ライフサイエンスコーパス: AKR

1 AKR control mice did not show the same severity of perio

2 AKR mice developed obesity and a prestage of metabolic s

3 AKR mice were sensitized with conalbumin followed by two

4 AKR mouse peritoneal macrophages (PM) were previously fo

5 AKR-PM failed to increase NOS mRNA synthesis and NO gene

6 AKR.H-2(b) congenic mice, although carrying the responde

7 AKR.H-2(b) veto cell inhibition is virus specific, MHC r

8 AKR.H-2b macrophages were shown not to be required to de

9 AKR/J mice display a hair interior defect (hid) phenotyp

10 AKR/J mice had significantly higher frequencies and numb

11 AKR/J, DBA/2J, and BALB/cByJ or BALB/cJ mice were highly

12 iral CTL restimulation cultures of either 1) AKR.H-2(b) veto cells or 2) a blocking Fas-Ig fusion pro

13 In humans, at least 15 AKR superfamily members have been identified so far.

14 d male mice from other strains (A/J, DBA/2J, AKR/J, BALB/cJ) supplemented with 17-beta-estradiol pres

15 induced anti-GBM disease in DBA/1, C57BL/6, AKR, and NOD mice with recombinant human alpha3(IV)NC1 t

16 ta2, mutated at a site (Y90F) that abolishes AKR-like catalytic activity in other family members, hav

17 he existence of a novel catalytically active AKR, which is associated with mitochondria and expressed

18 ic MMTV-PyMT mice were crossed with 25 AKXD (AKR/J x DBA/2J) recombinant inbred strains to produce F1

19 unit biogenesis and catalytic activity as an AKR oxidoreductase.

20 This results in a unique architecture for an AKR active site with scant catalytic power.

21 ereby the invariant catalytic tyrosine of an AKR has been mutated with retention of kcat values simil

22 ions in the conserved catalytic tetrad of an AKR yielded enzymes which were still catalytically activ

23 The deduced protein sequence revealed an AKR-3 motif located near the N terminus, unlike the othe

24 We used an AKR leukemia murine transplant model, analogous to human

25 tity of amino acid 117 determines whether an AKR can function as a 5 beta-reductase by reorienting th

26 disequilibrium mapping was performed in an (AKR x SAMP1/Fc) backcross to SAMP1/Fc, followed by seque

27 (BALB/c, C3H/HeN, C57BL/6, DBA.1, DBA.2, and AKR) showed progressive resolution of bladder infections

28 C57BL/6 and AKR mice developed a chronic disease course resulting in

29 sis of mice from crosses between C57BL/6 and AKR mice should allow the mapping and subsequent identif

30 oss and F2 progeny derived from C57BL/6J and AKR/J mice were infected with RSV, their lung titers wer

31 oss between two inbred strains (C57BL/6J and AKR/J) were exposed in utero to TCDD.

32 istance and glucose production in the B6 and AKR strains could provide a genetic system for the ident

33 C57BL/6J (B6) and AKR/J (AKR) inbred strains of mice develop a comparable

34 Lymph node cells from susceptible C3H and AKR mice also had increased ability to lyse YAC-1 target

35 re more PGS clusters in uninfected C57BL and AKR mice than in uninfected SAMP8 and SAMR1 mice.

36 ior horn neurons of immunosuppressed C58 and AKR mice and cause paralytic disease (age-dependent poli

37 h high endogenous stem cell numbers (DBA and AKR), but was unrelated to strain-specific progenitor ce

38 A/J and AKR/J mice received weekly injections of azoxymethane (1

39 consistently altered in lesions from A/J and AKR/J mice, respectively.

40 ility in vivo compared to native WT mice and AKR recipients of SAMP BM.

41 used in C3H to B6AF1 (class I mismatch) and AKR to C57BL/6 (complete mismatch) models.

