Search results for: NNT1
#34731707 
2021/10/30
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Synthetic Fe-rich nontronite as a novel activator of bisulfite for the efficient removal of tetracycline.
In this work, the iron-containing smectite nontronite (NNT) was artificially prepared by hydrothermal process and used as a heterogeneous catalyst to activate bisulfite (BS) for degradation of tetracycline (TC). Two NNT samples with different iron content (NNT1 and NNT2) were characterized by XRD, FTIR, XPS and SEM-EDS analysis. Under dark condition, the TC removal rates of NNT1/BS and NNT2/BS reached about 91.7% and 95.5% respectively at 60 min. Due to the heterogeneous catalysis of structural Fe(III), the NNT catalysts showed great catalytic activity and low iron leaching at the pH range 3.0-7.5. In addition, NNT particles were also stable and reusable in activating BS for TC removal. According to the EPR and radical quenching experiments, it could be proved that the precursor radical SO- was first generated in NNT/BS system, then SO- and OH were the active species that played a role in TC degradation. The synthetic NNT clay is a promising Fe-based catalyst for treatment of TC wastewater thanks to its high activity, good stability and effective reusability.Zixuan Zhang, Jingfang Li, Yunliang Zhao, Tong Wen, Tingting Zhang, Shaoxian Song
2666 related Products with: Synthetic Fe-rich nontronite as a novel activator of bisulfite for the efficient removal of tetracycline.
100 Plates100 assays1,000 tests10 Plates50 assays96 Tests100Tests100 plates100 tests10 plates
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#15890626 //
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A Caenorhabditis elegans mutant lacking functional nicotinamide nucleotide transhydrogenase displays increased sensitivity to oxidative stress.
Proton-translocating mitochondrial nicotinamide nucleotide transhydrogenase (NNT) was investigated regarding its physiological role in Caenorhabditis elegans. NNT catalyzes the reduction of NADP(+) by NADH driven by the electrochemical proton gradient, Deltap, and is thus a potentially important source of mitochondrial NADPH. Mitochondrial detoxification of reactive oxygen species (ROS) by glutathione-dependent peroxidases depends on NADPH for regeneration of reduced glutathione. Transhydrogenase may therefore be directly involved in the defense against oxidative stress. nnt-1 deletion mutants of C. elegans, nnt-1(sv34), were isolated and shown to grow essentially as wild type under normal laboratory conditions, but with a strongly lowered GSH/GSSG ratio. Under conditions of oxidative stress, caused by the superoxide-generating agent methyl viologen, growth of worms lacking nnt-1 activity was severely impaired. A similar result was obtained by using RNAi. Reintroducing nnt-1 in the nnt-1(sv34) knockout mutant led to a partial rescue of growth under oxidative stress conditions. These results provide evidence for the first time that nnt-1 is important in the defense against mitochondrial oxidative stress.Eva L Arkblad, Simon Tuck, Nikolay B Pestov, Ruslan I Dmitriev, Maria B Kostina, Jörgen Stenvall, Mattias Tranberg, Jan Rydström
2872 related Products with: A Caenorhabditis elegans mutant lacking functional nicotinamide nucleotide transhydrogenase displays increased sensitivity to oxidative stress.
1 kit(96 Wells)161 kit(96 Wells) 1 G100 µg1 module1 mL 25 G1 mg.1 module100ug Lyophilized
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#15253382 //
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New IL-6 (gp130) family cytokine members, CLC/NNT1/BSF3 and IL-27.
Masaaki Murakami, Daisuke Kamimura, Toshio Hirano
1154 related Products with: New IL-6 (gp130) family cytokine members, CLC/NNT1/BSF3 and IL-27.
1000 TESTS/0.65ml100ug100ug100 mg100ug 100 UG25 mg25 mg250 MG 1 G 100 G4 Arrays/Slide
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#15034937 //
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Characterizing the new transcription regulator protein p60TRP.
