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1 g mice carrying altered copies of a targeted gene ('knockout mice').
2 ood pressure (shared by some but not all BBS gene knockout mice).
3 rmed with the pharmacological inhibition and gene knockout mice.
4 ions in glucose metabolism in transgenic and gene knockout mice.
5 ble for IL-10 upregulation was determined in gene knockout mice.
6 on RI-stimulated mast cells derived from btk gene knockout mice.
7 d -0.6 kb of upstream sequence into beta3-AR gene knockout mice.
8 g the generation and analysis of conditional gene knockout mice.
9 evel of glutathione peroxidase using GSHPx-1 gene knockout mice.
10 ng-term potentiation between control and PrP gene knockout mice.
11 P4A mRNAs was also blocked in the PPAR alpha gene knockout mice.
12 ing into question negative results in single-gene knockout mice.
13  phenotypes appearing in previously analyzed gene knockout mice.
14 ere markedly reduced in TNF receptor 1 and 2 gene knockout mice.
15 s can predict the lethal phenotype of single-gene knockout mice.
16 where possible, testing of islet tissue from gene knockout mice.
17 out mice and sphingomyelin synthase 2 (Sms2) gene knockout mice.
18 rkedly reduced in tamoxifen-inducible Nkx2-5 gene knockout mice.
19 n responses, studies were performed in COX-2 gene knockout mice.
20 r mice, an adoptive cell transfer model, and gene knockout mice.
21 nt with neutralizing antibodies and cytokine gene knockout mice.
22 through use of the appropriate transgenic or gene knockout mice.
23 against this parasite has been studied using gene knockout mice.
24 ological inhibitors of iNOS, as well as iNOS gene knockout mice.
25 uli infection was further evaluated by using gene-knockout mice.
26 on using pharmacological inhibitors and iNOS gene-knockout mice.
27 neutrophils obtained from A(2A)AR and A(3)AR gene "knockout" mice.
28 bolished in pancreatic beta cells from Tpcn2 gene knockout mice [2].
29 ic effects, we analyzed these factors in Ada gene knockout mice (Ada(-/-)).
30 Our previous study reported that adiponectin gene knockout mice (Adipoq (-/-) ) develop GDM due to in
31 /6 major histocompatibility complex class II gene knockout mice and CD4 cell-depleted C3H mice (i.e.,
32                                        Using gene knockout mice and in vivo cellular depletion method
33 d lipolysis was observed in both adiponectin gene knockout mice and primary adipocytes from these mic
34                                        Using gene knockout mice and siRNA to silence mouse genes, we
35 ll as in plasma samples from six cholestatic gene knockout mice and six age- and gender-matched wild-
36 almitoyltransferase (SPT) subunit 2 (Sptlc2) gene knockout mice and sphingomyelin synthase 2 (Sms2) g
37             METHODS AND We used H- and K-Ras gene knockout mice and subjected them to pressure overlo
38 antibody-deficient muMT mice (immunoglobulin-gene knockout mice), and CD4(+) spleen T cells from immu
39                      Cataract development in gene-knockout mice appeared to progress from focal opaci
40 ecific mechanisms are unclear since the CB2R gene knockout mice are constitutive gene knockout.
41 tivator of transcription 4 (STAT4) and STAT6 gene knockout (-/-) mice as recipients of fully mismatch
42  smooth muscle-specific acid ceramidase (Ac) gene knockout mice (Asah1(fl/fl)/SM(Cre)) were used to d
43 ntribution to its etiology, including single-gene knockout mice associated with diaphragmatic defects
44                    Using B(2) kinin receptor gene knockout mice (B(2)(-/-)), we tested the hypothesis
45                           We generated Necl4 gene knockout mice, but found that disruption of Necl-4
46 feration were compared in wild-type and Zeb1 gene knockout mice by immunostaining, real-time PCR, and
47                             We have produced gene knockout mice by targeted disruption of the apobec-
48 f EP2 has been extensively studied using EP2 gene knockout mice, cellular models, and selective small
49 ed, major histocompatibility complex class I gene knockout mice compared with no deaths for wild-type
50 ncrease in nuclear light scattering (NLS) in gene-knockout mice compared with control animals.
