ライフサイエンスコーパス: congenic mice

1 onding decrease in hnRNP H protein in 114 kb congenic mice.

2 ress the IgM(b) allotype) to IgM(a) allotype congenic mice.

3 lymphoid and myeloid progenitors from CD45.1 congenic mice.

4 ransplantation method, into old or young Ly5 congenic mice.

5 severe EAE in NOD mice compared with Idd5.1 congenic mice.

6 leads to autoimmune cholangitis in NOD.Abd3 congenic mice.

7 mechanism of protection from diabetes in Idd congenic mice.

8 g the systemic administered MDSC from CD45.1 congenic mice.

9 notype of the lupus-like disease in NZM 2328 congenic mice.

10 14- to 15-day fetal thymic lobes from Thy-1 congenic mice.

11 The locus on chromosome 2 was confirmed in congenic mice.

12 P-1 were evaluated for immunogenicity in B10 congenic mice.

13 n and injected into lethally irradiated Ly-5 congenic mice.

14 mice showed responses similar to the normal congenic mice.

15 cra(b) with Tcra(a) or Tcra(c) haplotypes in congenic mice.

16 c segment of CD45 were transferred into CD45 congenic mice.

17 e in hypersusceptible BALB/c.DBA/2-Idh1-Pep3 congenic mice.

18 + expansion was absent in H-2IA(b)-deficient congenic mice.

19 transgenic cells adoptively transferred into congenic mice.

20 Prmt1 caused leukemia when transplanted into congenic mice.

21 on intratracheal adoptive cell transfer into congenic mice.

22 f them had fat mass as large as the original congenic mice.

23 controls, and comparable that to B6.TH-tabw2 congenic mice.

24 optively transferred into Rag1((-)/(-))Ly5.1 congenic mice.

25 ne marrow-derived dendritic cells from Cdcs1 congenic mice.

26 e measured in aging female gld and wild-type congenic mice.

27 uence adaptive immunity to Salmonella in MHC congenic mice.

28 s following the transfer of these cells into congenic mice.

29 gher resolution than that attained using the congenic mice.

30 fertile but weighed significantly less than congenic +/+ mice.

31 AKR.H-2(b) congenic mice, although carrying the responder H-2(b) ma

32 Using B6.129c1 congenic mice and adoptive transfer, we found that diver

33 ypes, NZB mice were bred with B6 or B6.Sle1c congenic mice and approximately 20 female offspring were

34 were compared between cohorts of B6.Sle2.lpr congenic mice and B6.lpr mice of ages up to 6 months.

35 In both B6.Sle2 congenic mice and C57BL/6 control mice, antibody-mediate

36 between lupus-prone B6.Sle1.Sle2.Sle3 triple-congenic mice and C57BL/6 controls at steady state relat

37 disease was observed in B10.Yaa.BXSB-Bxs2/3 congenic mice and caused 50% mortality by 12 mo.

38 LB/c mice with NK cells from BALB.B6-Cmv1(r) congenic mice and generated a mAb, designated 4E4, that

39 gene mRNA expression data in segregating and congenic mice and identify glutamate receptor metabotrop

40 In this study Bphs congenic mice and mice with a disrupted Hrh1 gene were u

41 We confirmed the presence of Blmpf1 in MHC congenic mice and narrowed the region to 2.7 cM in a red

42 QTL was coincident with a body weight QTL in congenic mice and Scg5 expression was negatively correla

43 nsferred CD45.1 CD8 OT-I T cells into CD45.2 congenic mice and subjected them to cecal ligature and p

44 Studies with various B10 congenic mice and their F(1) hybrids indicate that this

45 9S-Cdh23(c.753A) SNV and 129S1.B6-Cdh23(ahl) congenic mice, and a linkage backcross involving these s

46 f the Idd2 locus and found that NOD.B10-Idd2 congenic mice are highly resistant to diabetes.

47 ast, spontaneous virus-expressing AKR.H-2(b) congenic mice are low/nonresponders for the generation o

48 Although Idd5.1 congenic mice are resistant to diabetes, we found them m

49 Mixed marrow chimeras using TgB(+) and congenic mice as donors, and experiments using anti-IL-7

50 to nearly those of wild-type B6 in the B6/B6 congenic mice as follows: 83% rescue of low pial collate

51 In an earlier study, we used Ly5.1 congenic mice as transplant recipients to investigate th

52 DCC-susceptible C3H/He and B6.C3H(Dyscalc1) congenic mice at day 3 after injury.

53 blockade but is prolonged further in NOD Idd congenic mice bearing C57-derived chromosome 3 loci.

