ライフサイエンスコーパス: null mice

1 d on OL progenitor cells purified from Thap1 null mice.

2 reviously reported for Rnaseh2b- or Rnaseh2c-null mice.

3 le acid metabolism was also evident in Gpat3-null mice.

4 tion compensates for PKMzeta loss in PKMzeta-null mice.

5 ol6a2Deltaex5 mice than in gamma-sarcoglycan-null mice.

6 -type C57BL/6 mice, cIAP2-null mice, or XIAP-null mice.

7 nt or at the onset of RTT phenotype in Mecp2-null mice.

8 eletal muscle pathology in gamma-sarcoglycan-null mice.

9 btained from the developing calvaria of DSPP-null mice.

10 ge was seen among matrix metalloproteinase-8 null mice.

11 rginally higher compared with Akita and Ncf1 null mice.

12 ntagonist reduced ileal inflammation in SHIP-null mice.

13 ent, that were significantly induced in PGRN null mice.

14 esis, we crossed DYT1 knock-in with p58(IPK)-null mice.

15 of seminal vesicle epithelial cells in Pten-null mice.

16 ne opsins, features resembling those of Rpgr-null mice.

17 NOD/SCID/interleukin 2 receptor gamma chain null mice.

18 ull Sgta ablation in vivo using Cre-lox Sgta-null mice.

19 ntly increases in LTP maintenance in PKMzeta-null mice.

20 esicle-associated membrane protein 8 (VAMP8) null mice.

21 rescues disorganized growth plates of PTHrP-null mice.

22 investigated the cardiac phenotype of Scn2b null mice.

23 neration and juvenile lethality seen in Fig4 null mice.

24 but these effects were not observed in Fgf21-null mice.

25 econstitute the vascular dysfunction in CD36-null mice.

26 nt atrial fibrillation and hearts of decorin null mice.

27 ly prolonged lifespan compared with globally null mice.

28 le pathology compared with gamma-sarcoglycan-null mice.

29 as having the highest fold increase in MMP-9 null mice.

30 nd guidance, and mRNA expression in Munc18-1-null mice.

31 rm Western diet-fed wild type (WT) and Plin2-null mice.

32 ry are maintained without PKMzeta in PKMzeta-null mice.

33 veral of which also became depleted in Mecp2-null mice.

34 l and adrenal-specific scavenger receptor BI null mice.

35 MMP-1 and tissue inhibitor of MMP-4 in P2Y4-null mice.

36 d GABA transmission are decreased in calcyon null mice.

37 e than embryonic lethal phenotypes of Pofut2-null mice.

38 C development that occurred in otherwise FXR-null mice.

39 ation and vessel loss by using specific Dp71-null mice.

40 lar (CB) cells were nearly absent from Prdm8-null mice.

41 ently lost with disease progression in Mecp2-null mice.

42 -10 in nerve injury was assessed using IL-10-null mice.

43 ce but are profoundly impaired in BK channel-null mice.

44 of Whsc1 prevented tumor progression in PTEN-null mice.

45 PPARgamma suppression causes alopecia in VDR-null mice.

46 icantly increased in Mybphl heterozygous and null mice.

47 autophagy inhibition is attenuated in FGF15-null mice.

48 del of CKD-mineral bone disorder and alphaKL-null mice.

49 gets and in genes upregulated in miR-132/212 null mice.

50 e in the lung of wildtype but not caveolin-1-null mice.

51 th increased metastasis as compared with p53-null mice.

52 in (AG) and UAG were abolished in male GHS-R-null mice.

53 eased rate of arrhythmia in heterozygous and null mice.

54 CYP2A13/2F1-humanized mice than in Cyp2abfgs-null mice.

55 the exaggerated fibrosis observed in Twist1-null mice.

56 lial-to-mesenchymal transition (EMT) in Pten-null mice.

57 ng persistent DNA damage in p53R172H and p53-null mice.

58 were measured in 16HBE cells and claudin-18 null mice.

59 ut not purified immunoglobulin, into obese B(null) mice.

60 d P. falciparum-infected NOD-scid IL-2Rgamma(null) mice.

61 d under the kidney capsule of NOD-scid IL2Rg(null) mice.

62 man islets transplanted into NOD-scid IL-2Rg(null) mice.

63 in sublethally irradiated NOD-scid IL2rgamma(null) mice.

64 enotype seen in the cerebral cortex of Vldlr(null) mice.

