Pyridoxal 5-phosphate protection of trypsin cleavage site on the glucocorticoid receptor protein.
Pyridoxal 5-phosphate (PLP) treated rat liver triamcinolone acetonide complex was trypsin-digested followed by hydroxylamine treatment. This complex displayed a considerable fraction of DNA binding capacity of the intact complex, which was lost if trypsin digestion had not been preceded by PLP treatment. At the same time trypsin reduced the size of the complex regardless PLP pretreatment. These findings reveal that DNA binding does not require a large complex.
D000315:Adrenalectomy; D000818:Animals; D004247:DNA / Q000378:metabolism*; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D011732:Pyridoxal Phosphate / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D011965:Receptors, Glucocorticoid / Q000187:drug effects / Q000378:metabolism*; D011987:Receptors, Steroid / Q000378:metabolism*; D014222:Triamcinolone Acetonide / Q000378:metabolism*; D014357:Trypsin / Q000494:pharmacology*
D011965:Receptors, Glucocorticoid; D011987:Receptors, Steroid; D011732:Pyridoxal Phosphate; D004247:DNA; D014357:Trypsin; D014222:Triamcinolone Acetonide