54 Congenic mice bearing the disease loci Sle1 or Sle1 and

55 eous proliferation when transferred to naive congenic mice, both characteristic of central memory T c

56 not in C3H/HeJ or BALB/c (C.C3H Tlr4(lps-d)) congenic mice, both of which have a mutant TLR4 gene.

57 e or absence of the Stat5b mutation in these congenic mice but is correlated with the expression leve

58 erall disease progression in some strains of congenic mice but not in others.

59 B6.TH-tabw2 congenic mice, but not subcongenic mice, also had signif

60 chimerism was studied in nonirradiated Ly 5 congenic mice by quantitative intrathymic and intravenou

61 tandard backcross breeding scheme to produce congenic mice by the inclusion of genotype-based selecti

62 he profound protection from diabetes seen in congenic mice carrying an Idd3 protective allele is unli

63 moter and inhibits its expression in NOD.C3H congenic mice carrying C3H alleles at Idd6.3.

64 Congenic mice carrying introgressed DNA from DBA/2J on a

65 Congenic mice carrying the impulsivity locus (Impu1) con

66 gulatory T cells from diabetes-resistant NOD congenic mice compared to susceptible NOD mice.

67 Use of class II MHC-congenic mice confirmed that the enhancement of CTL resp

68 ne phenotypes can be isolated in recombinant congenic mice containing both genes.

69 used NZB.NZW-Lbw2 congenic (designated Lbw2 congenic) mice containing an introgressed fragment of Ne

70 + CD25- cells transferred into thymectomized congenic mice converted to CD4+ CD25+ cells that also su

71 These congenic mice, CRE3/Shp2-KO, developed obesity and diabe

72 ive transplant model, which uses Ly5.2/Ly5.1 congenic mice, cytokine-cultured Ly5.2 cells competed wi

73 gh-resolution marker of neuronal activation, congenic mice demonstrated significantly less neuronal a

74 on and IL-17 production in interval-specific congenic mice demonstrated that the two identified genet

75 rom T1D to the same extent as NOD.B10 Idd5.1-congenic mice, demonstrating that increased liCTLA-4 exp

76 B6.Sle1c congenic mice develop Abs to chromatin by 9 mo of age wi

77 The B6.TH-tabw2 congenic mice developed increased adiposity that became

78 ntrol, and the bacteria were inoculated into congenic mice differing only at Nramp1.

79 Analyzing these congenic mice enabled us to fine map the Par1 quantitati

80 Finally, while both KitW/KitW-v and congenic +/+ mice exhibited fatal active anaphylaxis, ma

81 Lbw2 congenic mice exhibited marked reductions in AEAs and sp

82 oliferator-activated receptor-gamma, and the congenic mice exhibited significantly reduced expression

83 ogenitor responded equally to DMBA and BP in congenic mice expressing the PAH-resistant AhR (AhR(d)).

84 generating lines of transgenic B10 (H-2(b)) congenic mice expressing three independent contiguous co

85 ich Nba2 genes accomplish this, we generated congenic mice expressing various Nba2 intervals where ge

86 ficantly dysregulated in arthritic joints of congenic mice; expression of these genes was also sex sp

87 Lyme arthritis in the reduced interval Bbaa1 congenic mice, formally implicating myostatin as a novel

88 urthermore, neomycin treatment protected Mx1 congenic mice from upper and lower respiratory infection

89 amine-induced locomotor activity in C57BL/6J congenic mice harboring DBA/2J polymorphisms.

90 UCP1-deficient congenic mice have a very pronounced cold-sensitive phen

91 NOD.Idd3/5 congenic mice have insulin-dependent diabetes (Idd) regi

92 t alcohol-avoiding male B6.D2 Alcp1 line 2.2 congenic mice have lower Ucn immunoreactivity in the EW

93 Analyses of lupus-prone congenic mice have pointed to an important role for the

94 s (Tregs), and we found that B10.S-Eae5(SJL) congenic mice have significantly greater numbers of lymp

95 ice with that observed in diabetes-resistant congenic mice having protective alleles at insulin-depen

96 C57BL/6-congenic mice heterozygous for the F508del CFTR mutation

97 MHV-68-specific CD4(+) T cells generated in congenic mice homozygous for disruption of the beta2-mic

98 chromosome 2 that could not be confirmed in congenic mice, however, probably because of epistasis.

