Sentence examples for binding of stat from inspiring English sources

Tyrosine phosphorylation results in STAT dimerization, nuclear translocation, and binding of STAT dimers to consensus elements upstream of regulated genes.

In accordance with this, our meta-analysis of genome-wide STAT binding sites in 29 different cell contexts showed that the binding of STATs to GAS sites was mostly defined by the cell type compared to other features such as the type of STATs and the cytokine.

IRF-1 is transactivated by binding of STAT-1 dimers to the GAS sequence of the IRF-1 promoter.

Moreover, the STAT-1 decoy ODN prevented binding of STAT-1/STAT-3 heterodimers from IFN-γ-stimulated synoviocytes to the SIE gel shift ODN.

Of particular importance, STAT-1 also regulates CD40 transcription in different cells, either by direct binding of STAT-1 to the γ-activated sequence (GAS) element in the CD40 promoter or by inducing the de novo synthesis of the transcription factor interferon regulatory factor-1 (IRF-1) [ 11, 12], which induces not only CD40 but also other mediators such as inducible nitric oxide synthase (iNOS).

The DNA-binding domain is involved in the direct binding of STATs to the corresponding sites in gene promoter.

Our results suggest that genomic binding of STATs is primarily determined by the cell type and further specificity is achieved in part by juxtaposed binding of cell-specific transcription factors.

Bluyssen and co-workers have recently used comparative in silico docking to study the binding specificity of STAT inhibitors stattic and fludarabine, and have concluded that ligands targeting only the highly conserved phosphotyrosine binding pocket of the SH2 domain (i.e. stattic) will lack selectivity towards STATs, as STAT1 and STAT3 have identical active residues at this site.

These common and cell-specific bindings of STATs to GAS sites in CRMs likely reflect context-dependent gene regulations in different cell types via STATs.

We conclude, therefore, that the binding of activated STAT-1 and/or STAT-3 to certain target gene promoters in macrophages and synoviocytes can be blocked by treatment with the administered STAT-1 decoy ODN in vitro and in vivo.

In addition to the quantitative aspect of genome-wide STAT binding, we determined that cell context was the foremost defining factor in the establishment of genome-wide binding positions of STATs.