Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.27.1 (RNase)
 16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A process for conformational modification of protein, which we have previously reported, was investigated as a means of generating fluorohydrolase activity in bovine ribonuclease (RNase). The resulting modified RNase had catalytic activity that depended upon the chosen modifier. Bovine pancreatic ribonuclease, modified by addition of hexamethylphosphoramide (HMPA) at pH 3, was derivatized with diimidates of chain lengths from C1 to C8. The derivative with the highest activity was obtained when RNase was crosslinked with dimethyl pimelimidate (C5). This derivative, which was active over a pH range of 6.5 to 8.0 with an optimum pH of 7.4, hydrolyzed phenylmethylsulfonylfluoride (PMSF) and the potent acetylcholinesterase inhibitor, diisopropyl phosphorofluoridate (DFP). The mean fluorohydrolase activity for four preparations using dimethyl pimelimidate was 0.8 +/- 0.2 U mg-1. Gel filtration on G-75 Sephadex and SDS-polyacrylamide gel electrophoresis showed components having a molecular weight of 13,000 and 27,000, with activity restricted to the 27,000 molecular weight fraction. After gel filtration, the specific activity was 9.1 +/- 2.4 U mg-1, resulting in a molecular activity of 125 min-1. The mechanism of this unique transformation of RNase into a fluorohydrolase is not known, nor has the location of the active site been determined.
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PMID:Semisynthetic fluorohydrolases prepared by chemical modification of ribonuclease. 136 89

Generation of a cytoplasmic factor(s) that induced IgG secretion in nonstimulated cells was demonstrated in TRF-stimulated cells by using red cell-mediated microinjection. Injection of the cytoplasm from a TRF-stimulated B lymphoblastoid cell line (CESS) into nonstimulated cells induced an increase of IgG-producing cells. Injection of TRF itself did not induce an increase of IgG-producing cells. Active substance(s) in the cytoplasm were generated at 2 hr after TRF stimulation, and IgG-producing cells reached their maximum level at 40 hr after injection of the factor(s). DFP, but not actinomycin D, inhibited the generation of the cytoplasmic factor(s). The activity of the cytoplasmic factor(s) was not destroyed by RNase and not absorbed with anti-IgG. These results suggested that binding of TRF with its acceptors induced the generation of the cytoplasmic factor(s) involved in the transmission of TRF-mediated signals from membrane to nuclei.
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PMID:IgG induction in a human B cell line by red cell-mediated microinjection of the cytoplasm from T cell factor-stimulated B cells. 698 Sep 30