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1                                                       Next, we crossed 5xFAD mice with pGFAP:BDNF mice (only males were u
2 o model the phenotypic variability observed among patients, we crossed a Drosophila model of NGLY1 deficiency onto a pane
3                 To understand this mechanism of resistance, we crossed a p110alpha conditional (p110alpha(flx/flx)) mouse
4                                              In this study, we crossed a transgenic prostate adenocarcinoma mouse model,
5        To determine the roles of Akt isoforms in this model we crossed Akt1(-/-), Akt2(-/-), and Akt3(-/-) mice with PV m
6 igate interactions between heterozygosity and recombination we crossed Arabidopsis lines carrying fluorescent crossover r
7                                                      First, we crossed ataxin-2 knockout mice with TDP-43 (also known as
8 y address the role of Runx1 in CBFB-MYH11-induced leukemia, we crossed conditional Runx1 knockout mice (Runx1f/f) with co
9 p of IKKbeta to HTT S13 phosphorylation and HD progression, we crossed conditional tamoxifen-inducible IKKbeta knockout m
10                                                             We crossed diabetic leptin receptor-mutant mice to mice lacki
11                                                             We crossed DO mice with syngeneic HER2 transgenic mice to stu
12                                                             We crossed Drp1+/- mice with APP transgenic mice (Tg2576 line
13                                                             We crossed Drp1+/- mice with Tau transgenic mice (P301L line)
14                                    To test this hypothesis, we crossed DYT1 knock-in with p58(IPK)-null mice.
15                                                    Finally, we crossed EP3R conditional knock-out mice with either VGluT2
16                                    To test this hypothesis, we crossed gamma-sarcoglycan-null mice, a model of limb-girdl
17                                                             We crossed Hdac3 conditional knockout mice with Mb1-Cre knock
18 Idh1 mutation as an oncogenic driver in the T-cell lineage, we crossed Idh1-KI mice with conditional Trp53 null mice, a w
19                                                             We crossed Irf6 heterozygous ( Irf6(+/-)) mice with transgeni
20 plore the function of KAT8 during mouse oocyte development, we crossed Kat8(flox/flox) mice with Gdf9-Cre mice to specifi
21                                       To test this further, we crossed Kit(W-sh/W-sh) mice with signal transducer and act
22                                                       Here, we crossed MA lines of the green alga Chlamydomonas reinhardt
23 ute 2 (MDM2)-p53 pathway to APC loss-induced tumorigenesis, we crossed mice bearing MDM2(C305F) mutation, which disrupts
24  that cooperate with STAT5 activation to initiate leukemia, we crossed mice expressing a constitutively active form of ST
25 d the role of IMP2 in hepatic triglyceride metabolism, here we crossed mice expressing albumin-Cre with mice bearing a fl
26                                            To address this, we crossed mice harboring floxed Glp1r alleles to mice expres
27  whether the upstream kinase JAK2 exerts similar functions, we crossed mice harbouring a hepatocyte-specific deletion of
28                   To disambiguate these the two mechanisms, we crossed mice in which channelrhodopsin is endogenously exp
29                                                             We crossed mice overexpressing human retinol-binding protein
30                                   To address this question, we crossed mice-bearing knock-out of Klf9, an ubiquitous tran
31                                                             We crossed MIP-TF mice with A(vy) mice which develop obesity
32                                                             We crossed one genome-edited dairy bull, homozygous for the d
33                                       In our current study, we crossed our Lpd conditional knockout mice with a mouse lin
34    To investigate the role of mTORC1 in the diabetic heart, we crossed OVE26 type 1 diabetic mice with transgenic mice ex
35                                                             We crossed p48-Cre;LSL-Kras(G12D/+);LSL-Trp53(R172H/+) (KPC)
36 e transcriptomic programs of pericytes during angiogenesis, we crossed Pdgfrb(BAC)-CreER(T2) mice into RiboTag(flox/flox)
37                                              In this study, we crossed populations of the intertidal copepod Tigriopus ca
38                                                             We crossed Sirt1-overexpressing mice with SCA7 mice and noted
39                                                             We crossed Tert heterozygous knockout mice (mTert (+/-) ) for
40 estigate the function of TET3 in adult postmitotic neurons, we crossed Tet3 floxed mice with a neuronal Cre-expressing mo
41                                                             We crossed the inducible erbB2 (MMTV-iErbB2) and Wnt (MMTV-Wn
42 he potential benefit of S6k1 loss on HD-related phenotypes, we crossed the R6/2 HD model with the long-lived S6k1 knockou
43                                                             We crossed these CD79-GFP lines to a recombination activating
44                                                             We crossed these drivers to conditional DREADD mouse lines to
45                                                             We crossed these mice with LSL-KrasG12D mice, which express a
46                                       In the present study, we crossed Thra1 (PV/+) mice with mice expressing a mutant Nc
47  effects of kallistatin on DN and its underlying mechanism, we crossed transgenic mice overexpressing kallistatin with OV
48                                              In this study, we crossed Trem2(+/+) (T2(+/+)) and Trem2(-/-) (T2(-/-)) mice
49                                       In the present study, we crossed two chicken breeds, White Leghorn (WL) and Cornish
50                                                             We crossed wild-type and HDAC6-deficient mice and subjected t