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

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