42 change in spine BMD in a cross of SAMP6 and AKR/J mice and conducted association mapping of the synt

43 strain that is resistant to senescence) and AKR/J (a progenitor of the SAM strains) mice were infect

44 /cByJ, A/J, CBA/J, 129/SvevTac, 129/SvJ, and AKR/J mice were screened for the development of latent i

45 intercrosses between C57BL/6J- tub / tub and AKR/J-+/+ F(1)hybrids (AKR intercross) and between C57BL

46 cells in the generation of C57BL/6 (B6) anti-AKR/Gross virus CTL, consistent with their expression of

47 ctivity is higher than that observed for any AKR to date.

48 ds of Mtv-7-containing mouse strains such as AKR.

49 chromosome 17 had been transferred onto a B6.AKR or a C3.SW background.

50 s of conplastic mice (B6.NZB, B6.NOD, and B6.AKR) by administration of dextran sodium sulfate or rect

51 ype as the fibrotic radiation response of B6.AKR-H2(k) mice was significantly less than that of B6 mi

52 on a strongly resistant genetic background, AKR/J (AKR), Min-induced adenoma multiplicity is reduced

53 important role in the transformation of both AKR-2B and NRK cells.

54 red strains: C57BL/6J (B6), BTBR/Pas (BTBR), AKR/J (AKR), and A/J.

55 eles of Mom7: the recessive, enhancing BTBR, AKR, and A/J alleles and the dominant, suppressive B6 al

56 Tolerance was confirmed by AKR skin grafting after antibody clearance.

57 the antiviral response that was decreased by AKR.H-2b spleen cells.

58 esponders were as sensitive to inhibition by AKR.H-2(b) modulator cells as were B6 responders, B6.lpr

59 Consistent with this model, inhibition by AKR.H-2(b) modulator cells was MHC restricted, and resul

60 The 129/Svev, C57BL/6, BALB/cByJ, AKR, and DBA/2 mice developed latent inhibition, but 129

61 al antibodies to high dose (5 x 10(7) cells) AKR (H-2k, MLS-1a) bone marrow.

62 e (3alpha-HSD, AKR1C9), a well-characterized AKR, the catalytic tyrosine is Tyr 55.

63 ays a high catalytic efficiency for a common AKR substrate 9,10-phenanthrenequinone (9,10-PQ).

64 differ in that one residue in the conserved AKR catalytic tetrad, His(120) (AKR1D1 numbering), is su

65 fusion protein (to cultures also containing AKR.H-2(b) veto cells) to block inhibition demonstrated

66 cts in ilea of uninflamed (parental) control AKR/J mice.

67 were shown not to be required to demonstrate AKR/Gross MuLV-specific inhibition, however, confirming

68 We show that B[a]P-7,8-trans-dihydrodiol (AKR substrate) and B[a]P-7,8-dione (AKR product) lead to

69 drodiol (AKR substrate) and B[a]P-7,8-dione (AKR product) lead to the production of intracellular rea

70 Fas mutant mice infused with high dose AKR bone marrow under the cover of antibody were toleran

71 A moth1 allele from either AKR/J, CAST/Ei or 129/Ola is sufficient to protect C57BL

72 lable, TPO nonpeptide mimetics (eltrombopag, AKR-501) bind and activate the TPO receptor by a mechani

73 -restricted epitope, KSPWFTTL, of endogenous AKR/Gross MuLV.

74 lation with tumors induced by the endogenous AKR/Gross murine leukemia virus (MuLV), C57BL/6 mice gen

75 sharp contrast, spontaneous virus-expressing AKR.H-2(b) congenic mice are low/nonresponders for the g

76 ells were susceptible to inhibition by FasL+ AKR.H-2(b) inhibitory cells as the basis for inhibition.

77 ype, are low responders or nonresponders for AKR/Gross MuLV-specific CTL, apparently due to the prese

78 IFN-alpha beta may be the primary reason for AKR-PM refractoriness to induction of NOS in response to

79 ic T-lymphocyte (CTL) responses specific for AKR/Gross murine leukemia virus (MuLV).

