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For competition binding assay, M13-Cry1Ac phages were incubated in presence of increasing concentrations of soluble Cry1Ac toxin and the phage binding was performed as described above.
The biochemical assay for peptide-HLA class I binding was performed as previously described [29], [30].
3H-CGP12177 whole cell binding was performed as previously described [25].
The biochemical assay for peptide MHC-I binding was peptide MHC-Ipreviously describinding].
The fluorescence polarization assay for SRC-1/PPARγ binding was performed as described previously [ 21].
Aven binding was performed as in panel B. PRMT1 depletion was confirmed by immunoblotting.
Similar(51)
EBA-175 erythrocyte blocking of binding studies and the determination of the IC50 for blocking of EBA-175 binding were performed as previously described, respectively [4], [17].
Steady-state kinetics and equilibrium binding were performed as previously described.
Gel mobility shift assays for Mor binding were performed as described by Ma and Howe (2004) except that approximately half (~0.38 nM) the prior amount of DNA probe was used.
The ELISA assay for dsDNA-binding was performed as described [29].
Karytyping and G-binding was performed as previously described [36] at Chinese Academy of Medical Science & Peking Union Medical College.
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