65 athways, we fed wild-type and Pparalpha(-/-) null mice a high fat diet supplemented with either fenof

66 was delivered intrathecally into adult Gjb1-null mice, a genetically authentic model of CMT1X that d

67 his hypothesis, we crossed gamma-sarcoglycan-null mice, a model of limb-girdle muscular dystrophy typ

68 crossed Idh1-KI mice with conditional Trp53 null mice, a well-characterized model of T-cell malignan

69 Here, AhR-null mice (AhR-/-) were used to explore whether AhR cont

70 sferase (Bhmt), or both genes (BHMT-null/SHP-null mice), along with mice with wild-type copies of the

71 or initiated, and consistent with this LRBA-null mice also demonstrate resistance to lethal GvHD.

72 Interestingly, the null mice also displayed low serum phosphate levels, whi

73 Upf3b-null mice also have a profound defect in prepulse inhibi

74 In ZBTB20-null mice, although lactotrope lineage commitment is nor

75 The apparent partial lipodystrophy in Reep1 null mice, although less severe, is reminiscent of the l

76 omain of CIZ1 and the E repeats of Xist CIZ1-null mice, although viable, display fully penetrant fema

77 f brain cholesterol homeostasis in 129.Mecp2-null mice, an experimental model of Rett syndrome.

78 dney epithelial cells derived from both Pkd1-null mice and ADPKD patients.

79 the in vivo role of RTN1, we generated RTN1-null mice and compared the effects of RTN1 and RTN3 on B

80 shed literature, Dlx1/Dlx2 double homozygous null mice and Dlx5 homozygous null mice both have clefts

81 explain the parturition differences in Cox-1 null mice and gestation-matched wild type (WT) controls.

82 was observed in the livers of PPARbeta/delta-null mice and in mouse primary hepatocytes when this rec

83 ophages from heme overload in heme-loaded Hx-null mice and reduces production of cytokines and reacti

84 We generated RBM20-null mice and show that they completely lack these titin

85 levels are significantly reduced in Slc7a10-null mice and spontaneous glycinergic postsynaptic curre

86 we investigated the bone phenotype in Bmpr1b null mice and the impacts of loss of Bmpr1b on osteoblas

87 By using intravital microscopy with DREAM-null mice and their bone marrow chimeras, we demonstrate

88 Tumor incidence was increased 32% in Ahr null mice and tumor multiplicity was approximately incre

89 AML cells xenografted in NOD-Scid-IL2rgamma(null)mice and markedly increased overall survival, revea

90 tinal inflammation in Inpp5d(-/-) mice (SHIP-null mice), and SHIP levels and activity in intestinal t

91 ostnatal lethality characteristic of Slc7a10-null mice, and implicate SLC7A10 as a candidate gene and

92 istance in endothelial nitric oxide synthase null mice, and multiple studies have reported that both

93 hyperacetylated in the mitochondria of SIRT3-null mice, and SIRT3 directly deacetylates the ceramide

94 early death; on the other hand heterozygous null mice are apparently normal.

95 t from being prone to tumor development, Arf-null mice are blind, and their male germ cells exhibit d

96 Sorcin-null mice are glucose intolerant, with markedly impaired

97 Moreover, because RIAM-null mice are healthy, fertile, and display no bleeding

98 t endoplasmic reticulum membranes from Plin2-null mice are markedly enriched in omega-3 and omega-6 l

99 It has been reported that SR-BI/II null mice are more sensitive than normal mice to endotox

100 Abcb6 null mice are more susceptible to pentobarbital-induced

101 Porcn-null mice are rescued from radiation lethality by treatm

102 increased chromosome instability, and Abro1-null mice are tumor-prone.

103 Here we show that LRBA-null mice are viable, but exhibit compromised rejection

104 ng activity was altered in ovaries from Gas2 null mice around the time of birth and during follicular

105 have been conducted in male Mecp2 hemizygous null mice as offspring of heterozygous dams.

106 We collected intestines from SHIP-null mice, as well as Inpp5d(+/+) mice (controls), and m

107 hmt (betaine-homocysteine methyltransferase)-null mice at age 4, 12, 24, and 52 wk (N = 8) and observ

108 es were found in the distal segment of IL-10-null mice at early (3 d) and late (14 and 21 d) time poi

109 d found to be significantly delayed in Cox-1 null mice at term.

110 nd elevated progesterone levels in the Cox-1 null mice at term.