80 xamined compared with specific pathogen-free AKR control mice of similar age.

81 Analysis of Acact cDNA from AKR mice revealed a deletion of the first coding exon an

82 eparate AKR.H-2b modulator spleen cells from AKR/Gross MuLV-primed responder cells or the direct tran

83 occurs in the early T-cell compartment from AKR/J mice, animals that are highly susceptible to the s

84 opic murine leukemia virus (MuLV) genes from AKR and C58 mice.

85 eins from tryptic digests of total hair from AKR/J-hid/hid mice, which were predominantly keratins (K

86 h CD4- CD8+ and CD4+ CD8- T lymphocytes from AKR.H-2b mice could inhibit the generation of AKR/Gross

87 s to the study of such diseases, pelage from AKR/J and two other mouse strains without this defect wa

88 e peptides generated among hair samples from AKR/J-hid/hid, FVB/NJ+/+, and LP/J+/+ mice indicated tha

89 Hair shafts from AKR/J mice were deficient in these projections and also

90 he demonstration that Kvbeta is a functional AKR.

91 sterol gallstones, we studied gonadectomized AKR/J mice of both genders that were implanted subcutane

92 lity complex (MHC)-matched (B10.BR[H-2k] --> AKR/J[H-2k]) and mismatched (B10.BR[H-2k] --> DBA/2[H-2d

93 BR (H-2k)) and engraftment (C57BL/6 (H-2b)-->AKR/J (H-2k)).

94 HC-matched murine transplant model (B10.BR-->AKR/J) was adapted.

95 e gene led to hepatic iron levels in Hfe -/- AKR mice that were 2.5 or 3.6 times higher than those of

96 he constitutively and widely expressed human AKR, aldehyde reductase (AKR1A1), will oxidize potent pr

97 ion ratio (V(max)/K(m)) than any other human AKR.

98 7BL/6J- tub / tub and AKR/J-+/+ F(1)hybrids (AKR intercross) and between C57BL/6J- tub / tub and CAST

99 JL/J) F1 offspring of D10 TCR-IgG1-immunized AKR/J mothers making D10 clonotypic Ab, the effect was i

100 In AKR mice, peripheral leptin significantly decreased food

101 a was increased significantly from week 2 in AKR/J mice and from week 4 in BALB/c mice and remained e

102 ald, a recessive allele in AKR inbred mice, is responsible for complete adrenocorti

103 lon, npas2, per1, and per2) were assessed in AKR/J, C57BL/6J, and DBA/2J mice, three strains that exh

104 sk whether adrenocortical lipid depletion in AKR mice results from an Acact mutation.

105 on the prevention of autoimmune diabetes in AKR mice in which the low-dose streptozocin (STZ) model

106 owever, the mechanism of Apc inactivation in AKR Min/+ mice often differs from that observed for B6 M

107 ing (MCF) viruses induce T-cell lymphomas in AKR/J strain mice.

108 h a strong mutagen increases tumor number in AKR Min/+ mice in an age-dependent manner, similar to re

109 y pregnenolone 16alpha-carbonitrile (PCN) in AKR/J mice can prevent the development of high-fat diet-

110 cotransfection of E2F-4-encoding plasmid in AKR-2B cells overcame p202-mediated inhibition of cell g

111 errin saturation, with the highest values in AKR mice and the lowest values in C3H mice.

112 One class, which includes AKR, did not initiate normal testis development in B6 T(

113 apparently due to the presence of inhibitory AKR.H-2(b) cells.

114 echanism based on the presence of inhibitory AKR.H-2b cells was examined.

115 B6.gld mice, indicating that the inhibitory AKR.H-2(b) cells express FasL.

116 Upon inoculation into AKR mice, mink cell focus-forming murine leukemia virus

117 ) bone marrow cells into lethally irradiated AKR/J recipients.

