Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two glucosamine (GCA)-requiring mutants have been isolated which grow on glucose minimal or nutrient sporulation medium only in the presence of either GCA or acetyl-GCA. They lack the l-glutamine-d-fructose-6-phosphate aminotransferase (EC 2.6.1.13), which is repressible by GCA and whose activity in the standard strain decreases after cessation of growth. But the mutants can grow on GCA as sole carbon and ammonia source, because GCA induces the synthesis of 2-amino-2-deoxy-d-glucose-6-phosphate ketol-isomerase (deaminating) (EC 5.3.1.10). With respect to sporulation, the GCA-requiring mutants are in a serious dilemma, as GCA represses the onset of massive sporulation and yet a small amount of GCA-6-phosphate derivatives is necessary to allow sporulation. When GCA is continuously provided in small quantities, sporelike particles are produced which contain little or no spore cortex but a normal spore coat. Apparently, GCA derivatives are needed especially for cortex formation. Many of the sporelike particles can produce colonies after octanol, but not after heat treatment. When they are purified by treatment with lysozyme and sodium dodecylsulfate, they do not show the decrease in optical density at 600 nm typical of germination nor do they produce offspring.
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PMID:Growth, sporulation, and enzyme defects of glucosamine mutants of Bacillus subtilis. 498 85

The preventive effect of Thea sinensis melanin (TSM) against cisplatin-induced nephrotoxicity was studied on ICR mice. Animals were given 20mg/kg i.p. of cisplatin, and TSM was injected i.p. in doses 10-40 mg/kg 2h before intoxication. The protective effects were evidenced by a complete inhibition of the cisplatin-induced elevation of serum Blood Urea nitrogen (BUN), prevention of oxidative stress, and complete blockade of cisplatin-induced elevation of serum creatinine. TSM by itself, however, did not affect the renal functional parameters, including serum BUN and creatinine. Real-time RT-PCR was applied to quantify mRNA levels of cisplatin-treated mouse kidney compared to normal mouse kidney for selected marker genes. Cisplatin treatment increases mRNA levels 40-fold for glutathione-S-transferases (Gstp2), 15-fold for soluble epoxide hydrolase (Ephx1), 15-fold for lipocalin 2 (Lcn2), 9-fold for lysozyme (Lyz), 5-fold for UDP glycosyltransferase 2 (Utg2b), 30-fold for survival motor neuron (Smn1), 30-fold for guanidinoacetate methyltransferase (Gamt), 80-fold for urine retinol binding protein (Rbp4), 60-fold for aminopeptidase N (Apn), 60-fold for cytochrome P450 (Cyp2d18), and 100-fold for ornithine aminotransferase (Oat). Pre-administration of TSM restored normal expression of marker genes for cisplatin-treated mouse kidneys. TSM by itself, however, did not affect the transcription for marker genes. Results obtained demonstrate that TSM pre-administration can prevent the renal toxic effects of cisplatin.
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PMID:Thea sinensis melanin prevents cisplatin-induced nephrotoxicity in mice. 1730 99