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  • Tubule-specific ablation of endogenous β-catenin aggravates acute kidney injury in mice. 22622501

    β-Catenin is a unique intracellular protein functioning as an integral component of the cell-cell adherens complex and a principal signaling protein mediating canonical Wnt signaling. Little is known about its function in adult kidneys in the normal physiologic state or after acute kidney injury (AKI). To study this, we generated conditional knockout mice in which the β-catenin gene was specifically disrupted in renal tubules (Ksp-β-cat-/-). These mice were phenotypically normal with no appreciable defects in kidney morphology and function. In the absence of β-catenin, γ-catenin functionally substituted for it in E-cadherin binding, thereby sustaining the integrity of epithelial adherens junctions in the kidneys. In AKI induced by ischemia reperfusion or folic acid, the loss of tubular β-catenin substantially aggravated renal lesions. Compared with controls, Ksp-β-cat-/- mice displayed higher mortality, elevated serum creatinine, and more severe morphologic injury. Consistently, apoptosis was more prevalent in kidneys of the knockout mice, which was accompanied by increased expression of p53 and Bax, and decreased phosphorylated Akt and survivin. In vitro activation of β-catenin by Wnt1 or stabilization of β-catenin protected tubular epithelial cells from apoptosis, activated Akt, induced survivin, and repressed p53 and Bax expression. Hence, endogenous β-catenin is pivotal for renal tubular protection after AKI by promoting cell survival through multiple mechanisms.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo

  • Exercise reverses high-fat diet-induced impairments on compartmentalization and activation of components of the insulin-signaling cascade in skeletal muscle. 17623749

    The aims of this investigation were 1) to determine whether endurance exercise training could reverse impairments in insulin-stimulated compartmentalization and/or activation of aPKCzeta/lambda and Akt2 in skeletal muscle from high-fat-fed rodents and 2) to assess whether the PPARgamma agonist rosiglitazone could reverse impairments in skeletal muscle insulin signaling typically observed after high-fat feeding. Sprague-Dawley rats were placed on chow (NORCON, n = 16) or high-fat (n = 64) diets for 4 wk. During a subsequent 4-wk experimental period, high-fat-fed rats were allocated (n = 16/group) to either sedentary control (HFC), exercise training (HFX), rosiglitazone treatment (HFRSG), or a combination of both exercise training and rosiglitazone (HFRX). Following the 4-wk experimental period, animals underwent hindlimb perfusions. Insulin-stimulated plasma membrane-associated aPKCzeta and -lambda protein concentration, aPKCzeta/lambda activity, GLUT4 protein concentration, cytosolic Akt2, and aPKCzeta/lambda activities were reduced (P less than 0.05) in HFC compared with NORCON. Cytosolic Akt2, aPKCzeta, and aPKClambda protein concentrations were not affected in HFC compared with NORCON. Exercise training reversed the deleterious effects of the high-fat diet such that insulin-stimulated compartmentalization and activation of components of the insulin-signaling cascade in HFX were normalized to NORCON. High-fat diet-induced impairments to skeletal muscle glucose metabolism were not reversed by rosiglitazone administration, nor did rosiglitazone augment the effect of exercise. Our findings indicate that chronic exercise training, but not rosiglitazone, reverses high-fat diet induced impairments in compartmentalization and activation of components of the insulin-signaling cascade in skeletal muscle.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo

  • Cholesterol diet-induced hyperlipidemia impairs the cardioprotective effect of postconditioning: role of peroxynitrite. 19734363