99 Neutropenic congenic mice, however, were susceptible only to wild-ty

100 Bone marrow-derived macrophages from Bbaa1 congenic mice implicated this locus as a regulator of ty

101 Here, we showed that housing Mx1 congenic mice in low relative humidity makes mice more s

102 by comparing alpha7 receptor development in congenic mice in which the DBA/2 allele of Chrna7 has be

103 welve-month-old C3H.SW-H2b/SnJ mice (C3H/HeJ congenic mice in which the H2k purported susceptibility

104 diation sensitivity, we conducted studies on congenic mice in which the linked region on chromosome 1

105 trains (often C57BL/6J) typically results in congenic mice in which the targeted gene is flanked by E

106 NOD.B10 Idd9 congenic mice, in which the NOD Idd9 chromosomal region

107 ordance of phenotypes between Tgfb2(+/-) and congenic mice indicates that HSPC frequency and cycling

108 In reciprocal chromosome 5 congenic mice, introgressed D2 alleles increased HSC num

109 In reciprocal chromosome 3 congenic mice, introgressed D2 alleles increased HSC num

110 These NOD.C6 congenic mice lack the NOD islet cell antigen to which t

111 In this study, we used wild-type and congenic mice lacking various components of the immune s

112 ated effector CD4(+) T cells into tumor-free congenic mice mediates rejection of tumor challenge 9 mo

113 Crry derived from B6.Sle1c congenic mice migrated at a higher m.w. by SDS-PAGE comp

114 total) to detect underlying genetic loci; 2) congenic mice (n = 23) to replicate the identified locus

115 1 diabetes, and changes between NOD and NOD congenic mice (NOD.Idd3/Idd10 and NOD.B10Sn-H2(b)), whic

116 We used congenic mice of black, yellow, and albino coat colors t

117 Importantly, Ob-deficient and vic1 I/LnJ congenic mice on other genetic backgrounds produce antiv

118 round or DR4.Ab(0)- and DQ8.Ab(0)-transgenic/congenic mice on the arthritis-susceptible BALB/c geneti

119 dependency, we used genetically modified and congenic mice on the C57BL/10 background and in vitro T-

120 hat macrophages obtained from sst1-resistant congenic mice possess superior ability to kill L. monocy

121 gene (designated Tnfrsf9) in NOD.B10 Idd9.3 congenic mice protected from type 1 diabetes (T1D).

122 m multilineage chimerism is achieved in CD45 congenic mice receiving high bone marrow doses with or w

123 tion of these cells into lethally irradiated congenic mice resulted in efficient gene transfer into h

124 using major histocompatibility complex (MHC)-congenic mice revealed probable contributions by both MH

125 ysis of iNKT cell number and function in Idd congenic mice revealed that neither iNKT cell number nor

126 Transplantation of Vk*MYC tumor cells into congenic mice selected for a more aggressive disease tha

127 ained with independent inbred strains and H2 congenic mice show that the genetic control of all three

128 As previously reported, B6.TH-tabw2 congenic mice showed a significantly larger fat mass tha

129 e onset of autoimmunity, B cells from triple-congenic mice showed an elevated glycolysis and mitochon

130 Analysis of a panel of subinterval congenic mice showed that the full effect of Lbw2 on AEA

131 prisingly discover that the UBC-GFP BALB/cBy congenic mice still retain the H-2(b) MHC haplotype of t

132 Surprisingly, in NOD congenic mice that are almost completely protected from

133 Here, we examined B6.Sst1(S) congenic mice that carry the 'susceptible' allele of the

134 We generated congenic mice that confirm a quantitative trait locus (Q

135 ted at human chromosome 5q23-35, we examined congenic mice that differed at the homologous chromosoma

136 have developed novel NOD.B10-Idd9 (line 905) congenic mice that predominantly harbor islet-reactive C

137 tations to the reported genetically modified congenic mice that were generated using 129-strain ESCs

138 Congenic mice that were genetically deficient in B cells

139 However, unlike NOD.B6 Idd3 congenic mice, the knockin mice were not protected from

140 We have previously shown that AKR.H-2b congenic mice, though carrying the responder H-2b major

141 Previous studies have used congenic mice to examine the function of major histocomp

142 ific imbalances in tumors from backcross and congenic mice to refine the location of Skts1.

143 In this study, we use congenic mice to show that BMC rejection is regulated by

144 s can be fine-mapped by crossing appropriate congenic mice to the background strain, and complex gene

145 ting the cells into lethally irradiated Ly-5 congenic mice together with "compromised" marrow cells.

146 ransplantation into lethally irradiated Ly-5 congenic mice together with compromised marrow cells.

147 e cultured cells to lethally irradiated Ly-5 congenic mice together with compromised marrow cells.

