ライフサイエンスコーパス: double-mutant mice

1 replication stress in vivo, we used Hus1/Atm double mutant mice.

2 DSBs, we generated Fancd2(-/-)/Prkdc(sc/sc) double mutant mice.

3 single LRP6 mutant mice as well as LRP6/Lef1 double mutant mice.

4 , resulting in an increased life span of the double mutant mice.

5 ons were significantly increased in lungs of double mutant mice.

6 he retinal pigment epithelium and choroid of double mutant mice.

7 ice, it failed to do so in CB1(-/-)/CB2(-/-) double mutant mice.

8 sceral pathology was similar in the NP-C and double mutant mice.

9 P-C disease was substantially reduced in the double mutant mice.

10 macrophages was not reduced significantly in double mutant mice.

11 mber was reduced and length was increased in double mutant mice.

12 ) mutant, SNCA transgenic (tg), and Gba-SNCA double mutant mice.

13 and dendritic spines in Tau mice relative to double mutant mice.

14 e Itsn genes, we generated Itsn1, Itsn2, and double mutant mice.

15 to normal levels in osteoclasts derived from double mutant mice.

16 ant mice were augmented in DBH (-/-)/APP/PS1 double mutant mice.

17 al projections in Brn3a and Brn3b single and double mutant mice.

18 of tooth morphogenesis in Msx1(-/-)Osr2(-/-) double mutant mice.

19 edly ameliorated in Ptpn11(D61G/+)/Gab2(-/-) double mutant mice.

20 loss of Fgf8a, we generated Fgf17 and Fgf8a double mutant mice.

21 MEN1, we characterized p18-Men1 and p27-Men1 double mutant mice.

22 to sustain molecular rhythmicity in mPer1/2 double-mutant mice.

23 ytokine withdrawal was also increased in the double-mutant mice.

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

25 ation, in the renal tubules of Tsc1 and rpS6 double-mutant mice.

26 ssin mRNA levels are increased in CRFR2- and double-mutant mice.

27 tex was aggravated in Fmr1(-/y); Cyfip2(+/-) double-mutant mice.

28 we generated and analyzed Nkx2.5 and Nkx2.6 double-mutant mice.

29 pulmonary inflammation characteristic of E/P double-mutant mice.

30 e, but these were less extensive than in E/P double-mutant mice.

31 of these transcription factors by analyzing double-mutant mice.

32 errantly long telomeres were observed in the double-mutant mice.

33 protective effects are lost in Atg16L1/Nod2 double-mutant mice.

34 fovea in NPHP6-LCA, we generated rd16;Nrl-/- double-mutant mice.

35 knock-in mice was also markedly decreased in double-mutant mice.

36 of mice deficient in either SLRP gene and in double-mutant mice.

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

38 g were boosted in tumor tissues of Apc Olfm4 double-mutant mice.

39 n parkin null alpha-synuclein-overexpressing double-mutant mice.

40 2 g at 6 mo) and the Acox1-deficient (ob/ob) double-mutant mice (23.8+/-4.6 g at 6 mo), the ob/ob mic

41 The resultant double-mutant mice 5xF:pGB mice displayed a full rescue

42 ibited few RGC axon guidance defects, but in double mutant mice a large additional chiasm developed a

43 Double mutant mice also exhibit a high predisposition to

44 Double-mutant mice also display an even greater impairme

45 prx-1; prx-2 double-mutant mice also displayed extreme shortening and

46 Tissues and cells from double-mutant mice also showed indications of spontaneou

47 cochlear sensory epithelium were present in double mutant mice and cochlear stereocilia exhibited a

48 GFR-positive cell lines derived from Nf1:p53 double mutant mice and human MPNST.

49 MEN1, we characterized p18-Men1 and p27-Men1 double mutant mice and showed that p18, but not p27, fun

50 is dependent on CDK4, we generated p18; Cdk4 double-mutant mice and examined the organs and tissues w

51 (-/-)-mutant mice and Xpc(-/-)G1-G3Terc(-/-) double-mutant mice and exposed them to UV radiation.

52 compared the generation of T cells in these double-mutant mice and IIo or TAPo mice.

53 In this study, we generated Camk2a/Camk2b double-mutant mice, and observed that loss of CAMK2, as

54 CRF mRNA levels are elevated in CRFR1- and double-mutant mice, and urocortin III and vasopressin mR

55 The double mutant mice are also significantly more glucose i

56 Interestingly, ICE-/-/type I IL-1R-/- double mutant mice are resistant to high dose LPS.

57 Remarkably, Casp8(-/-)Rip3(-/-) double mutant mice are viable and mature into fertile ad

58 The alterations observed in double-mutant mice are distinct from the phenotypes obse

59 Double-mutant mice are suitable for assessing the severi

60 These double-mutant mice are unable to cleave leukotriene C(4)

61 from PN0 through PN23, and in rd-1/caspase-3 double mutant mice at PN14, -16, and -18.