118 t on alloengraftment, sublethally irradiated AKR mice underwent transplantation with TCD B6 BM plus l

119 NA from cog/cog mice and unaffected isogenic AKR/J mice.

120 ferent time points, SAMP and parental AKR/J (AKR) control mice were sacrificed, and mandibles were pr

121 C57BL/6J (B6) and AKR/J (AKR) inbred strains of mice develop a comparable degree

122 The AKR/J (AKR) strain carries alleles that correlate with a strong

123 ains: C57BL/6J (B6), BTBR/Pas (BTBR), AKR/J (AKR), and A/J.

124 trongly resistant genetic background, AKR/J (AKR), Min-induced adenoma multiplicity is reduced by abo

125 strain SAMP6 and control strains SAMR1, A/J, AKR/J, BALB/c, C3H/HeJ, C57BL/6J, and DBA/2J.

126 rent inbred mouse strains (129S1/SvImJ, A/J, AKR/J, BALB/cByJ, BTBR T+ tf/J, C3H/HeJ, C57BL/6J, C57L/

127 tested 12 inbred mouse strains (129/J, A/J, AKR/J, BALB/cJ, C3H/HeJ, C57BL/6J, C57BL/10J, C58/J, CBA

128 sucrose (10%) intake in eleven inbred (A/J, AKR/J, BALB/cJ, CBA/J, C3H/HeJ, C57BL/6J, C57BL/10J, DBA

129 era-injected mice and anti-GBM-injected A/J, AKR/J, C3H/HeJ, DBA/2J, MRL/MpJ, NOD/LtJ, P/J, SJL/J, an

130 st treatment was not achieved in three (A/J, AKR/J, CBA/J) inbred mouse strains.

131 A/J, AKR/N, C3H, and DBA/1J mice also had higher peak parasit

132 fed murine strains C57L/J, C57BL/6J, SWR/J, AKR/J, PE N-methyltransferase (PEMT) knockout (KO), PEMT

133 SJL/NCr, BALB/cAnNCr, A/JCr, C3H/HeJ, SWR/J, AKR/NCr, CBA/NCr, C58/J, DBA/2NCr, C3H/HeNCr, C3HeB/FeJ,

134 ) and is a member of the aldo-ketoreductase (AKR) superfamily.

135 ent comparable to that attained by the known AKR inhibitor epalrestat.

136 hia muris infection in immunocompetent mice (AKR and C57BL/6 strains) correlated with their antibody

137 sparate (DBA/2 to B6AF1), complete mismatch (AKR to C57BL/6), and xenograft (ACI rat to B6AF1).

138 In an in vivo thymocyte repopulation model, AKR/J thymocytes had a selective advantage over healthy

139 ent TF promoter/ reporter construct in mouse AKR-2B fibroblasts.

140 of basal SmalphaA enhancer activity in mouse AKR-2B stromal fibroblasts.

141 When injected into neonatal AKR mice, MCF ProEn was more pathogenic than the parenta

142 repubescent female C57BL/6J, DBA/2J, FVB/NJ, AKR/J, A/J, and BALB/cJ mice towards prepubescent DBA/2J

143 ee obese strains of mice: diet-induced obese AKR/J, New Zealand Obese (NZO), and Ay.

144 e B6 mice are more glucose intolerant, obese AKR mice are more insulin resistant.

145 on was shown not to be due to the ability of AKR.H-2b cells to function as unlabeled competitive targ

146 This combination of AKR modifiers can almost completely suppress spontaneous

147 production), dependent on direct contact of AKR.H-2(b) cells in a dose-dependent manner with the res

148 nhibition was dependent on direct contact of AKR.H-2b cells in a dose-dependent manner with the respo

149 This partial deficiency of AKR-PM to lipid A stimulation was reconstituted complete

150 tudy, we examined the cellular expression of AKR family member, succinic semialdehyde reductase (AKR7

151 are low/nonresponders for the generation of AKR/Gross MuLV-specific CTL.

