Disease relevance of Btg2

• BACKGROUND: An increased biosynthesis of nitric oxide (NO) has been implicated in the hyperdynamic circulation and development of collaterals of portal hypertension (PHT) because of its potent vasodilatory effects [1].
• Role of nitric oxide in blood-brain barrier permeability, brain edema and cell damage following hyperthermic brain injury. An experimental study using EGB-761 and Gingkolide B pretreatment in the rat [2].
• CONCLUSIONS: An ethanol diet sensitizes rats to pancreatitis caused by CCK-8 [3].
• Alcohol-induced testicular atrophy. An experimental model for hypogonadism occurring in chronic alcoholic men [4].
• Selective binding, uptake, and retrograde transport of tetanus toxin by nerve terminals in the rat iris. An electron microscope study using colloidal gold as a tracer [5].

High impact information on Btg2

• While the endothelial cell is a well known source of NO(.), recent studies suggest that tubular epithelial cells may constitutively generate NO(.). An inducible isoform of nitric oxide synthase which produces far greater quantities of NO. exists in some cell types [6].
• CONCLUSIONS: An ARE in the rat hepatocyte iNOS promoter confers redox sensitivity and augments IL-1beta-mediated iNOS gene and protein expression in the setting of superoxide treatment [7].
• Threonine was the only amino acid phosphorylated in peptide 1/1'. An additional peptide, referred to as peptide 2, was phosphorylated in the beta subunit [8].
• Expression of basic fibroblast growth factor and its receptor by smooth muscle cells and endothelium in injured rat arteries. An en face study [9].
• (iii) An N-terminal antibody-uptake experiment indicated that Syt IV-containing vesicles in the neurites of NGF-differentiated PC12 cells undergo Ca(2+)-dependent exocytosis, whereas no uptake of the anti-Syt IV-N antibody was observed in undifferentiated PC12 cells [10].

Chemical compound and disease context of Btg2

• METHODS: An adenoviral construct that transfers bcl-2 under the control of a tetracycline inducible promoter was generated (advTetOn bcl-2) and used with a second adenovirus that transfers the repressor protein (advCMV Rep) [11].
• 1. An enhanced production of nitric oxide (NO) from L-arginine, related to the diffuse expression of an inducible NO synthase (iNOS), contributes to the pathogenesis of endotoxic shock [12].
• STUDY DESIGN/SETTING: An established L5-L6 rat laminectomy model with a unilateral L5-6 disc injury was employed to assess postoperative proliferative fibrosis of the L5 spinal nerves using quantitative biochemical hydroxyproline assessment of the collagen content in four experimental groups [13].

Biological context of Btg2

• Furthermore, PC3TIS21/BTG2 protects from apoptosis elicited by NGF deprivation in terminally differentiated PC12 cultures [14].
• Such effects might be a consequence of the arrest of cell cycle exerted by PC3TIS21/BTG2, or expression of a sensitizing (neurogenic) property of the molecule [14].
• Intracellular degradation of insulin stores by rat pancreatic islets in vitro. An alternative pathway for homeostasis of pancreatic insulin content [15].
• Loss of haem from cytochrome P-450 caused by lipid peroxidation and 2-allyl-2-isoprophylacetamide. An abnormal pathway not involving production of carbon monoxide [16].
• Cell proliferation in pancreatic islets of rat fetuses and neonates from normal and diabetic mothers. An in vitro and in vivo study [17].

Anatomical context of Btg2

• We have previously shown that PC3TIS21/BTG2 is induced by nerve growth factor (NGF) at the onset of neuronal differentiation in the neural crest-derived PC12 cell line, and is a marker for neuronal birth [14].
• Presence of three acyl-CoA oxidases in rat liver peroxisomes. An inducible fatty acyl-CoA oxidase, a noninducible fatty acyl-CoA oxidase, and a noninducible trihydroxycoprostanoyl-CoA oxidase [18].
• RESULTS: An 18-amino acid peptide (type I peptide) with anti-angiogenic and TGF-beta-activating sequences decreased mesangial and glomerular endothelial cell proliferation in vitro and in vivo and reduced microaneurysm formation and proteinuria in experimental glomerulonephritis [19].
• BACKGROUND: An imbalance between protein load and folding capacity is referred to as endoplasmic reticulum (ER) stress [20].
• BACKGROUND/AIMS: An increase in proliferative activity and other distinct hepatocellular alterations--resembling preneoplastic foci and progressing to hepatocellular tumors--have been shown to develop in liver acini draining the blood from islets of Langerhans, transplanted through the portal vein into the liver of streptozotocin-diabetic rats [21].

Associations of Btg2 with chemical compounds

• RESULTS: An impaired response to norepinephrine observed in sham-operated, portal-vein-stenosed and cirrhotic rats at days 1 and 4 compared with controls was reversed after L-NNA and aminoguanidine [22].
• 4. An NO synthase inhibitor, NG-nitro-L-arginine monomethyl ester (L-NAME) was administered at graded intravenous doses [23].
• Hormonally sensitive cyclic AMP phosphodiesterase in liver cells. An ecto-enzyme [24].
• Possible role of free radicals generated by pseudohypoxia in the regulation of hepatic glucose output. An in vitro model using rat liver microsomal glucose 6-phosphatase [25].
• RESULTS: An increase in diffusible NO generated by constitutive NO synthase was observed immediately after administration of lipopolysaccharide, reaching a plateau (145 +/- 18 nmol/L) after 540 +/- 25 s [26].

Analytical, diagnostic and therapeutic context of Btg2

• METHODS: An mRNA differential display method was used to identify genes with altered expression during differentiation of lens epithelial cells [27].
• BACKGROUND: An isolated arteriole fails to dilate in response to endotoxin unless a segment of aorta is included in the perfusion system [28].
• Healing of a left colon anastomosis after early colostomy closure. An experimental study in the rat [29].
• METHODS: An experimental pancreas transplantation model was established using diabetic SD rats as the recipient, induced by applying streptozocin (STZ) [30].
• BACKGROUND: An intravenous injection of diphenylthiocarbazone (dithizone), a zinc chelator, induces selective killing of Paneth cells which have a large amount of zinc in their cytoplasmic granules [31].

References