62 Double mutant mice (bpk -/-; cftr -/-) developed massive

63 We monitored Brg1+/-, Brm-/- double-mutant mice but did not observe any tumors resemb

64 urrence of skin and pulmonary disease in E/P double-mutant mice but not E/L/P triple-mutant mice sugg

65 d thymic apoptosis was suppressed in Atm/p53 double-mutant mice but not in Atm/p21 double mutants, de

66 In Neurod2/6 double-mutant mice, callosal axons lack expression of th

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

68 Double mutant mice carrying the Scn2a(Q54) transgene tog

69 esis and synaptic proteins were increased in double mutant mice compared with Tau (P301L) mice.

70 taneous testicular tumors in XPC-/- TrpS3-/- double mutant mice compared with XPC+/+ Trp53-/- mice.

71 el complexes could be detected in single- or double-mutant mice compared to control animals.

72 ctivity were increased in proximal aortas of double-mutant mice compared with controls.

73 MRF4/myogenin double mutant mice contained a comparable number of resi

74 Using double mutant mice created by F2 generation crosses of C

75 The coat-color phenotype of young homozygous double-mutant mice deficient in subunits of BLOC-3 (HPS1

76 Double-mutant mice, deficient in dystrophin and perforin

77 urned to normal in Rasgrp1(Anaef)Mtor(chino) double-mutant mice, demonstrating that increased mTOR ac

78 Furthermore, we showed that in compound double mutant mice, deregulation of Wnt signaling was th

79 In this study we report that double mutant mice develop a lupus-like disease as well

80 The double mutant mice develop a wider spectrum of tumors, i

81 Furthermore, p53-/- scid double mutant mice develop lymphoma earlier than p53-/-

82 At approximately 6 mo of age, double-mutant mice develop amyloid pathology, with signs

83 e mutant mice were asymptomatic, Prkdc/Mpv17 double-mutant mice developed mtDNA depletion and recapit

84 , IL-4 -/- BCL-6 -/- and STAT6 -/- BCL-6 -/- double-mutant mice developed the same TH2-type inflammat

85 When compared with Tau mice, double mutant mice did better on the Morris Maze (reduce

86 Unlike the NP-C model mice, these double mutant mice did not exhibit central nervous syste

87 However, double-mutant mice died at lower frequency from tumors t

88 The double-mutant mice died at relatively young ages and dev

89 We have found that although the female double-mutant mice display anxiolytic-like behavior, the

90 -), Kcnq5(dn/dn) nor Kcnq4(-/-)/Kcnq5(dn/dn) double mutant mice displayed circling behavior found wit

91 The double mutant mice displayed significant loss of thermal

92 Moreover, eEF2(G717R/G717R)/OVCA1(-/-) double mutant mice displayed the milder phenotypes of th

93 OPN and dystrophin were generated and termed double-mutant mice (DMM mice).

94 ith behavioral data from mPer2/3 and mPer1/3 double-mutant mice, either mPER1 or mPER2 alone can sust

95 ot completely inhibited in P-selectin/ICAM-1 double-mutant mice (eosinophil recruitment inhibited app

96 These double mutant mice exhibit a novel phenotype, including

97 les to promote muscle regeneration, as MSulf double mutant mice exhibit delayed myogenic differentiat

98 phaSyn mice manifest motor symptoms, and the double mutant mice exhibit more exacerbated synaptic and

99 Likewise, heterozygous double mutant mice exhibited severe circling behavior, w

100 Cul9-p53 double-mutant mice exhibited indistinguishable tumor phe

101 The double-mutant mice exhibited phenotypes very close to or

102 ility of Mre11 complex mutants; however, the double-mutant mice exhibited synergistic defects in DNA-

103 These double mutant mice expressed GM3 as their major ganglios

104 c factor Bax, as demonstrated in conditional double mutant mice for Bcl-x and Bax.

