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In peripheral blood mononuclear cells from diabetic patients with chronic microvascular lesions increased NFAT5 DNA binding activity was demonstrated [ 16].
The integrity of the clones was confirmed by sequencing and the binding activity was demonstrated by ELISA using both the SAI/II antigen and S. mutans cells.
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The specificity of the NF- κB DNA-binding activity was demonstrated by competitive inhibition in the presence of a 100 ng excess of unlabelled probe (not shown).
Utilizing a purified recombinant human perlecan domain 1 (rhPln.D1) expressed from HEK 293 cells with HS and CS GAGs, tight binding and dose-enhancement of rhBMP-2 activity was demonstrated in vitro.
Our experiments demonstrated that after acute prion infection of Bos2 neuroblastoma cells with PrPSc (RML6), NF-κB binding activity was detectable but no transcriptional activity.
NF-κB binding activity was also increased markedly.
Pleasingly, simultaneous binding activity was confirmed.
DNA binding activity was assessed by EMSA.
It has been shown that the LEPR Gln223Arg polymorphism is associated with variation in ligand binding; higher levels of ligand binding activity has been demonstrated in individuals homozygous for the G (LEPR Arg223Arg) allele than for carriers of the A (LEPR 223Gln) allele [ 16].
Progesterone binding activity has been demonstrated in nuclei purified from the adrenal cortex of guinea pigs, but the binding protein was considered distinct from classical PR, partly since a monoclonal antibody known to recognise guinea pig classical nuclear uterine PR failed to identify the protein [ 10].
Elevated NF-κB DNA binding activity has been demonstrated both in breast cancer cell lines and primary breast cancer tissues [ 37, 38].
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