Active cell death ('apoptosis' or 'programmed cell death') is essential in the development and homeostasis of multicellular organisms and abnormal inhibition of apoptosis is an indicator of cancer and autoimmune diseases, whereas excessive cell death might be implicated in neurodegenerative disorders such as Alzheimer's disease (AD). Using bioinformatics-, Western-blotting-, yeast-two-hybrid-system-, polymerase chain reaction (PCR)-, and fluorescence microscopy-analyses, we demonstrate here that the neuroprotective protein p60TRP (p60-transcription-regulator-protein) is a basic helix-loop-helix (bHLH) domain-containing member of a new protein family that interacts with the Ran-binding-protein-5 (RanBP5) and the protein-phosphatase-2A (PP2A). The additional findings of its influence on NNT1 and p48ZnF (new-neurotrophin-1, p48-zinc-finger-protein)-signaling and its down-regulation in the brain of AD subjects point to a possible pivotal role of p60TRP in the control of cellular aging and survival.K Heese, T Yamada, H Akatsu, T Yamamoto, K Kosaka, Y Nagai, T Sawada
1765 related Products with: Characterizing the new transcription regulator protein p60TRP.
3100 U 100ul1mg1100μg101 mg 25UG100μg2100
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#12843240 //
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Glial reactivity in ciliary neurotrophic factor-deficient mice after optic nerve lesion.
There is evidence that ciliary neurotrophic factor (CNTF), in addition to its neurotrophic activity, positively regulates astrogliosis after CNS injury. CNTF and its receptor, CNTFRalpha, are strongly upregulated in activated astrocytes. Application of CNTF upregulates GFAP expression in cultured astrocytes and induces various aspects of gliosis in the intact brain. Here we examined whether inactivation of the CNTF gene results in the expected changes in glial reactivity by analyzing gliosis in the superior colliculus (SC) after optic nerve crush. Basal expression levels of GFAP and vimentin in unlesioned CNTF-deficient mice were reduced by 66 and 37%, respectively. Absolute numbers of astrocytes were found not to be different. Surprisingly, however, lesion induced robust activation of astrocytes in CNTF-deficient mice; the time course of activation was even accelerated as compared with wild-type animals. At later time points, activation reached the same level. With respect to microglial cells, basal expression of microglial markers was unaltered in CNTF-knock-out animals. Lesion-induced upregulation of Iba-1, ICAM-1, and F4/80 in microglial cells was unaffected in CNTF-deficient animals. Differences were observed with respect to the time course of microglial activation, different markers being affected differentially. We further demonstrate that lesion induces upregulation of CNTF-related cytokines (LIF, NNT-1) and, interestingly, a more pronounced upregulation of cytokine receptor components (LIF receptor beta, gp130) and TGFbeta in CNTF-deficient animals. Our results thus indicate that CNTF is required for the development and maintenance of the mature astrocyte phenotype and provide evidence that CNTF is part of the complex regulatory network modulating lesional glial reactivity after lesion.Aliki Martin, Hans-Dieter Hofmann, Matthias Kirsch
1045 related Products with: Glial reactivity in ciliary neurotrophic factor-deficient mice after optic nerve lesion.
2ug5ug0.1 mg100 ug1mg96T100.00 ug100ug50 ul100ug100 μg20 ul
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#12385838 //
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Leukemia inhibitory factor and interleukin-11: cytokines with key roles in implantation.
Members of the interleukin-6 family of cytokines include leukaemia inhibitory factor (LIF), interleukin-6, interleukin-11, cardiotrophin, ciliary neurotropic growth factor, oncostatin M and the recently discovered cardiotropin-like cytokine (NNT-1). These ligands signal via heterodimeric receptors composed of ligand-specific alpha chains and the common signal-transducing subunit gp130. Gene targeting in mice provided the first indication of a role for interleukin 6 family cytokines in implantation with the generation of mice with a null mutation of the gene encoding LIF. LIF null female mice were infertile because of failure of blastocyst implantation. More recently, interleukin-11 signalling has been shown to be required for the uterine decidualization response. This review describes the insights into the role of interleukin-6 family cytokines in female fertility that have come from gene targeting experiments in mice.Lorraine Robb, Eva Dimitriadis, Ruili Li, Lois A Salamonsen