105 king myogenin alone and myoblasts from those double mutant mice formed differentiated multinucleated

106 These double mutant mice had longer skulls than Axin2(-/-) mic

107 Double mutant mice had more overt diabetic nephropathy,

108 Double mutant mice had novel phenotypes in which the ros

109 -specific immune responses were quantitated, double-mutant mice had 100-fold more antigen-specific me

110 The double-mutant mice had no shortening of lifespan and no

111 The obtained hSOD1/rag2 double mutant mice have been characterized.

112 e is compensatory upregulation of Grg4Grg3/4 double mutant mice have severe dysregulation of the panc

113 l mutant mice by gene targeting, we produced double mutant mice homozygous for both Agtr1a and Agtr1b

114 The p27; Cdk4 double-mutant mice, however, displayed phenotypes interm

115 We generated Hyp and klotho double-mutant mice (Hyp/klotho(-/-)).

116 crossed together to generate Ku70, Ku80, and double-mutant mice in the same genetic background raised

117 Most notably, the clinical phenotype of the double mutant mice, in the absence of CNS ganglioside ac

118 The analysis of Rag2-/- Ctsl(nkt)/Ctsl(nkt) double-mutant mice indicates that the skin defect remain

119 ations (100 nM) is absent in Mel(1a)-Mel(1b) double-mutant mice, indicating that the Mel(1b) receptor

120 RF8 (IFN consensus sequence binding protein) double mutant mice (IRF4,8(-/-)).

121 In fact, the body weight of these double-mutant mice is only approximately 17% of normal a

122 Furthermore, 3-week-old double mutant mice lacked auditory brainstem responses,

123 king the P2X2 receptor subunit (P2X2-/-) and double mutant mice lacking both P2X2 and P2X3 subunits (

124 Similar defects were observed in double mutant mice lacking Cadm3 and Cadm2 (i.e., Cadm3(

125 thesis, we have characterized two strains of double mutant mice lacking either p18(INK4c) and p27(KIP

126 s1 and Irs2 in Igf1r signaling, we generated double mutant mice lacking Igf1r specifically in pancrea

127 with those of myogenin or MyoD, we generated double mutant mice lacking MRF4 and either myogenin or M

128 In contrast with the Igf2r/Igf2 double mutants, mice lacking IGF2R/CI-MPR and CD-MPR sur

129 Nevertheless, double-mutant mice lacking beta-actin and expressing fas

130 re(+) mice to myd88(f/f) animals, generating double-mutant mice lacking both Lyn and the adaptor prot

131 e primacy of cholesterol storage, neurons of double-mutant mice lacking both NPC1 and an enzyme requi

132 Double-mutant mice lacking dystrophin and perforin showe

133 Double-mutant mice lacking function of both Lhx1 and Lhx

134 nent, genetic alteration of both pathways in double mutant mice leads to expansion of phenotypic HSCs

135 In the double-mutant mice, maintenance of axo-glial adhesion is

136 Hps5/Hps5,Hps6/Hps6 and Hps3/Hps3,Hps6/Hps6 double mutant mice mimic, in coat and eye colors, in mel

137 In Olig1/2 double-mutant mice, motoneurons are largely eliminated,

138 s c-Jun activation by comparing C3 mice with double mutant mice, namely C3 mice in which c-Jun had be

139 electro-olfactogram (EOG) recordings on the double-mutant mice, NCKX4(-/-);CNGB1(DeltaCaM), which ar

140 Rather, as revealed by analysis of double-mutant mice, Nkx2.1 and Gsh2 act cooperatively in

141 mical, and histochemical characterization of double-mutant mice overexpressing mutant human A53T alph

142 The absence of Cdx1 function in Rb/p130 double mutant mice partially reverted the histologic phe

143 eptor stimulation, peripheral B cells in the double mutant mice phenocopy hyperresponsive CD45 E613R

144 Occasionally, double-mutant mice progressed to locally invasive PDAC w

145 Further, these double mutant mice provide an unprecedented viable anima

146 The double-mutant mice rescued the angiogenic deficit associ

147 me of the skeletal defects seen in single or double mutant mice resemble defects seen in human skelet

148 ioral rhythms of mPer1/mPer3 and mPer2/mPer3 double-mutant mice resembled rhythms of mice with disrup

149 uggest that the severe kidney disease in the double-mutant mice results from a combination of immunol

150 ordings in cerebellar slices from Wnt7a/Dvl1 double mutant mice reveal a defect in neurotransmitter r

151 Creation of Hand1/2 double mutant mice revealed gene dose-sensitive function

152 ns and sleep architecture is also altered in double mutant mice (S1/2(-/-)).