152 KR.H-2b mice could inhibit the generation of AKR/Gross virus-specific CTL in vitro.

153 beta-induced anchorage-independent growth of AKR-2B cells.

154 s blocked in SAMP1/Fc mice by inheritance of AKR alleles on chromosome 6 in the region of Pparg .

155 ed with the mesenteric lymph nodes (MLNs) of AKR control mice, SAMP1/YitFc MLNs contain a 4.3-fold ex

156 in the membrane-spanning domain of p15TM of AKR/Gross murine leukemia viruses (MuLV).

157 samples from reciprocal cross F1 progeny of AKR and PWD mouse strains and quantified the allele-spec

158 strating that this was a general property of AKR-generated PAH o-quinones.

159 t, as demonstrated by indefinite survival of AKR skin grafts.

160 This resulted in increased survival of AKR/J early thymocytes, shown by the decreased frequency

161 Compared with adipose tissue of AKR mice, adipose tissue of B6 mice contained about thre

162 -induced proliferation and transformation of AKR-2B and NRK fibroblasts.

163 cytometry, enabling direct visualization of AKR.H-2(b) veto cell-mediated depletion of these CTL.

164 ised by nonrelated mothers from the AKR/Ola (AKR) and C3H/He (C3H) strains exhibiting low- and high-p

165 e crossed C57Bl/6J mice with either SWR/J or AKR/J mice and examined the effect of MPTP on F1 C57BL/6

166 ocated near the N terminus, unlike the other AKR family members where it is confined to the C terminu

167 the AKR-3 motif that is similar to the other AKR members.

168 In contrast with other AKR enzymes, which are mostly cytosolic, AKR1B15.1 co-lo

169 , BALB/cJ, and FVB/J) but not in the others (AKR/J, 129/svJ, and C57BL/6J).

170 At different time points, SAMP and parental AKR/J (AKR) control mice were sacrificed, and mandibles

171 ulated NOD2 signaling compared with parental AKR control mice.

172 aphylaxis was a strain-dependent phenomenon, AKR/J and BALB/c mice also received multiple i.m. pAra h

173 nteraction mechanism: viral antigen-positive AKR.H-2(b) cells expressing FasL inhibit antiviral T cel

174 hese purified recombinant proteins possessed AKR activity using various cytotoxic aldehydes including

175 ted in either C57BL/6 or DBA/2 (and possibly AKR) mice.

176 Homozygosity for the protective AKR allele of Mor1 restores cell adhesion in Rs1tmgc1 mi

177 A putative AKR in complex with a Kv channel has led to the hypothes

178 Stimulation of quiescent AKR-2B mouse fibroblasts with transforming growth factor

179 sublethally irradiated (800 cGy) recipients (AKR/J, H-2k) is dependent on the presence of mature dono

180 ed a novel member of the aldoketo reductase (AKR) superfamily of cytosolic NAD(P)(H)-dependent oxidor

181 eroid dehydrogenase, or aldo-keto reductase (AKR) 1C2, eliminates the androgen signal in human prosta

182 Aldo-keto reductase (AKR) family 1, member 7 (AKR1B7), a member of the AKR su

183 Aldo-keto reductase (AKR) inhibitors blocked this effect, suggesting that ben

184 known structure in the aldo-keto reductase (AKR) superfamily and may provide a paradigm for other ma

185 ymes are members of the aldo-keto reductase (AKR) superfamily and possess catalytic tetrads differing

186 1C9) is a member of the aldo-keto reductase (AKR) superfamily which inactivates circulating steroid h

187 AKR1C4), members of the aldo-keto reductase (AKR) superfamily, activate trans-dihydrodiols by convert

188 SD/DD), a member of the aldo-keto reductase (AKR) superfamily, oxidizes PAH trans-dihydrodiols to red

189 nels are members of the aldo-keto reductase (AKR) superfamily.

190 rogenases (HSDs) of the aldo-keto reductase (AKR) superfamily.

