389) to Ala mutant mice, we show that failure to inactivate nuclear

275 In contrast, Tsc1 single-mutant mice were all alive and had far fewer renal cysts

276 ynaptic density in wild-type and GluA1-S845A mutant mice were compared using western blot analysis.

277 Filaggrin mutant mice were generated on the proallergic BALB/c bac

278 Consequently, the mutant mice were impaired in locomotor activity and spat

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

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

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

282 singly, nerves of Schwann cell-specific Pex5 mutant mice were unaltered regarding axon numbers, axona

283 eled (ScxGFP) reporter and Scx-knockout (Scx-mutant) mice were used to assess bone morphometry and th

284 We generated KLHL41 mutant mice, which display lethal disruption of sarcomer

285 hat cochlear amplification is absent in Nptn mutant mice, which is consistent with the failure of OHC

286 teoclast impairment also occurs in Msx2 null mutant mice, which is restored by overexpression of the

287 re, administration of JH4 to LmnaG609G/G609G-mutant mice, which phenocopy human HGPS, resulted in a m

288 and elevated angiostatin levels in plasma of mutant mice, which reduced endothelial cell proliferatio

289 marrow failure occurring in DNA-PKcs(3A/3A) mutant mice, which require bone marrow transplantation (

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

291 with high efficiency to generate non-mosaic mutant mice with a high germline transmission rate.

292 tor-induced anaphylaxis was blunted in Stat3 mutant mice with AD-HIES and in wild-type mice subjected

293 calmodulin-dependent kinase II (alphaCaMKII) mutant mice with altered dendritic localization of alpha

294 Heterozygous mutant mice with deletion of hypoxia-response element in

295 Mutant mice with elevated or reduced levels of transcyto

296 ce1-null mice most closely resembled that of mutant mice with impaired ciliogenesis and/or ciliary mo

297 al common pathway in Cnp-deficient and other mutant mice with minor myelin abnormalities.

298 more, pharmacologic treatment of Tsc1 single-mutant mice with rapamycin reduced hyperphosphorylation

299 We characterized two lines of mutant mice with Shank3 mutations linked to ASD and schi

300 W131A mutant mice with wild-type T cell receptor (TCR) reperto