Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.4.3 (phospholipase C)
 18,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By using a suckling mouse assay, heat-stable enterotoxin (ST) was purified from the culture filtrate of Yersinia enterocolitica isolated from a diarrheal patient. The purification procedures involve ultrafiltration with an Amicon HIP-10 hollow fiber, ethanol fractionation, protamine sulfate treatment, diethylaminoethyl-Sephacel and hydroxylapatite column chromatographies, and Sephacryl S-200 superfine gel filtration. About 408-fold purification was achieved, with a yield of 12.0%. The minimal effective dose of purified ST was about 110 ng in the suckling mouse assay. The molecular weight of purified ST was 9,000 by Sephadex G-100 superfine gel filtration. The purified ST was stable to heating (100 degrees C for 20 min, 121 degrees C for 20 min) and did not lose its toxicity after treatment with protease, trypsin, lipase, phospholipase C, ribonuclease, deoxyribonuclease, beta-glucosidase, and neuraminidase. The purified ST was separated by isoelectric focusing into two active fractions, with pI's of 3.29 (ST-1) and 3.00 (ST-2), respectively. Antiserum from guinea pigs immunized with the purified ST neutralized the activity of both Y. enterocolitica ST and Escherichia coli ST.
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PMID:Partial purification and characterization of heat-stable enterotoxin produced by Yersinia enterocolitica. 721 60

In according with the mechanism for an adaptive response (AR) offered in [Bodnarchuk I.A.//Radiat. biologiya. Radioecologiya. 2002. V. 42. No. 1. P. 36-43], the low-dose irradiation of mammalian cells leads to the activation of such enzymes as Ras, ceramid-activated protein kinase, phospholipase C (PL C) and phosphatidilinostol 3-kinase (PI 3-K). All of them initiate apoptosis and eliminate the most radiosensitive cells form the population before the damaging irradiation. The function of PL C and PI 3-K accompanied by protein kinase C (PK C) activation. PK C activates transcription of the poly(ADP-ribose)polymerase (PARP) gene and DNA polymerase beta gene, and makes posttranslation activation of apurinic/apyrimidinic endonuclease APE, which are participating in the base excision repair (BER). PK C, APE and PARP activate the transcription factor p53, PK C and APE also activate the transcription factor AP-1, AP-1 and p53 take part in the initiation of nucleotide excision reapir (NER). The function of BER, NER and p53 after the damaging irradiation is accompanied by the G1-arrest of cell cycle progression. During G1-arrest there is p53-dependent activation of nonhomologous ends joining (NHEJ) and the inhibition of homologous recombination repair (HRR) of the DNA double-strand breaks takes place. Passing through the NHEJ the cells will outgo from G1-arrest and follow by HRR. AP-1 takes part in outgoing of cells from G1-arrest. So, the preliminary low-dose irradiation causes the decrease of quantity of cells died apoptotically after damaging irradiation as a result of inability to overcome G1-arrest. Thus, AR is the combination of processes: the removal of radiosensitive subpopulation of cells, and/or the activation of DNA repair, and/or the increase of cells ability to overcome the cell cycle delay.
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PMID:[Analysis of the role of DNA repair, regulation of cell cycle and apoptosis in the radiation-induced adaptive response of mammalian cells]. 1267 54


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