191 t liver 3 alpha-HSD, an aldo-keto reductase (AKR) that plays critical roles in steroid hormone inacti

192 hat Kvbeta resembles an aldo-keto reductase (AKR), an enzyme that catalyzes a redox reaction using an

193 LR2), a NADPH-dependent aldo-keto reductase (AKR), is widely distributed in mammalian tissues and has

194 Human aldo-keto reductase (AKR)1C isoforms have been shown to act as 3alpha/3beta-h

195 Aldo-keto reductases (AKR) are monomeric oxidoreductases that retain a conserv

196 hol dehydrogenases and aldo-keto reductases (AKR).

197 We bred SAMP1/Fc to disease-resistant AKR mice to identify additional susceptibility genes tha

198 red at high risk, whereas ACF from resistant AKR/J mice were considered at low risk for tumorigenesis

199 SWR mice but not in the gallstone-resistant AKR mice.

200 n of leptin to peripherally leptin-resistant AKR mice on 45% fat diet resulted in a robust response t

201 catalysts for aminolytic kinetic resolution (AKR) of a variety of terminal epoxides and glycidyl ethe

202 an eight-way cross of C57BL/6, BALB/c, RIII, AKR, DBA/2, I, A/J and C3H inbred mouse strains.

203 exhibits the most robust EEG response to SD (AKR/J) exhibited dramatic increases in expression of bma

204 rom GCV-treated chimeric mice into secondary AKR recipients failed to cause GVHD indicating that dono

205 emipermeable membranes were used to separate AKR.H-2b modulator spleen cells from AKR/Gross MuLV-prim

206 This inhibition is specific (AKR.H-2(b) modulator spleen cells do not inhibit allogen

207 This inhibition was specific: AKR.H-2b modulator spleen cells did not inhibit allogene

208 es (Sry(DOM) alleles, e.g., Sry(POS) and Sry(AKR)) onto the C57BL/6J (B6) mouse strain causes abnorma

209 bout half the level of Sry(RIII) whereas Sry(AKR) and Sry(RIII) were equally expressed.

210 TL responses stimulated in vitro by standard AKR/Gross MuLV-induced tumor cells.

211 the Mor1 allele from the inbred mouse strain AKR/J diminishes the severity of the schisis phenotype i

212 However, the other resistant strain (AKR) did not show a Th2-dominated response pattern, in t

213 (moth1), whose wildtype alleles from strains AKR/J, CAST/Ei and 129P2/OlaHsd protect tubby mice from

214 d in an intercross between the mouse strains AKR/J and C57L/J.

215 scores of SCCs whereas the resistant strains AKR/J, 129/svJ, and C57BL/6J failed to develop any SCCs.

216 ll as four common inbred laboratory strains (AKR/J, HRS/J, C3H/HeJ, and C57BL/6J).

217 different genetically defined mouse strains (AKR, C57BL/6, and C3H), which differ in basal iron statu

218 C57BL/6 (B6; H-2(b)) mice mount strong AKR/Gross murine leukemia virus (MuLV)-specific CD8(+) C

219 inal nematode Trichuris muris in susceptible AKR mice, which mount a Th1 response, is associated with

220 Obesity-susceptible AKR mice were fed with high-fat diet (HFD) or normal low

221 ongenic strains, derived from 129S6/SvEvTAC, AKR/J, APN, BALB/cJ, BTBR-T+ tf/tf, C3H/HeJ, C57BL/6J, D

222 le mice from 14 inbred strains (129S1/SvImJ, AKR/J, BALB/cJ, BALB/cByJ, BTBR T+tf/J, C3H/HeJ, C57BL/1

223 , including 10 resistant strains (129X1/SvJ, AKR/J, C3H/HeJ, C57BL/6J, DBA/2J, NZB/BlnJ, CAST/EiJ, SP

224 insulin and are more insulin sensitive than AKR mice.

