Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.4.2.30 (PARP)
 13,611 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of staphylococcal epidermal cell differentiation inhibitor (EDIN), an ADP-ribosyltransferase targeting the small GTP-binding protein rho p21, was examined using Bacillus subtilis. A recombinant plasmid, containing B. licheniformis alpha-amylase promoter flanking either a beta-glucanase or a B. cereus sphingomyelinase signal sequence, and a DNA fragment corresponding to mature EDIN were constructed and used to transform B. subtilis KN2. Transformants were designated ED7 and ED8, respectively. ED7 extracellularly produced recombinant protein, which was purified to homogeneity through column chromatography using SP-Toyopearl 650 cation-exchange gel and the HA1000 hydroxyapatite HPLC column. ED8 did not grow in broth culture. Biochemical and biological studies of purified protein revealed that ED7 produced a correctly processed recombinant EDIN, indistinguishable from natural EDIN.
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PMID:Expression and purification of epidermal cell differentiation inhibitor (EDIN) from Bacillus subtilis. 951 71

Alcohol abuse is associated with both acute and chronic pancreatitis. Repeated episodes of acute pancreatitis or pancreatic injury may result in chronic pancreatitis. We investigated ethanol-induced pancreatic injury using a mouse model of binge ethanol exposure. Male C57BL/6 mice were exposed to ethanol intragastrically (5 g/kg, 25% ethanol w/v) daily for 10 days. Binge ethanol exposure caused pathological changes in pancreas demonstrated by tissue edema, acinar atrophy and moderate fibrosis. Ethanol caused both apoptotic and necrotic cell death which was demonstrated by the increase in active caspase-3, caspase-8, cleaved PARP, cleaved CK-18 and the secretion of high mobility group protein B1 (HMGB1). Ethanol altered the function of the pancreas which was indicated by altered levels of alpha-amylase, glucose and insulin. Ethanol exposure stimulated cell proliferation in the acini, suggesting an acinar regeneration. Ethanol caused pancreatic inflammation which was indicated by the induction of TNF-alpha, IL-1beta, IL-6, MCP-1 and CCR2, and the increase of CD68 positive macrophages in the pancreas. Ethanol-induced endoplasmic reticulum stress was demonstrated by a significant increase in ATF6, CHOP, and the phosphorylation of PERK and eiF-2alpha. In addition, ethanol increased protein oxidation, lipid peroxidation and the expression of iNOS, indicating oxidative stress. Therefore, this paradigm of binge ethanol exposure caused a spectrum of tissue injury and cellular stress to the pancreas, offering a good model to study alcoholic pancreatitis.
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PMID:Binge ethanol exposure causes endoplasmic reticulum stress, oxidative stress and tissue injury in the pancreas. 2752 70