111 r0b2 (called small heterodimer partner [SHP]-null mice), betaine-homocysteine S-methyltransferase (Bh

112 ble homozygous null mice and Dlx5 homozygous null mice both have clefts of the secondary palate.

113 itions in HSCs derived from wild-type or App-null mice but in no comparable way when HSCs were fixed

114 rupts late-LTP and spatial memory in PKMzeta-null mice but not in wild-type mice.

115 changed in enamel organs of Ae2a,b- and Cftr-null mice but reduced in Dra-null mice by 36%.

116 t delay in AML progression in NOD/SCID/IL2Rg(null) mice, but the persistence of adoptively transferre

117 e2a,b- and Cftr-null mice but reduced in Dra-null mice by 36%.

118 for a loss-of-function, we generated NaV1.4 null mice by deletion of exon 12.

119 In C1ql2/3 double-null mice, CA3 synaptic responses lost the slow, KAR-med

120 Therefore, Xist-null mice can develop to term in spite of a deficiency o

121 ity, were significantly increased in nAChRa7 null mice (Chrna7(-/-)) relative to wild-type mice.

122 unchanged in cultured DRG neurons from TrpC3 null mice compared to wild type.

123 ced by a high fat diet was mitigated in Nox2-null mice compared with wild-type mice after 3 or 9 mont

124 In addition, Task1-null mice, compared with their controls, became overweig

125 of cell death in intestinal tissue of cIAP1-null mice, compared with wild-type C57BL/6 mice, cIAP2-n

126 e mTert gene in the first generation of Tert null mice compromised tumor growth, with reduced VEGF ex

127 nputs at end stages of disease (>/=P56 Mecp2 null mice) concomitant with synapse loss.

128 We found that claudin-2-null mice conserve sodium to the same extent as WT mice,

129 Ldlr(-/-) (low-density lipoprotein receptor null) mice deficient in miR-146a develop less atheroscle

130 Finally, the hearts of VWF-null mice demonstrate an abnormal endothelial phenotype

131 Ptrh2 null mice demonstrate multiple degenerating and regenera

132 However, ADF-null mice demonstrated increased intestinal permeability

133 Analysis in Ret wild-type and Ret-null mice demonstrates specific expression of Sema3a, Se

134 Null mice developed a robust immune phenotype characteri

135 Instead, C9orf72 null mice developed progressive splenomegaly and lymphad

136 Strikingly, these conditional gp96-null mice developed spontaneous colitis, had increased l

137 As Alpl-null mice die before weaning, we aimed to generate mouse

138 Consequently, prostasin null mice die shortly after birth.

139 onary function and cytokine profiles in Htr4-null mice differed little from their wild-type controls.

140 In Tshz3-null mice, differentially expressed genes include layer-

141 fects, cortical pyramidal neurons from Upf3b-null mice display deficient dendritic spine maturation i

142 The miR-183/96/182 null mice display impairment of the visual, auditory, ve

143 Here we report that Naa10-null mice display partial embryonic lethality, growth re

144 ort that mice lacking Nogo receptors (NgR123-null mice) display complete CC agenesis due to axon misd

145 Similar to Rac1 knockouts, Cdc42 null mice displayed a severe loss of pigmentation, and m

146 Notably, Kv3.1-null mice displayed baseline hyperlocomotion, reduced an

147 ly, tumors growing in C/EBPalpha conditional null mice displayed greater MDSC infiltration, increased

148 Young adult St3gal2/3 double-null mice displayed impaired motor coordination, disturb

149 We showed that adult P2Y4-null mice displayed microcardia resulting from defective

150 Contrary to expectation, Cox-1 null mice displayed normal uterine contractility; theref

151 By 18 months of age, P2X7-null mice displayed phenotypic characteristics consisten

152 NgR123-null mice displayed reduced motor coordination and hyper

153 Furthermore, Nrf2-null mice displayed slower regeneration marked by dysreg

154 istologic observations illustrated that Nrf2-null mice displayed smaller, immature TA muscle fibers c

155 of reeler mutants, while Reln(CTRdel)/Vldlr(null) mice do not.

156 y, expression of Mg29 in the hearts of Csrp3 null mice (encoding muscle LIM protein, MLP) partially r

157 sion only in GABAergic neurons of male Mecp2 null mice enhanced inhibitory signaling, extended lifesp

158 Unexpectedly, male UTX-null mice escape embryonic lethality due to expression o

159 urrent is absent in cochlear cells of Piezo2-null mice, even though the normal MT current persists.

