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1 t been previously explored in the context of gene ablation.
2 rgone excision to assess the consequences of gene ablation.
3 or gene recapitulates the phenotype of PTHrP gene ablation.
4 o specifically target dermal condensates for gene ablation.
5 tely eliminated in isogenic cells with CASP3 gene ablation.
6 diac BNIP3 and NIX/BNIP3L overexpression and gene ablation.
7 smooth muscle cells (VSMC) using conditional gene ablation.
12 erive mice deficient for Klf4 by conditional gene ablation and analyze their vascular phenotype follo
16 ntal phenotype depends on the degree of Igf2 gene ablation and the interplay between placental and fe
18 n mouse line for corneal epithelium-specific gene ablation and to analyze the allelic selection of th
20 dy used bioinformatics, expression analysis, gene ablation, and specific pharmacologic inhibitors to
22 ze and contrast data obtained using integrin gene ablation approaches in mice with other experimental
23 n total phospholipid mass was reduced 17% by gene ablation, ascribed to a 27% and 32% reduction in th
24 ild-type genes, and Cre recombinase-mediated gene ablations at the single-cell level in the context o
25 models, we demonstrate that beta-arrestin-2 gene ablation augments beta-agonist-mediated airway smoo
27 The first group is heterozygous for betaARK1 gene ablation, betaARK1(+/-), and the second is not only
28 second is not only heterozygous for betaARK1 gene ablation but is also transgenic for cardiac-specifi
29 re, implementing spatiotemporally restricted gene ablation by way of the Cre recombinase/loxP system,
30 (Fra-1) is activated in multiple cancers and gene ablation can suppress the invasive phenotypes of ma
33 floxed Alpl allele, allowing for conditional gene ablation (conditional knockout [cKO]) when crossed
34 e Genetics Project, where the treatment is a gene ablation, demonstrates the benefits of the new pipe
35 ylation by conventional or conditional cMLCK gene ablation did not affect troponin-I or myosin-bindin
39 dothelial-specific MAP4K4 gene silencing and gene ablation experiments in Apoe(-/-) mice, we show tha
43 Constitutive neuroplastin deficiency or Nptn gene ablation in adult mice causes substantial electroph
48 od pressure and sodium balance, in that Drd3 gene ablation in mice results in hypertension and failur
49 ments using dominant negative constructs and gene ablation in mice suggested that two phosphoinositid
50 drives lymphatic morphogenesis through Mmp2-gene ablation in mice, mmp2 knockdown in zebrafish and i
51 s achieved by complete or epithelia-specific gene ablation in mice, results in defective mammary morp
56 estin-CreER(T2)/R26R-YFP mouse for inducible gene ablation in stem cells and their progeny in vivo in
57 We show that mice with Tgfbr2 conditional gene ablation in the CNC have complete cleft secondary p
64 genetic manipulations, such as transgenesis, gene ablation (knockouts) and targeted mutagenesis (knoc
65 in many cases, the phenotype resulting from gene ablation might not provide a complete picture of th
68 We used constitutive and neuron-specific gene ablation models targeting an integral subunit of ne
69 spase 1 into inflammasomes, and consistently gene ablation of ASC abolishes caspase 1 activation and
70 ensation on N-cadherin deletion, SC-specific gene ablation of beta-catenin was generated and characte
71 is required in APC/C function; specifically, gene ablation of CBP by RNA-mediated interference marked
73 tified all intestinal miRNAs and shown using gene ablation of Dicer1 that miRNAs play a vital role in
77 e of N-cadherin, mice displaying SC-specific gene ablation of N-cadherin were generated and character
79 n in engulfment of apoptotic cells, although gene ablation of PSR has resulted in a variety of phenot
82 e we show that pharmacological inhibition or gene ablation of the Ep3 receptor in mice suppresses acc
90 estigated the consequences of PDE4B or PDE4D gene ablation on cAMP signaling at a subcellular level u
92 disease model, we evaluated the effect of C3 gene ablation on disease development in MRL/lpr-Daf-1(-/
93 on of CD99L2 on peripheral neutrophils, only gene ablation on endothelial cells but not on myeloid ce
94 To address this issue, the effect of L-FABP gene ablation on liver cytosolic LCFA-CoA binding, LCFA-
95 -arrestin-1 or beta-arrestin-2 inhibition or gene ablation on signaling and function of multiple GPCR
99 hanced by Runx2 deficiency that results from gene ablation or RNA interference, whereas induction of
100 alpha inhibition (with etanercept), TNFalpha gene ablation, or p38 inhibition, prevents atrial struct
101 rotein expression using short hairpin RNA or gene ablation prevented the sensitizing effects of ethan
102 er by spontaneous mutation or by conditional gene ablation, prevented the induction of p21(CIP1) and
103 n sensory neurons is a direct effect of Klf7 gene ablation, rather than a secondary effect of cell de
104 s provided three new insights: First, L-FABP gene ablation reduced maximal, but not initial, uptake o
106 scence photobleaching recovery, where L-FABP gene ablation reduced the cytoplasmic, but not membrane,
113 ically or via complete or conditional NFATc1 gene ablation, stem cells are activated prematurely, res
114 e transcription factors STAT1 and STAT2, and gene ablation studies have demonstrated that both STAT1
119 nsation in the animal kingdom, identified by gene ablation studies, has raised questions about whethe
122 ysis ('ChIP-on-chip') and cell type-specific gene ablation that the winged helix transcription factor
123 c DP precursors for labeling, isolation, and gene ablation that will greatly enhance investigations i
124 insulin promoter, has been shown by targeted gene ablation to be required for pancreatic development.
126 rphic Fgf8 allele (Fgf8neo) and Cre-mediated gene ablation to show that Fgf8 is essential for the sur
127 del in vivo, we utilized hepatocyte-specific gene ablation to study the binding of HNF6 to its target
129 is an acidic noncollagenous protein shown by gene ablations to be critical for the proper mineralizat
130 ncluding a model derived using Car6 and CHOP gene ablations, to delineate a role for CAVI-b in ischem
131 se (SOD1), reduction of MMP-9 function using gene ablation, viral gene therapy, or pharmacological in
135 in C3H mice carrying the type I IFN receptor gene ablation, which effectively blocks all autocrine/pa
136 em, enabling tamoxifen inducible conditional gene ablation while controlling for genetic background a
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