51           The analysis of vanilloid receptor gene knockout mice confirms the involvement of this chan
52                                           In gene knockout mice deficient in either CD3delta or CD3ga
53 e production in Schistosoma mansoni-infected gene knockout mice deficient in either CD8 lymphocytes o
54                 However, studies in connexin-gene knockout mice demonstrated significant CV slowing o
55 % compared with only 49% in control beta3-AR gene knockout mice, demonstrating that the human beta3-A
56 indicated that IFN-gamma-/- and IL-12 p40-/- gene knockout mice developed CTL responses equivalent to
57 n an unexpected result, lenses in the alphaB gene knockout mice developed normally and were remarkabl
58 -1(-/-)) and heterozygous (Flt-1(+/-)) Flt-1 gene knockout mice display increased endothelial cell pr
59                                   Adult IL-2 gene-knockout mice displayed exaggerated gamma c express
60 ut mice into R. australis-infected IFN-gamma gene knockout mice dramatically reduced the infectious r
61 nsgene) were bred with apo E or LDL receptor gene knockout mice (E0 or LDLr0 mice).
62 , fetal liver-derived macrophages from SHIP2 gene knockout mice enhanced activation of Akt in respons
63 al intracerebral hemorrhage, whereas AbetaPP gene knockout mice exhibited reduced hemorrhage size.
64 ontrol, perforin gene-knockout, and granzyme gene-knockout mice exposed by the realistic pulmonary ro
65  deletion of CB1, CB2, or GPR55 receptors in gene-knockout mice failed to alter BCP's action against
66 le wild-type mice and in the original single gene knockout mice for ERalpha (ERalphaKO(Chapel Hill) [
67 promoter and interbreeding of transgenic and gene knockout mice for generating a mouse strain that ex
68                                 Data from B7 gene knockout mice further clarify the importance of CD8
69 n colon carcinogenesis, we generated gastrin gene knockout mice (GAS-KO).
70                                    In double gene knockout mice generated by crossing these animals (
71 pared with the wild-type controls, the B(2)R gene knockout mice had a higher baseline BP (109.7+/-1.1
72 nt in E. faecalis infection, since IFN-gamma gene knockout mice had reduced mortality and massive coa
73 ce, interleukin-4, but not interferon-gamma, gene knockout mice had significantly less S. aureus bind
74     Recently, the use of transgenic mice and gene-knockout mice has allowed investigators to evaluate
75                                    As yet no gene knockout mice have been engineered, and so there is
76 revious in vitro studies with transgenic and gene-knockout mice have shown that lenses with elevated
77          We have used interleukin-10 (IL-10) gene knockout mice (IL-10-/-) to examine the role of end
78                           We have used IL-10 gene knockout mice (IL-10T) to examine the role of endog
79 C. parvum was then evaluated in C57BL/6 IL-4 gene knockout mice (IL-4(-/-)).
80 llicular pathway is significantly delayed in gene knockout mice in which both the endothelial and neu
81  similar deficit has been reported in Hoxa-1 gene knockout mice in which pattern formation of the hin
82                                       Use of gene-knockout mice indicates that depletion of BM B cell
83  and susceptible mice as well as in cytokine gene knockout mice infected with Trypanosoma brucei rhod
84 of wild type BALB/C mice or interferon-gamma gene knockout mice, interleukin-4, but not interferon-ga
85 r of immune CD8 T lymphocytes from IFN-gamma gene knockout mice into R. australis-infected IFN-gamma
86 subset depletion studies and the analysis of gene knockout mice, it is evident that CD8(+) T cells co
87                                      The ACE gene knockout mice lack both isozymes and they exhibit l
88 (kb) of human beta3-AR genomic sequence into gene knockout mice lacking beta3-ARs.
89  all effects of CL were completely absent in gene knockout mice lacking beta3-ARs.
