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  • Overexpression of SUMO perturbs the growth and development of Caenorhabditis elegans. 21253676

    Small ubiquitin-related modifiers (SUMOs) are important regulator proteins. Caenorhabditis elegans contains a single SUMO ortholog, SMO-1, necessary for the reproduction of C. elegans. In this study, we constructed transgenic C. elegans strains expressing human SUMO-1 under the control of pan-neuronal (aex-3) or pan-muscular (myo-4) promoter and SUMO-2 under the control of myo-4 promoter. Interestingly, muscular overexpression of SUMO-1 or -2 resulted in morphological changes of the posterior part of the nematode. Movement, reproduction and aging of C. elegans were perturbed by the overexpression of SUMO-1 or -2. Genome-wide expression analyses revealed that several genes encoding components of SUMOylation pathway and ubiquitin-proteasome system were upregulated in SUMO-overexpressing nematodes. Since muscular overexpression of SMO-1 also brought up reproductive and mobility perturbations, our results imply that the phenotypes were largely due to an excess of SUMO, suggesting that a tight control of SUMO levels is important for the normal development of multicellular organisms.
    Document Type:
    Reference
    Product Catalog Number:
    07-371
    Product Catalog Name:
    Anti-Histone H2B Antibody

  • An association of multiple endocrine neoplasia 2B, a RET mutation; constipation; and low substance P-nerve fiber density in colonic circular muscle. 16481266

    BACKGROUND: Multiple endocrine neoplasia (MEN) 2B is a rare hereditary syndrome that results from an activating mutation of the RET proto-oncogene. The RET gene is involved in the development of the enteric nervous system. Patients with MEN 2B have enlarged enteric ganglia and may be affected by gastrointestinal dysmotility. A deficiency of the neurotransmitter substance P (SP) has been identified in both pediatric and adult patients with chronic constipation. METHODS: Three patients, in whom constipation was the presenting symptom and MEN 2B had been provisionally diagnosed, underwent genetic analysis. Seromuscular colonic biopsies were taken for immunofluorescence imaging in all 3 patients. A retrospective review of the patient notes was undertaken. RESULTS: All 3 patients had constipation refractory to conservative treatment. Genetic analyses in the 3 patients confirmed an identical RET mutation (Met918Thr). Immunofluorescence imaging in all 3 patients identified grossly enlarged myenteric plexus ganglia but surprisingly a low density of SP-labeled nerve fibers in the colonic circular muscle. Nitric oxide synthase and vasoactive intestinal peptide labeling were not reduced. CONCLUSION: The results show an association between MEN 2B and its most common RET mutation, colonic dysmotility, and low density of SP in the colonic circular muscle. Larger numbers of patients need to be studied to investigate whether low SP is primarily associated with the constipation or RET mutation and if it is a common feature of MEN 2B.
    Document Type:
    Reference
    Product Catalog Number:
    AB5380
    Product Catalog Name:
    Anti-Nitric Oxide Synthase I Antibody

  • Toxicity of penta- and decabromodiphenyl ethers after repeated administration to rats: a comparative study. 20020105

    Until recently, pentabromodiphenyl (PentaBDE) and decabromodiphenyl (DecaBDE) ethers were commonly used as flame retardants in a wide array of products, mostly in the production of plastics utilized in the electric, electronic and textile industries. The aim of this study was to compare the toxicity of PentaBDE and DecaBDE after their repeated (7-28 days) intragastric administration to rats. The compounds were given at doses of 2, 8, 40 or 200 mg/kg/day (PentaBDE) and 10, 100 or 1,000 mg/kg/day (DecaBDE). The repeated administration of PentaBDE disturbed redox homeostasis, which was manifested by lower total antioxidant status and increased activity of glutathione reductase in serum and higher concentrations of glutathione reduced and malondialdehyde in the liver. The occurrence of these effects was not observed after DecaBDE administration. The results of histopathological examination showed fatty degeneration after administration of the highest dose of PentaBDE. The repeated administration of PentaBDE also caused the increase in relative liver mass, dose-dependent increase in the activity of CYP 1A (EROD) and CYP 2B (PROD), 7-12- and 2-8-fold, respectively, as well as enhanced level of CYP 1A1 (5-30-fold) and CYP 4A (2-4.5-fold). The administration of DecaBDE induced much less pronounced changes: a maximum 2.8-fold increase in the activity of CYP 1A, a twofold increase in CYP 2B, and no alterations in other parameters under study. Contrary to DecaBDE, PentaBDE disturbed redox homeostasis, and induced liver microsomal enzymes. Fatty degeneration in liver caused by this compound was also found.
    Document Type:
    Reference
    Product Catalog Number:
    AB1280
    Product Catalog Name:
    Anti-Cytochrome P450 Enzyme CYP4A1/2/3 Antibody