160 In addition, CA1 pyramidal neurons from IK1 null mice exhibit a characteristic sAHP current.

161 However, Mmp25-null mice exhibit a defective innate immune response cha

162 Phlpp1 null mice exhibit decreased bone mass and notable change

163 These Upf3b-null mice exhibit deficits in fear-conditioned learning,

164 Functionally, Inpp5f-null mice exhibit enhanced recovery of motor functions i

165 Akin to the human phenotype, Gpt2-null mice exhibit reduced brain growth.

166 Ctip2-null mice exhibit reduced HF density during embryonic de

167 In this study, we found that Pierce1-null mice exhibit severe laterality defects, including s

168 ns appear in OA cartilage and that nidogen-2-null mice exhibit typical osteoarthritic features.

169 static synaptic scaling [3-6], but TNF-alpha-null mice exhibited no apparent cognitive or emotional a

170 we found that neutrophils derived from Cebpe null mice exhibited normal Lbr gene and protein expressi

171 Whereas prostasin null mice exhibited partial embryonic and complete perin

172 d bone-marrow-derived macrophages from IL-10-null mice failed to downregulate expression of proinflam

173 Conversely, Sgpp2-null mice failed to mount a DSS-induced systemic inflamm

174 Fam13a null mice (Fam13a(-/-)) were generated and exposed to ci

175 Fam13a null mice (Fam13a(-/-)) were resistant to chronic cigare

176 In BHMT-null and BHMT-null/SHP-null mice fed a control liquid, lipid vacuoles were obse

177 Indirect calorimetry showed that Cyp2e1-null-mice fed FF exhibited consistently higher total ene

178 ls were cultured from wild-type and tryptase null mice, followed by an assessment of their profile of

179 We tested TrpC3 null mice for beta-alanine induced itch, and found that

180 advanced lung tumours from Kras(G12D/+);p53-null mice frequently exhibit Kras(G12D) allelic enrichme

181 e, intestinal FXR reactivation protected FXR-null mice from spontaneous HCC development that occurred

182 mice, whereas all WT mice survived, and Nrf2 null mice had a defect in clearance, particularly at the

183 Compared with wild-type mice, NgR123-null mice had a sharp increase in the glial marker glial

184 SHP-null mice had altered timing in expression of genes that

185 The addition of I3C to the diet of AHR null mice had less of an impact than in AHR heterozygous

186 Eosinophils from CF null mice had reduced lifespan, reduced granularity, and

187 Claudin-18 null mice had significantly higher serum IgE levels and

188 At 12 months of age, P2X7-null mice had thickening of Bruchs membrane and retinal

189 ZnT8 null mice have a mild phenotype with a slight decrease i

190 particular dysfunction, in part because GAN null mice have a very mild phenotype.

191 etnlbeta (mouse ortholog of human RETNLbeta) null mice have an enhanced or reduced susceptibility for

192 We show here that TBP2 null mice have an intact regeneration potential upon inj

193 In addition, neural stem cells from Upf3b-null mice have impaired ability to undergo differentiati

194 Piezo2-null mice have largely normal hearing, exhibiting up to

195 Heterozygous null mice have latent myasthenia and a right shift of th

196 Our previous studies show that Shh null mice have smaller, aparathyroid primordia in which

197 Lrig1-null mice (homozygous Lrig1-CreERT2) and wild-type mice

198 Female JDP2 null mice, however, exhibited early puberty, observed as

199 ge cells; early embryonic lethality in Bag-1 null mice, however, has limited the investigation of BAG

200 ied evidence of partial lipoatrophy in Reep1 null mice in addition to prominent spastic paraparesis.

201 We used CD151-null mice in an in vivo model of IAV infection and clini

202 ophil infiltration was also observed in P2Y4-null mice in LPS-induced inflammation model.

