Using a solid-phase ELISA-based binding assay, we determined that ISM binds αv β5 integrin with a K d around 40 μM, in the range of integrin ECM ligand binding affinities (Supplementary Figure S6).
Using this in vitro binding assay, we determined that PARP-1 binds directly to NEIL1.
Reporter assay studies determined that NF-κB transcriptional activity is stimulated within an hour of HSV-1 binding, peaks between two and three hours post-binding and declines to background levels by five hours after induction.
Using a Leishmania-binding assay (Fig. 3 and 4) it was determined that macrophages show parasite binding after 1 hour of macrophage- Leishmania interaction and that the use of C5 deficient sera (serum dependent system) markedly increased the parasite burden.
Notably, Metushi et al. [42] determined that only acyclovir significantly increased peptide binding with HLA-B*57 01 HLA-B*57 01adio-labelled peptide competitive binding assay.
Using cellular ELISA based receptor binding assay we determined binding capacity of GLP-1/hIgG2 in INS-1 cells.
This higher protein binding capacity translates to a greater venom specific IgE binding capacity, and may account for the observation that, on average, the CAP assay determined there was more venom sIgE present compared to the DELFIA assay.
The FLECS assay is a simple binding assay that enables proteins tagged with fluorophors to be rapidly and quantitative screened against small-molecule libraries.
Importantly, unlike brain homogenates from mice injected with PBS, brain homogenates from mice injected with MSA and iLBD patient brain extracts were able to seed alpha-synuclein aggregation in vitro as determined by ThT binding assays, suggesting that these mouse brains contained abnormal misfolded alpha-synuclein that was seeding competent.
To specifically determine that VX-809 facilitates increased binding of ΔF508 CFTR with NHERF1, we utilized a competition-based assay.