225 reputial gland homogenates demonstrated that AKR mice had an ACAT protein with a lower molecular mass

226 versible inhibitor emetine demonstrated that AKR.H-2(b) cells had to be metabolically active and capa

227 cells) to block inhibition demonstrated that AKR.H-2(b) veto cells begin to inhibit B6 precursor CTL/

228 Previously, we determined that AKR/J (susceptible) mice developed high lung RSV titers

229 otective allele of Mtap1a, and we found that AKR is not protective for hearing in the (DW/JxAKR) Pou1

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

231 The AKR/J (AKR) strain carries alleles that correlate with a

232 The AKR/J chromosome 17 locus was not sufficient to increase

233 The AKR/J Obq3 allele confers increased adiposity in a nearl

234 e B6 Y chromosome (Y(B6)) is replaced by the AKR Y chromosome (Y(AKR)), B6 Fog2-/+ XY(AKR) mice devel

235 tures, relieved the inhibition caused by the AKR.H-2(b) cells if the primed responders were from eith

236 ed responder B6 antiviral precursor CTL, the AKR.H-2(b) cells function as "veto" cells that actively

237 First, the AKR strain carries modifiers of Min in addition to Mom1.

238 egion likely to have been inherited from the AKR mouse strain.

239 tein sequences with representatives from the AKR superfamily, the proteins were ascribed not to the A

240 s were raised by nonrelated mothers from the AKR/Ola (AKR) and C3H/He (C3H) strains exhibiting low- a

241 dione formation in A549 cells implicates the AKR pathway in the metabolic activation of PAH in human

242 th a LOD score of 33.4 ( P < 10(-33)) in the AKR intercross (181 mice) and of 6.0 ( P < 10(-6)) in th

243 is similar to other binary complexes in the AKR superfamily in that NADP+ binds at the C-terminal en

244 hymocytes and thymic lymphoma in mice of the AKR and NFS strains when they are inoculated neonatally.

245 The relative contribution of the AKR and P450 pathways to cell cycle arrest was assessed.

246 family 1, member 7 (AKR1B7), a member of the AKR superfamily, has been suggested to play an important

247 autosomal genes, and (3) the presence of the AKR Y chromosome.

248 its ability to induce transformation of the AKR-2B and NRK fibroblasts but was later found to be a p

249 tumors initiated by allelic silencing on the AKR Apc(Min) genetic background is strongly skewed towar

250 In this genetic region, the AKR strain is known to carry a mutation in the tyrosinas

251 Since the AKR function of Kvbeta has never been demonstrated, a di

252 a renal-specific reductase belonging to the AKR family, representational difference analyses of cDNA

253 bit antiviral T cells ("veto" them) when the AKR.H-2(b) cells are recognized.

254 we have generated a mouse line in which the AKR allele of Mom1 is carried on the sensitive B6 geneti

255 s genome includes at least 21 genes with the AKR signature, very little is known of their functions.

256 /J-Pou1f1dw/+ carriers were crossed with the AKR strain, which also carries a protective allele of Mt

257 peptide (Met-Ala-Lys-Ser) located within the AKR-3 motif that is similar to the other AKR members.

258 8+ T cell population was unperturbed in the (AKR/J x SJL/J) F1 offspring of D10 TCR-IgG1-immunized AK

259 ention of quinone reductase activity in this AKR in the absence of Tyr 55 with kcat versus pH rate pr

260 ther nuclear receptor known to regulate this AKR isoform.

261 tinal tumors from both untreated and treated AKR Min/+ mice.

262 Irradiated or mitomycin C-treated AKR.H-2b spleen cells function as in vitro stimulator ce

263 SAMP mice receiving wild-type (AKR) BM developed severe ileitis, whereas SAMP BM did no

264 tly through either chaperone-like or typical AKR catalytic activity.

265 erage video intensity, in SAMP vs uninflamed AKR mice (P < .001) or SAMP given nonspecific MB (P < .0

266 ility to lethal GHVD when transplanted using AKR/J donors.