203 to rescue most of the abnormalities of Fig4 null mice, including juvenile lethality and extensive ne

204 ctive prostasin are viable, unlike prostasin null mice, indicating that at least some prostasin funct

205 In FXR-null mice, intestinal selective FXR reactivation normali

206 Furthermore, crossing HSPB7 null mice into an Lmod2 null background rescued the elon

207 transplantation from platelet-specific ERK5 null mice into hyperlipidemic apolipoprotein E null mice

208 pite GC losses, retinal organization in Brn3 null mice is remarkably similar to that of wild-type con

209 ed that increased proliferation in p27(kip1)-null mice is reverted by concomitant deletion of stathmi

210 A significant feature of Gcgr-null mice is the high circulating concentrations of GLP-

211 n MDM2-ALT1 is ubiquitously expressed in p53 null mice it leads to increased incidence of spindle cel

212 singly, damaged white matter tracts in Olig1-null mice lacked Olig2(+) OPCs, and instead proliferatin

213 ited to postsynaptic sites in C1ql2/3 double-null mice, leading to reduced recurrent circuit activiti

214 od in both germline and conditional Six2(p53-null) mice, linking p53-mediated defects in kidney devel

215 docytopathy was completely preserved in MC1R-null mice, marked by reduced albuminuria and diminished

216 d small intestinal transit observed in Lrig1-null mice may be due, at least in part, to loss of the I

217 Reduced beta3 gene dosage in elastin-null mice mitigates pathological aortic muscularization,

218 The phenotype of Pierce1-null mice most closely resembled that of mutant mice wit

219 rmline liver fatty acid (FA) binding protein null mice (Mttp-LKO, i.e., double knockout mice) hepatic

220 Infarct regions from wild-type and MMP-9 null mice (n=8 per group) analyzed by glycoproteomics sh

221 cally reducing NF-kappaB signalling in Mecp2-null mice not only ameliorates CPN dendritic complexity

222 ophagy, but these effects are blunted in SHP-null mice or LSD1-depleted mice.

223 compared with wild-type C57BL/6 mice, cIAP2-null mice, or XIAP-null mice.

224 Consistent with these data, caveolin-1-null mice overexpressing K-Ras(G12D) display accelerated

225 eveloped in the embryos of Haao-null or Kynu-null mice owing to NAD deficiency.

226 gion, with 7 overlapping those found in Bhmt-null mice (P < 0.001).

227 ressor effect of I3C was not observed in Ahr null mice (P < 0.05).

228 Similar to Pgr null mice, Pgr null rats were infertile because of defic

229 ssue homeostasis, we generated germline PKM2-null mice (Pkm2(-/-)).

230 tissues and intestinal macrophages from SHIP-null mice produced higher levels of IL1B and IL18 than i

231 imary tumor burden, Notch activation in Pten-null mice promoted epithelial-mesenchymal transition and

232 he lack of a developmental phenotype in TBP2 null mice prompted further analysis to determine whether

233 n-cell-autonomous fashion, and that in Mecp2-null mice, re-expression of Mecp2 preferentially in astr

234 sfer experiments, matrix metalloproteinase-8 null mice receiving wild-type marrow had a survival adva

235 g-term memory in wild-type mice, and PKMzeta-null mice recruit compensatory mechanisms.

236 ric oxide synthase-deficient mice or alphaKL-null mice reduced serum phosphate levels.

237 Furthermore, MDM2-ALT1-expressing p53 null mice represent a novel mouse model of fusion-negati

238 sively in the somatosensory neurons of Mecp2-null mice rescues tactile sensitivity, anxiety-like beha

239 hat initial host defense is enhanced in Nrf2 null mice, resulting in less recruitment of neutrophils.

240 on of specific DNA loci in the liver of Bhmt-null mice results in repression of Iqgap2 and F2rl2 and

241 )-induced premature senescence in caveolin-1-null mice results in the formation of more abundant lung

242 Studies with scavenger receptor-A1 null mice reveal reduced IL-13 generation following expo

243 ion of the transcription factor RBPJ in Pten-null mice revealed that endogenous canonical Notch signa

244 ted retinal degeneration in Cln3(Deltaex1-6) null mice, revealing classic 'fingerprint' lysosomal sto

245 lysis of both male and female maternal Ube3a-null mice reveals that microcephaly in the AS mouse mode

246 In RTN3-null mice, RTN1 expression was slightly elevated.

247 We suggest Upf3b-null mice serve as a novel model system to decipher cell

248 l pulmonary fibrosis; however, in telomerase-null mice, short telomeres predispose to emphysema after

249 BMI1-null mice show severe defects in growth, development, an

250 Experiments in Fmr1 null mice show that FMRP regulates axonal protein expres

251 first-generation TERT-null mice, unlike Terc-null mice, show delayed onset of MYC-induced lymphomagen

252 ll mice into hyperlipidemic apolipoprotein E null mice showed decreased platelet accumulation and inc

253 lusion is based on the observations that Ahr null mice showed increased number of colorectal tumors,

254 CF null mice showed reduced pulmonary pathology in a model

255 Experiments in kisspeptin receptor-null mice, showed that kisspeptin was the critical neuro

256 y and hepatocellular carcinoma found in Sod1 null mice (Sod1(-/-)).

