Disease relevance of DNA Footprinting

• Gel band mobility shift and DNA footprint experiments were used to demonstrate that the CYS3 protein, expressed in Escherichia coli, binds to three distinct sites in the 5' upstream DNA of cys-14, the structural gene for sulfate permease II [1].

High impact information on DNA Footprinting

• DNA footprint analysis with dimethyl sulfate demonstrated that the 7-mer region of the RSS was strongly protected when complexed with the binding protein [2].
• DNA footprinting with hydroxyl radical [3].
• Mouse nuclear factors that bind to an upstream metal regulatory element of the mouse metallothionein-I gene have been identified by DNA footprinting and oligonucleotide band shift assays [4].
• On the basis of extended DNA footprints of Region I-deleted holoenzyme, we also propose that Region I prevents RNA polymerase isomerization, a conformational change necessary for access to and the subsequent stable association of holoenzyme with melted DNA [5].
• The nuclear factor binding to the c-fos CRE is likely to be transcription factor CREB (CRE nuclear binding protein), because an affinity-purified 43-kD CREB isolated from PC12 cells binds efficiently in a DNA footprinting assay [6].

Biological context of DNA Footprinting

• Exonuclease III mediated in vivo DNA footprinting and dimethyl sulfate in vivo footprinting revealed DNA protection of a 32-bp region and two guanosines (G) within this region protected from methylation, respectively [7].
• In vivo binding of the OmpR protein to the ompF and ompC promoter regions was observed using an in vivo dimethyl sulfate DNA footprinting technique [8].
• Mutation of the two 5'-nucleotides decreased the affinity of thyroid hormone receptor alpha 1 for this DNA sequence approximately 5-fold, and the importance of those nucleotides in receptor binding was confirmed by DNA footprinting [9].
• This approach, combined with mutational analysis and DNA footprinting, led to the identification of the seven-base pair sequence GGGGTCA as the highest affinity retinoid X receptor binding site [10].
• Here we show by DNA footprinting analysis that MPG, but not UDG, bound to base-pair mismatches especially to less stable pyrimidine-pyrimidine pairs, without catalyzing detectable base cleavage [11].

Associations of DNA Footprinting with chemical compounds

• Inducible in vivo DNA footprints define sequences necessary for UV light activation of the parsley chalcone synthase gene [12].
• In vivo DNA footprinting revealed specific modifications of the ERE region in ERalpha-positive but not ERalpha-negative cells upon treatment with 17beta-estradiol (E2), indicative of estrogen-dependent chromatin remodelling [13].
• Deletion of the sequence between the two guanosines protected by in vivo dimethyl sulfate DNA footprinting (GAAGAGTG) in a luciferase construct (-1,094 bp to +23 bp) abolished the constitutive promoter activity [7].
• To demonstrate DNA binding of MtlR to a region upstream of the mannitol promoter, by DNA footprinting, MtlR was overproduced and purified [14].
• High resolution hydroxyl radical DNA footprinting showed protection centered around the tetrahydrofuran residue [15].

Gene context of DNA Footprinting

• Fractionation of yeast extracts on heparin-agarose revealed the presence of a DNA footprinting activity that interacted specifically with the 5'-upstream region of TEF1 and TEF2 genes coding for the protein synthesis elongation factor EF-1 alpha, and of the ribosomal protein gene RP51A [16].
• Protein-DNA binding studies using electrophoretic mobility shift and DNA footprinting assays showed that both Sp1 and Sp3 proteins bound this region of the VEGF promoter [17].
• The results of DNA footprinting analysis show that FadR binds downstream of the uspA promoter in the noncoding region [18].
• The MLPE site primarily binds USF1/USF2 and ERalpha, and gel mobility shift and DNA footprinting assays show that the AhR complex decreases binding of these transcription factors to the MLPE [19].
• In vivo DNA footprinting shows a specific loss of occupancy at the IFN response factor element site in Caki-2 cells, whereas Caki-1 cells show full promoter occupancy [20].

Analytical, diagnostic and therapeutic context of DNA Footprinting

• The binding of two symmetric bis-benzimidazole compounds, 2,2-bis-[4'-(3"-dimethylamino-1"-propyloxy)phenyl]-5,5-bi-1H-benzimidazole and its piperidinpropylphenyl analog, to the minor groove of DNA, have been studied by DNA footprinting, surface plasmon resonance (SPR) methods and molecular dynamics simulations in explicit solvent [21].

References