Disease relevance of Abp1

• Effect of intestinal ischemia on diamine oxidase activity in rat intestinal tissue and blood [1].
• Diamine oxidase activity in regenerating rat liver and in 4-dimethylaminoazobenzene-induced and Yoshida AH 130 hepatomas [2].
• A large increase in diamine oxidase activity, as compared to the values of normal liver, was also observed in 4-dimethylaminoazobenzene and Yoshida ascites hepatomas [2].
• While weight loss should be taken into consideration when interpreting cause and effect relationships in streptozotocin-treated animals, epididymal ABP levels appear to be well correlated with the altered metabolic state characteristic of diabetes [3].
• 4. We propose that by 3-5 weeks of chronic hypoxia renal function was normalized, principally because arterial O2 content was normalized by the increase in haematocrit and because ABP and renal haemodynamics were normalized: acute hypoxia in N rats produces a fall in ABP [4].

High impact information on Abp1

• Here we examine how glutamate receptor interacting protein (GRIP, also known as AMPAR binding protein or ABP) and protein interacting with C-kinase-1 (PICK) regulate subunit trafficking and plasticity [5].
• Diamine oxidase, an enzyme shown here to metabolize agmatine, was localized by immunohistochemistry in kidney glomeruli and other nonrenal cells [6].
• The mast cell stabilizer, lodoxamide, an H1- (but not an H2-) receptor antagonist, and diamine oxidase (histaminase) were also effective in reducing the LAE and albumin leakage elicited by Tx-A [7].
• Binding of diamine oxidase activity to rat and guinea pig microvascular endothelial cells. Comparisons with lipoprotein lipase binding [8].
• To assess the influence of diamine oxidase activity on the adaptive process of the small bowel after resection, we administered aminoguanidine, a potent diamine oxidase inhibitor, to rats for 10 days after either small bowel transection (n = 5) or 80% jejunoileal resection (n = 7) [9].

Chemical compound and disease context of Abp1

• 4. In an additional nine rats, alpha,beta-methyleneADP (160 micrograms kg-1, i.v.) which inhibits the 5'-ectonucleotidase that degrades AMP to adenosine, reduced the peripheral vasodilatation (fall in arterial blood pressure, ABP) induced by ATP infusion, but had no effect on the increase in FVC or decrease in ABP evoked by systemic hypoxia [10].
• Therefore, RA appears to have a broader range of desirable effects on bone, body weight, uteri and cholesterol than ABP or EE2 in ovariectomized rats [11].
• The effect of a single dose (2 g/kg, body weight) of ethanol on diamine oxidase activity of the upper gastrointestinal tract was studied in fasted rats [12].
• In the prolonged ischemic group (60-min ischemia), both histamine concentration and diamine oxidase activity in the mucosa decreased, contributing to an increase in circulating histamine [13].
• Such findings indicate that an increase in oxidative putrescine catabolism via diamine oxidase takes place in transformed cells and in gliomas and is probably linked to an activation of polyamine synthesis and turnover [14].

Biological context of Abp1

• Isolation of a rat amiloride-binding protein cDNA clone: tissue distribution and regulation of expression [15].
• To study further the regulation of gene expression in sodium-transporting epithelia by corticosteroids, we have cloned an amiloride-binding protein (ABP) cDNA from rat descending colon and kidney [15].
• 3. Concomitantly, maintenance of eucapnia reduced the increase in heart rate (HR) and fall in arterial pressure (ABP), the effects being significant at Fi,O2 0.08 and/or 0.06 [16].
• The adenosine receptor antagonist 8-phenyl-theophylline (8-PT, 10 mg kg-1) reduced the secondary fall in VE, the fall in ABP and muscle vasodilatation, indicating they were partly mediated by adenosine [17].
• In both glomeruli and tubules, the diamine oxidase inhibitor, amino-guanidine, abolished the production of acid metabolites while amodiaquine and pyrilamine, inhibitors of the methylation pathway, markedly reduced the production of N tau-methylhistamine [18].

Anatomical context of Abp1

• Low to undetectable levels of rat ABP were expressed in the descending colon and kidney [15].
• Our data suggest that ProSAPs may serve to localize Abp1 to dendritic spines, thus serving as attachment points for the dynamic postsynaptic cortical actin cytoskeleton [19].
• The distribution of Abp1, ProSAP1, and ProSAP2 overlaps within the brain, and all three proteins are part of the PSD and are particularly enriched in cortex and hippocampus [19].
• This study examines the effect of increasing duration of intestinal ischemia on the mucosal integrity and the release of the enzyme diamine oxidase from the small intestine [1].
• Diamine oxidase activity was measured in the intestinal lumen, mucosa, lymph, and serum [1].

Associations of Abp1 with chemical compounds

• The distribution of rat ABP is not as would be predicted for an aldosterone-induced gene and is thus unlikely to be a component of the amiloride-sensitive electrogenic sodium channel [15].
• These results suggest that aldehyde-metabolizing enzymes present in homogenate may interfere with the amount of delta 1-pyrroline formation and that the use of acetaldehyde may give better information on tissue diamine oxidase activity [2].
• Acetaldehyde did not modify the activity of a preparation of hog kidney diamine oxidase, while chloral hydrate and disulfiram, respectively, enhanced and depressed the activity of this enzyme [2].
• In addition, none of the three NK cell lines were found to contain histaminase-sensitive histamine [20].
• We tested the effect of 2-amino-5-bromo-6 phenyl-4 pyrimidinol (ABPP), an interferon (IFN) inducer, on NK cell cytotoxicity in various tissues of athymic and euthymic rats [21].

Other interactions of Abp1

• Importantly, different paradigms of neuronal stimulation induce a redistribution of Abp1 to ProSAP-containing synapses [19].
• Coimmunoprecipitation of endogenous Abp1 and ProSAP2 and colocalization studies of Abp1 and ProSAPs in hippocampal neurons indicate the in vivo relevance of the interactions [19].
• A small (twofold) increase in S-adenosylmethionine decarboxylase activity in the small intestine was observed after food, but there was no change in diamine oxidase activity [22].
• Ileal mucosal homogenates from the resection group receiving aminoguanidine, when compared with those from resection controls, showed no diamine oxidase activity with increased putrescine content and ornithine decarboxylase activity [9].
• Ornithine decarboxylase, transglutaminase, diamine oxidase and total diamines and polyamines in maternal liver and kidney throughout rat pregnancy [23].

Analytical, diagnostic and therapeutic context of Abp1

• We investigated the role of PDZ proteins (GRIP, ABP, and PICK1) interacting with the C-terminal GluR2 by infusing a ct-GluR2 peptide ("pep2-SVKI") into CA1 pyramidal neurons in hippocampal slices using whole-cell recordings [24].
• Diamine oxidase activity, which was very low in normal liver, increased rapidly in regenerating liver and reached maximum values between 16 and 48 hr after hepatectomy [2].
• One (ABP kinase peak 1) coelutes with the peak of RSK2 as judged by immunoblotting and S6 peptide kinase assays [25].
• The liver activities of histamine-metabolizing enzymes, histamine-N-methyltransferase and histaminase, decreased to 1/3.4 and 1/6.0 times those of the nontreated group, respectively, 12 weeks after treatment with CCl4, whereas blood histaminase increased about 9.2 times [26].
• The binding of iodinated ABP to the receptor was similar to that of photoaffinity-labelled ABP in gel filtration [27].

References