153 is; however, in Brn3a single and Brn3a;Brn3b double mutant mice, sensory afferent axons from the DRG

154 In Slit1;Slit2 or Robo1;Robo2 double mutant mice, sensory axons enter the spinal cord

155 Third, double mutant mice show a split sternum that is not dete

156 ressed by SAG neurons, and plexinA1/plexinA3 double mutant mice show defects in afferent projections

157 Double mutant mice show no reversion or improvement in t

158 e display anxiolytic-like behavior, the male double-mutant mice show significantly more anxiety-like

159 ole as a mediator of mdm pathology, C3KO;mdm double mutant mice showed no change in the progression o

160 The neocortex of the Lis1-Nde1 double mutant mice showed over 80% reduction in surface

161 The Abcc6(-/-)Alpl(+/-) double-mutant mice showed 52% reduction of mineralizatio

162 Double-mutant mice showed greater lesion area compared w

163 ity of the lung pathology in the beta c/IL-3 double-mutant mice showed normal hemodynamic parameters

164 Analysis of double-mutant mice showed that loss of Smad4 significant

165 tial embryonic lethality, with the surviving double-mutant mice showing synergistic increases in geno

166 Unlike the double-mutant mice, single mutants deficient in either L

167 increased lysosomal enzyme levels in lung of double mutant mice suggest a cause of a major clinical p

168 reduced EphA2 expression in hoxa1 and hoxb1 double mutant mice, suggest that expression of EphA2 gen

169 pe mice and normalized in cells derived from double mutant mice, suggesting a cell-autonomous effect

170 not affected in follicles from the single or double mutant mice, suggesting that diffusion of cAMP is

171 These double-mutant mice survived longer than NHEJ/p53 double-

172 (TCR)-alpha-/- mice was explored by creating double mutant mice (TCR-alpha-/- x immunoglobulin (Ig)mu

173 t risk factor, oxidative stress, we produced double-mutant mice (Tg-MYOC(Y437H/+)/Sod2(+/-)) bearing

174 observed on the lateral migration pathway in double-mutant mice that also lack MGF.

175 ole, we have initiated a program to generate double-mutant mice that are deficient in more than one f

176 double-mutant embryos or neonates; miR-133a double-mutant mice that survive to adulthood succumb to

177 Although in Apc-Grp78 double mutant mice the Wnt signature was lost, these int

178 In double-mutant mice, this phenotype was dependent on both

179 n-deficient mice (ob/ob) and ob/ob, CAR(-/-) double mutant mice to identify a metabolic role of CAR i

180 T-VII(-/-), low density lipoprotein receptor double-mutant mice to evaluate the roles of E- and P-sel

181 requency of spontaneous TGCTs in single- and double-mutant mice to identify combinations that show ev

182 The immune response of the beta c/IL-3 double-mutant mice to Listeria mono-cytogenes was normal

183 ce, a model of human diabetes, and generated double-mutant mice using the ACE2 knockout (KO) mice (Ak

184 tumor burden in the distal colon of Muc2/Apc double mutant mice was similar to the phenotype observed

185 inflammatory phenotype of p50(-/-)relB(-/-) double-mutant mice was markedly increased in both severi

186 By analyzing CoupTFI(-/-);Foxc1(H/L) double mutant mice we provide evidence that CoupTFI is r

187 Using single- and double-mutant mice, we show that loss of mast cells neit

188 Using double-mutant mice, we show that synapses do form in the

189 Mex3c and Leptin double mutant mice were growth retarded and obese and ha

190 BCL-6-/-IL-4-/- double-mutant mice were also susceptible to L. major inf

191 The double-mutant mice were apparently normal and fertile.

192 We found that Six1 (-/-) Six2 (-/-) double-mutant mice were born with severe craniofacial de

193 Double-mutant mice were created by crossing TCRalpha-/-

194 nous DNA damaging agent, ionizing radiation, double-mutant mice were exquisitely sensitive to low dos

195 In contrast, mPer1/mPer2 double-mutant mice were immediately arrhythmic.

196 TLR2(-/-)/scid double-mutant mice were infected with B. burgdorferi to

197 By contrast, BCL-6-/-STAT6-/- double-mutant mice were resistant to L. major infection

198 ifically for this study from Hoxa 11/Hoxd 11 double-mutant mice, were also modified to give cell popu

199 rm cells, we examined testes from Bclw/c-kit double mutant mice, which lack germ cells from birth.

200 mphatic vascular defects seen in Fgfr1/Fgfr3 double mutant mice, while HK2 overexpression partly resc

201 The double-mutant mice will help elucidate the pathophysiolo

202 Here, using double mutant mice with genetic deletions of Cav1 and NO

203 opment by comparing phenotypes in Emx1; Emx2 double mutant mice with wild-type and Emx1 and Emx2 sing

204 ene-2 x common cytokine receptor gamma-chain double-mutant mice with Syk-/- fetal liver cells.