257 We used wild-type and Olig1-null mice subjected to neonatal stroke and postnatal neu

258 esponses were persistently augmented in Nrf2-null mice suggesting that regulation of the regeneration

259 droxycholesterol (24S-OHC) found in B6.Mecp2-null mice suggests the occurrence of changes in brain ch

260 ium-phosphate cotransporter Npt2a in alphaKL-null mice supporting direct actions of cKL in the absenc

261 al excitability to a greater degree in Mecp2-null mice than in the WT.

262 ree different atherosclerosis models in ApoE null mice that prolonged systemic treatment with LyP-1 t

263 ted, streptozotocin-treated ghrelin receptor-null mice that were administered GcgR monoclonal antibod

264 ot establish infection in NOD-scid IL2rgamma(null) mice that lack B cells, T cells, NK cells, and lyt

265 In CLCa-null mice, the germinal centers have fewer B cells, and

266 In null mice, the prevention of NAD deficiency during gesta

267 le these data by showing that exposing Fsp27-null mice to a substantial energetic stress by crossing

268 e growth factor 1 (IGF-1) treatment on CDKL5 null mice to restore the synaptic deficits.

269 Ldlr(-/-) (low-density lipoprotein receptor null) mice transplanted with bone marrow (BM) cells from

270 Wnt7a-null mice under de novo conditions and in both the strai

271 , we demonstrated that first-generation TERT-null mice, unlike Terc-null mice, show delayed onset of

272 n conclusion, the phenotype of the Retnlbeta null mice unravels new aspects of inflammation-mediated

273 Also increased in expression in Mecp2-null mice was another extrasynaptic GABAAR subunit, alph

274 ygen consumption in the kidneys of claudin-2-null mice was markedly increased, resulting in medullary

275 ary cause of podocyte abnormalities in Rhpn1-null mice was the result of cell-autonomous, Rhophilin-1

276 eveloped in p53 wild-type ((+/+)) versus p53 null ((-/-)) mice, we observed higher GMPS expression in

277 Here, using male wildtype (WT) and Pxr-null mice, we examined PXR-mediated regulation of chroni

278 Msh2-null mice were also impaired in locomotive activity and

279 Male wild-type (WT) and Cyp2e1-null mice were fed standard chow or FF for 2, 12, and 24

280 Plaa-null mice were generated and prostaglandin E2 levels wer

281 Plaa-null mice were perinatal lethal with reduced brain level

282 ed by CB1 receptor genetic ablation, and CB1-null mice were resistant to THC-induced alterations.

283 paired LTD and extinction learning in ASIC1a null mice were restored by virus-mediated expression of

284 ent visceral fat and Th2 responses in Chi3l1 null mice were reversed by Sirt1 inhibition.

285 elinated corpus callosum projections of Msh2-null mice were smaller than wild-type mice, whereas unmy

286 ctor-erythroid 2 p45-related factor 2 (Nrf2) null mice were studied.

287 NOD-Scid-IL2Rgamma null mice were transplanted with human hematopoietic CD3

288 n this report, humanized NOD/scid-IL2Rgammac(null) mice were used to establish that impaired Sonic he

289 e dental pulp cells and odontoblasts of DSPP-null mice when compared with wild-type mice.

290 gly increased from 15 to 31 and 100% in Nrf2 null mice, whereas all WT mice survived, and Nrf2 null m

291 owever, progressively reseals in older Akap9 null mice, which correlates with a reduction in germ cel

292 We report that in contrast to kindlin-3-null mice, which die perinatally of severe bleeding and

293 Similar to P4ha1 null mice, which die prenatally, the muscle tissue from

294 ng hormone axons was reduced in adult Magel2-null mice, while the density of orexigenic agouti-relate

295 To this end, we generated FXR-null mice with re-expression of constitutively active FX

296 alphaKL-null mice with sustained AAV-cKL expression had a 74%-78

297 wed greater sensitivity to NA than Cyp2abfgs-null mice, with greater depletion of nonprotein sulfhydr

298 and extended the life span of treated Mecp2-null mice without adverse side effects.

299 A improves glucose intolerance in obese MC4R-null mice without affecting body weight or circulating i

300 memory in wild-type mice, but not in PKMzeta-null mice without the target mRNA.