148 These results validate the approach of using congenic mice together with genome-wide analysis of tiss

149 esis of EAE, we generated phenotype-selected congenic mice using EAE-resistant B10.S and EAE-suscepti

150 In our present study, we generated Par1 congenic mice using two mouse strains A/J (Par1/-) and M

151 Congenic mice validated these loci and demonstrated epis

152 d that increased expression of Ifi202 in the congenic mice was associated with inhibition of E2F1-med

153 Retinal function of the resultant congenic mice was evaluated using electroretinographic a

154 A panel of B10 congenic mice was immunized with rCIX emulsified with Fr

155 lls, and Treg cells, a panel of C57BL/6 (B6) congenic mice was tested.

156 strain mapping using autoimmune NOD.C57BL/6J congenic mice, we demonstrated previously that the type

157 Using congenic mice, we determined that the Ts cells in recipi

158 Using congenic mice, we found CD1d polymorphisms affect the th

159 ransfer of CD45.1-positive cells into CD45.2 congenic mice, we show that CD11c(+)Gr-1(+) cells migrat

160 Using H-2 congenic mice, we show that the genetic basis for the va

161 Using H2-congenic mice, we show that the observed difference in f

162 Using NOD congenic mice, we validate that both the MHC and the chr

163 urine samples from each of two panels of MHC congenic mice were analyzed by gas chromatography.

164 ient (C5(-/-)) macrophages derived from B.10 congenic mice were found to be defective in killing intr

165 erived LSK(-) cells upon transfer into naive congenic mice were found to differentiate predominantly

166 type C57/Bl6 mice and LDL-receptor deficient congenic mice were randomly assigned for infection with

167 After colonic preparation, 20 anesthetized congenic mice were scanned with high-resolution microCT.

168 in-dependent variation as well, we generated congenic mice where the telomeric region of chr.4 was in

169 pared with CD4(+) T cells from NOD.H2(b) MHC-congenic mice (which have an H2(b) MHC region introgress

170 tablished in NOD.Cg-Rag1(tm1Mom)Prf1(tm1Sdz) congenic mice, which are devoid of NK cell activity.

171 In this study, we used C57BL/6.S (B6.S) congenic mice, which carry H-2(s) MHC genes instead of H

172 nificantly increased in the B6.C3H(Dyscalc1) congenic mice, which carry only the Dyscalc1 locus with

173 neration compared with T cells from NOD.Idd3 congenic mice, which carry the protective Idd3 allele fr

174 es in splenic cells from lupus-prone B6.Nba2 congenic mice, which express increased levels of p202, w

175 ing pancreatic IL-10 backcrossed to B10.H2g7 congenic mice, which have no Idd alleles other than NOD

176 hem susceptible to Salmonella, and BALB/c.D2 congenic mice, which have the wild-type Nramp1 gene that

177 ses of CD4(+) T cells from NOD and B6.G7 MHC congenic mice, which share the H2(g7) MHC region but dif

178 that differ genetically only at the MHC (MHC congenic mice), while they cannot distinguish geneticall

179 class II-deficient mice engrafted readily in congenic mice, while HSC from class I-deficient donors (

180 ssion for RP1 disease, the authors generated congenic mice with a gene-targeted retinitis pigmentosa

181 er infection of different inbred strains and congenic mice with a single isolate of H. felis.

182 We showed previously that C57BL/6 congenic mice with an introgressed homozygous 70 cM (125

183 e examined by inferior vena cava ligation in congenic mice with and without alpha2-antiplasmin (alpha

184 We reconstituted lethally irradiated congenic mice with bone marrow progenitors transduced wi

185 lated from the paws of male and female Pgia8-congenic mice with collagen antibody-induced arthritis.

186 Second, in MHC-congenic mice with identical non-MHC genes, is response

187 However, the use of congenic mice with limited phenotypes in this study has

188 In reciprocal C57BL/6 congenic mice with NOD-derived Idd loci, skin allograft

189 newly identified plasmacytomas from NFS.V(+) congenic mice with plasmacytomas of IL6 transgenic, Fasl

190 these modifier(s), we generated recombinant congenic mice with quantitative trait loci (QTL) contain

191 then compared the phenotypes of these triple congenic mice with that of previously characterized B6.S

192 producing the phenotype observed for DC from congenic mice with the NZB c1 70-100 cM interval.

193 in genetically resistant BALB/c.D2(Slc11a1) congenic mice with the wild-type Nramp1 locus.

194 Using congenic mice with varying levels of extracellular super