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In B. subtilis, ComGA is absolutely required for initial DNA binding to the cell surface as comGA point mutants are unable to bind to extracellular DNA 66.
The binding enthalpies of the specific and non-specific DNA binding to the protein differed significantly.
Previous studies to quantify DNA binding to cells have used radiolabeled DNA.
DNA binding to cell-surfaces has been documented in several studies.
Combination of these regions synergistically modifies DNA binding to further enhance specificity.
Upon addition of double stranded DNA to the aqueous phase, the transfer of electrolyte anions was diminished, due to DNA binding to the acridine moiety at the ITIES.
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Similarly, we expect, for example, accidental transcription factor-DNA binding to go on at some rate, so assuming that transcription equals function is not good enough.
However, the tandem zinc fingers of REST are Krüppel-like zinc fingers that mediate sequence-specific DNA-binding to RE1-elements in promoters [50], [51].
In conclusion, cyclosporine repressed HNF4α/HNF1α expression, DNA-binding to targeted promoters and subsequent expression of genes involved in glucose metabolism and pancreatic β-cell function.
First, unlike the proposal for DNA-binding to E. coli GyrA, the model requires minimal distortion of protein and DNA molecules [19].
Loss of HNF4α DNA-binding to targeted promoters resulted in reduced expression of genes coding for glucose transport and metabolism and of insulin secretion from pancreatic ß-cells [28].
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