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1 NOX2 subunits in MDSC was controlled by the STAT3 transcription factor.
2 A cells through activation of Src kinase and STAT3 transcription factor.
3 CR signal transduction and the activation of STAT3 transcription factor.
4 R signal transduction, and the activation of STAT3 transcription factor.
5 phosphorylation and nuclear translocation of STAT3 transcription factor.
6 outgrowth and constitutive activation of the Stat3 transcription factor.
7 leukin 6-dependent pathway that involves the STAT3 transcription factor.
8 din by IFN-alpha was seen, controlled by the STAT3 transcription factor.
9 y, acting at least in part through c-Jun and STAT3 transcription factors.
10 ial protein substrates such as the STAT1 and STAT3 transcription factors.
11 bioimaging to the assessment of NFkappaB and STAT3 transcription factor activated reporters during th
12 e of inhibiting TCR signaling and activating STAT3 transcription factor activity as efficiently as wi
13 transducer and activator of transcription 3 (Stat3) transcription factors and re-enter the cell cycle
14 T was also associated with activation of the STAT3 transcription factor, and the combination of STAT3
16 decrease constitutive phosphorylation of the STAT3 transcription factor at Tyr705 in the pancreatic c
17 osine kinase inhibitor in combination with a STAT3 transcription factor decoy, we found enhanced anti
18 ther Bcl-2 antisense or NF-kappaB, STAT1 and STAT3 transcription factor decoys oligodeoxyribonucleoti
19 ses, related to defective MyD88 adaptor- and Stat3 transcription factor-dependent T follicular regula
23 ed the DNA-binding activity of the STAT1 and STAT3 transcription factors in nuclear extracts and also
28 ha mRNA expression through activation of the STAT3 transcription factor pathway and subsequent expres
29 ncreases in the binding of the NF-kappaB and STAT3 transcription factors shortly after PH failed to o
31 es the tyrosine phosphorylation of STAT1 and STAT3, transcription factors that can mediate the induct
32 implicated in ROS generation via binding of Stat3 transcription factor to a central component of the
34 ere activated predominantly by the STAT5 and STAT3 transcription factors, whereas transcription of Eg
35 to the cytokine IL-6 activates the oncogenic STAT3 transcription factor, which directly represses the
36 ecific interaction between PAX3-FKHR and the STAT3 transcription factor, which results in a dramatic
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