267 Propranolol (beta-blocker) as a key step via AKR of single racemic naphthylglycidyl ether with Boc-pr

268 Viable AKR.H-2b spleen cells were also able to cause dramatic (

269 n of viral antigens and Kb, untreated viable AKR.H-2(b) spleen cells cause dramatic inhibition of the

270 In contrast, untreated viable AKR.H-2b spleen cells functioned very poorly as stimulat

271 Furthermore, when viable AKR.H-2(b) spleen cells are cocultured with primed respo

272 In vitro, AKR 1A and 1B catalyzed the reduction of AGE precursors,

273 on by lamina propria lymphocytes (P <.05 vs. AKR controls).

274 Crossing Acact-/- with AKR (ald/ald) mice yielded postpubertal male offspring c

275 entage of B6 tetramer(+) CTL cocultured with AKR.H-2(b) veto cells was annexin V positive and Fas(hig

276 everely impaired in these mice compared with AKR mice (controls).

277 SAMP mice showed greater ABL compared with AKR mice by 12 weeks of age, with maximal differences ob

278 BALB/cT females were crossed with AKR/J males to generate F1 females.

279 al CTL response to in vitro stimulation with AKR/Gross MuLV-induced tumor cells.

280 2 M-MULV-induced tumor DNAs from C57BR/cdJ x AKR/J F1 (BRAKF1) hybrid mice.

281 xpressed in the mammary glands of (BALB/cT x AKR/J)F1 mice, acquired a specific DNA sequence from BAL

282 Foster nursing of BALB/cT mice on (BALB/cT x AKR/J)F1 mothers resulted in the generation of a new mou

283 The (SJL/J x AKR/J) F1 offspring of immunized female SJL/J mice were

284 In D10 TCR-IgG1 maternally immunized (SJL x AKR/J) F1 mice, the T cell responses to pCA(134-146) wer

285 mutant mice from a B6-Tulp1(tm1Pjn/tm1Pjn) x AKR/J intercross were genotyped with a panel of single n

286 re identified in a B6-Tulp1(tm1Pjn/tm1Pjn) x AKR/J intercross.

287 uses develop ovaries and ovotestes and B6 XY(AKR) fetuses have delayed testis cord development.

288 range of aberrant testis development: B6 XY(AKR), B6 XY(POS), and (BXD-21 x B6-Y(POS))F1 XY(POS).

289 Furthermore, DBA/2J (D2) Fog2-/+ XY(AKR) mice and (B6 x D2)F1 hybrid Gata4(ki)/+ XY(AKR) mic

290 the AKR Y chromosome (Y(AKR)), B6 Fog2-/+ XY(AKR) mice develop ovaries, and B6 Gata4(ki)/+ XY(AKR) mi

291 mice develop ovaries, and B6 Gata4(ki)/+ XY(AKR) mice develop ovaries and ovotestes (gonads containi

292 ) mice and (B6 x D2)F1 hybrid Gata4(ki)/+ XY(AKR) mice develop testes.

293 development in B6 Fog2-/+ or Gata4(ki)/+ XY(AKR) mice.

294 nd that Sry is transcribed in B6 T(Orl)/+ XY(AKR) fetal gonads but at a reduced level.

295 s development was restored in B6 T(Orl)/+ XY(AKR) mice carrying a Mus musculus Sry transgene.

296 normal testis development in B6 T(Orl)/+ XY(AKR) mice results from a biologically insufficient level

297 e been developed with either transient (B6-Y(AKR)) or severe (B6-Y(TIR)) XY(DOM) sex reversal.

298 In B6-Y(AKR), penetrance of the trait is low; however, in B6-Y(T

299 -derived Sry allele (B6-Y(POS,RIII) and B6-Y(AKR,RIII)).

300 (B6)) is replaced by the AKR Y chromosome (Y(AKR)), B6 Fog2-/+ XY(AKR) mice develop ovaries, and B6 G