  • Relationship of opioid receptors with GABAergic neurons in the rat inferior colliculus. 17040471

    The inferior colliculus is a critical structure for processing auditory information and receives ascending and descending synaptic auditory projections. In addition to GABAergic and glutamatergic innervations, other neurotransmitter systems are also reported in the inferior colliculus, including opioid peptides. In the present study, the relative distribution of each type of opioid receptor, mu (MOR), delta (DOR) and kappa (KOR) within GABAergic neurons in the inferior colliculus was examined. GABA immunoreactivity was expressed by small, medium and large neurons and distributed in the central nucleus and the pericentral nucleus of the inferior colliculus. Immunostaining for MOR, DOR and KOR receptors was found in both disc-shaped cells and stellate cells. Punctiform beta-endorphin immunolabelling was observed in the proximity of GABA-positive neurons. Co-localization of GABA and MOR receptors was observed in neurons and nerve terminals in the central nucleus, dorsal cortex and external cortex of the inferior colliculus. Quantification of the co-localization patterns determined that a higher proportion of GABA neurons was associated with MOR receptors compared with KOR or DOR receptors.
    Document Type:
    Reference
    Product Catalog Number:
    MAB316
    Product Catalog Name:
    Anti-GABA Antibody, clone 5A9

  • Superoxide production by mitochondria of insulin-sensitive tissues: mechanistic differences and effect of early diabetes. 19765776

    Obesity and mild hyperglycemia are characteristic of early or "prediabetes." The associated increase in fatty acid flux is posited to enhance substrate delivery to mitochondria, leading to enhanced superoxide production that results in mitochondrial dysfunction and progressive worsening of the hyperglycemic state. We quantified superoxide production by gastrocnemius muscle, heart, and liver mitochondria in a rodent model that mimics the pathophysiology of prediabetes by administering low-dose streptozotocin to rats fed high fat (HF). Superoxide was rigorously determined indirectly as H(2)O(2) largely released from the matrix and by electron paramagnetic resonance spectroscopy that directly detects superoxide released externally. Both HF and low-dose streptozotocin mildly increased glycemia (P < .05 by 2-way analysis of variance). Matrix and external superoxide production by gastrocnemius mitochondria respiring on the complex II substrate succinate and matrix superoxide production by liver mitochondria respiring on the complex I substrates glutamate plus malate were significantly reduced by HF feeding but not affected by mild hyperglycemia. Superoxide production was not significantly altered by either treatment in heart mitochondria fueled by either complex I or II substrates. The functional status of the mitochondria was assayed as simultaneous respiration and membrane potential that were not affected by HF or mild hyperglycemia. Comparison of substrate and inhibitor effects on superoxide release implied marked differences in the redox mechanisms regulating mitochondrial superoxide production from liver mitochondria compared with muscle and heart. In summary, superoxide production from mitochondria of different insulin-sensitive tissues differs mechanistically. However, in any case, excess superoxide production as an intrinsic property of mitochondria of insulin-sensitive tissues does not result from conditions mimicking the pathophysiology of pre- or early diabetes.
    Document Type:
    Reference
    Product Catalog Number:
    06-984
    Product Catalog Name:
    Anti-Mn-SOD Antibody

  • Biased binding of class IA phosphatidyl inositol 3-kinase subunits to inducible costimulator (CD278). 21188463

    To better understand T lymphocyte costimulation by inducible costimulator (ICOS; H4; CD278), we analyzed proteins binding to ICOS peptides phosphorylated at the Y(191)MFM motif. Phosphorylated ICOS binds class IA phosphatidyl inositol 3-kinase (PI3-K) p85α, p50-55α and p85β regulatory subunits and p110α, p110δ and p110β catalytic subunits. Intriguingly, T cells expressed high levels of both p110α or p110δ catalytic subunits, yet ICOS peptides, cell surface ICOS or PI3-kinase class IA regulatory subunits preferentially coprecipitated p110α catalytic subunits. Silencing p110α or p110δ partially inhibited Akt/PKB activation induced by anti-CD3 plus anti-ICOS antibodies. However, silencing p110α enhanced and silencing p110δ inhibited Erk activation. Both p110α- and p110δ-specific inhibitors blocked cytokine secretion induced by TCR/CD3 activation with or without ICOS costimulus, but only p110α inhibitors blocked ICOS-induced cell elongation. Thus, p110α and p110δ are essential to optimal T cell activation, but their abundance and activity differentially tune up distinct ICOS signaling pathways.
    Document Type:
    Reference
    Product Catalog Number:
    06-195