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Carbohydrate-dependence of the binding was analysed by addition of 50 mM lactose as a pan-galectin inhibitor and 50 mM sucrose as control.
Peptide binding was analysed by confocal laser microscope (Leica TCS-SP5) with 488 λ ex and 530 550 λ em.
The STAT3-DNA binding was analysed by EMSA using a P-labelled high-affinity sis-inducible element (hSIE) probe as previously described (Yu et al, 1995).
However, when PolII binding was analysed by ChIP on other regions along STL1, PolII recruitment was clearly defective on the 3′ end of the coding region in rsc9 ts mutant cells.
The STAT3 DNA binding was analysed by electrophoretic mobility shift assay (EMSA) using a P-labelled high-affinity sis-inducible element (hSIE) probe (5′-CTTCATTTCCCGTAAATCCCTA-AAGCT-3′ and 5′-AGCTTTAGGGATTTACGGGAAATGA-3′) as previously described (Bhutani et al, 2007).
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Differences in expression levels, expression ratios, constitutive activity measured using [S]-GTPγS binding and receptor activation by LTD4 using [S]-GTPγS binding were analysed by using Student's t-test.
Data of the 5-HTT binding were analysed by means of non-linear least squares regression using a commercial program GraphPad PRISM™ (GraphPad, San Diego, CA, USA) and obtained parameters compared with t-tests.
AP-2 α levels were estimated by Western blotting and AP-2 DNA binding activity was analysed by gel retardation experiments (EMSA).
Receptor binding specificity of A/Quzhou/1/2015(H7N9) was analysed by a solid phase direct binding assay as previously described.
DNA-binding was analysed fluorometrically by quantitative PCR after separation on agarose gels.
Snail binding to serpinA1 promoter was analysed by chromatin immunoprecipitation (ChIP) assays.
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