90                                   In C57BL/6 gene knockout mice lacking either functional TCRs or MHC
91 is enhancement was lost almost completely in gene knockout mice lacking either TCRs or MHC class II m
92                       Recently, we generated gene knockout mice lacking functional beta3-ARs and demo
93 ouse embryonic fibroblast cells derived from gene knockout mice lacking the gene for RNase L(-/-) or
94 lyceride metabolism in lysosomal acid lipase gene knockout mice (lal-/-) results in severe pathogenic
95   Based on studies with LPS-nonresponder and gene-knockout mice, LPS-induced proliferation of CD44(hi
96                      Finally, in cathepsin L gene knockout mice, [Met]enkephalin levels in brain were
97                                   The use of gene-knockout mice permits an increased insight into the
98 d a significant increase in opacification in gene-knockout mice relative to control animals of the sa
99 ice were adoptively transferred into various gene-knockout mice rendered T cell-deficient by subletha
100 contrast, deletion of PN2/AbetaPP in AbetaPP gene knockout mice resulted in a significant increase in
101                                  Analysis of gene knockout mice revealed that CAR is also indispensab
102                     Furthermore, analyses of gene knockout mice revealed that Nfia is specifically re
103 e organ of Corti of homozygous Cx26 and Cx30 gene knockout mice show that cochlear hair cells degener
104 ing to echocardiography, we found that Efnb3 gene knockout mice showed enhanced constriction in the c
105     Accordingly, cultured T-cells from Spry1 gene knockout mice showed increased proliferation in res
106 -deficient Tc2 cells generated from perforin gene knockout mice showed no differences in therapeutic
107                                       Single gene-knockout mice showed roles for both TRPA1 and TRPV1
108 onsisted of a single population spike in PrP gene knockout mice similar to that recorded from control
109  manganese superoxide anion dismutase (SOD2) gene-knockout mice (SOD2+/-), in which SOD2 activity is
110 ol mice only until day 8 p.i., in all of the gene knockout mice studied except those lacking C3 and C
111                                              Gene knockout mice studies indicate that urokinase-type
112               Furthermore, studies involving gene knockout mice suggest that long-term depression, a
113                                 Studies with gene knockout mice suggested that IL-10, but not IL-4, c
114 eased after pulmonary infection of IFN-gamma gene knockout mice, suggesting a protective role for IFN
115 otective effect of A(1)AR activation in iNOS gene-knockout mice suggests a direct cause-and-effect re
116 ponse to pathogens, it was noted that in CD4 gene knockout mice, the CD8 population made significant
117 With the use of three distinctive strains of gene knockout mice, the current study has provided the f
118 strumental for the susceptibility of the HFE gene knockout mice to cardiac injury.
119 nimal model for DMD, were crossed with Flt-1 gene knockout mice to create a model with increased vasc
120           In the present study, we have used gene knockout mice to define an essential role for MyD88
121                              We used various gene knockout mice to examine the role of donor T cells
122                                      We used gene knockout mice to explore the role of Angiopoietin-l
123                                 We used CaSR gene knockout mice to investigate the role of the CaSR i
124 om hippocampal slices of prion protein (PrP) gene knockout mice to investigate whether the loss of th
125 d a streptozotocin-induced DKD model in FHL2 gene-knockout mice to determine the possible role of FHL
126                 In fibroblast cells from p53 gene knockout mice, transfection with E6 also conferred
127 he central corneal epithelium of C57BL/6 and gene knockout mice was abraded, and 1 x 10(7) S. marcesc
128  Cutaneous wound healing model in miR-29a/b1 gene knockout mice was used to identify miR-29 targets i
129                         In this study, using gene knockout mice, we show that Rap1b is the dominant i
130                            P- and E-selectin gene knockout (-/-) mice were immunized with antigens ex
131 r mammalian-cell viability in vivo: calnexin gene knockout mice were carried to full term, although 5
132                The observation that perforin gene knockout mice were more than 100-fold more suscepti
133                 Gamma interferon (IFN-gamma) gene knockout mice were more than 100-fold more suscepti
134  that inducible nitric oxide synthase (iNOS) gene knockout mice were resistant to endotoxin-induced b
135                                          The gene knockout mice were screened for cataract with slit
136 in systemic autoimmunity, IL-4 and IFN-gamma gene knockout mice were studied for susceptibility to th
137                                  MHC class I gene knockout mice were the most susceptible, more than
138                               When IFN-gamma gene knockout mice were used as graft recipients, the re
139                           TRPA1/TRPV1 double gene-knockout mice were more susceptible to adhesion of
140 by targeted disruption of the 5-lipoxygenase gene (knockout mice) were studied following intratrachea
141 % of CD4+ T cells, or from MHC-class II I-Ab gene knockout mice, where they constitute 42% of CD4+ T
142        This idea is supported by analysis of gene-knockout mice, which uncovered crucial roles of sev
143 g the estrogen-synthesizing enzyme aromatase gene knockout mice with APP23 transgenic mice, a mouse m
144 of lens in vivo by comparing lens changes of gene-knockout mice with age-matched control animals.
145    Tamoxifen-inducible podocyte-specific Yap gene knockout mice (Yap(podKO)) exhibited accelerated an

 
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