    The aim of the present study was to investigate if hyperlipidemia interferes with the infarct size-limiting effect of postconditioning and to study the involvement of peroxynitrite in this phenomenon. Rats were fed a 2% cholesterol-enriched or normal diet for 12 wk. Infarct size by triphenyltetrazolium chloride staining was measured in hearts isolated from both groups and subjected to 30 min coronary occlusion followed by 120 min reperfusion with or without the postconditioning protocol induced by six cycles of 10 s coronary occlusion and 10 s reperfusion at the onset of the reperfusion. Postconditioning significantly decreased infarct size in the normolipidemic but not in the hyperlipidemic group. Postconditioning increased cardiac 3-nitrotyrosine concentration (a marker for peroxynitrite formation) in the normal but not in the cholesterol-fed group when measured at the 5th min of reperfusion. Next, we tested if the postconditioning-induced acute increase in peroxynitrite is involved in the cardioprotection in normolipidemic animals in separate experiments. Postconditioning failed to decrease infarct size in the presence of the peroxynitrite decomposition catalyst 5,10,15,20-tetrakis-[4-sulfonatophenyl]-porphyrinato-iron [III] (20 mg/l) in normolipidemic animals. We conclude that an early increase in peroxynitrite after postconditioning plays a role in cardioprotection. Furthermore, hyperlipidemia blocks the cardioprotective effect of postconditioning at least in part via deterioration of the postconditioning-induced early increase in peroxynitrite formation.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB5404
    Nombre del producto:
    Anti-Nitrotyrosine Antibody, clone 2A8.2

  • Galactolipid deficiency in the early pathogenesis of neuronal ceroid lipofuscinosis model Cln8mnd : implications to delayed myelination and oligodendrocyte maturation. 22044361

    CLN8 deficiency underlies one of a group of devastating childhood neurodegenerative disorders, the neuronal ceroid lipofuscinoses. The function of the CLN8 protein is currently unknown, but a role in lipid metabolism has been proposed. In human CLN8 diseased brains, alterations in lipid composition have been detected. To further investigate the connection of CLN8 to lipid metabolism, we characterized the lipid composition of early symptomatic Cln8-deficient mouse (Cln8(mnd)) brains.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB5320
    Nombre del producto:
    Anti-NG2 Chondroitin Sulfate Proteoglycan Antibody

  • N-terminal tail of a viral histone H4 encoded in Cotesia plutellae bracovirus is essential to suppress gene expression of host histone H4. 19196351

    An endoparasitoid wasp, Cotesia plutellae, possesses a symbiotic bracovirus (CpBV), which facilitates parasitism of a specific host, such as larvae of the diamondback moth, Plutella xylostella. A viral histone H4 (CpBV-H4) has been found in the CpBV genome and its gene product plays a role in impairing the host insect cellular immune response. Based on its high similarity to histone H4 of P. xylostella apart from its extended N-terminal tail, it has been suspected to alter host gene expression. Histone subunits were purified from parasitized P. xylostella larvae and found to contain both host and viral H4s, confirming a previous report of a possible epigenetic mode of action. Moreover, this study showed that the host H4 levels in the parasitized larvae clearly decreased during the parasitization period, whereas CpBV-H4 levels maintained a significant level without significant changes. To understand the decrease of host H4 levels, transcription levels of host H4 were monitored by quantitative reverse-transcriptase PCR (RT-PCR) and showed a significant decrease in parasitized P. xylostella larvae, whereas no significant change of the mRNA level was detected in nonparasitized larvae. This transcriptional control of host H4 expression was also observed by inducing transient expression of CpBV-H4 in nonparasitized P. xylostella. Moreover, co-injection of CpBV-H4 and its specific double-stranded RNA recovered the host H4 expression level. To identify a functional domain of CpBV-H4 involved in the transcriptional control, the extended N-terminal tail of CpBV-H4 was removed by preparing a truncated viral H4 construct in an expression vector by deleting the N-terminal tail of 38 amino acid residues and inducing its expression in nonparasitized P. xylostella larvae. The truncated CpBV-H4 clearly lost its inhibitory effects on host H4 transcription. Moreover, the presence of CpBV-H4 affects the spreading of host haemocytes by an epigenetic effect, which is at least partly restored in larvae expressing the truncated version of CpBV-H4. This study suggests that the viral H4 encoded in CpBV can alter host gene expression with its extended N-terminal tail.
    Tipo de documento:
    Referencia
    Referencia del producto:
    05-858
    Nombre del producto:
    Anti-Histone H4 Antibody, pan, clone 62-141-13, rabbit monoclonal

  • Extracellular matrix-induced transforming growth factor-beta receptor signaling dynamics. 20101206

    Matrix remodeling, degradation, inflammation and invasion liberate peptide fragments that can subsequently interact with cells in an attachment-independent manner. Such 'soluble' matrix components, including collagens, fibronectin and laminin, induced Smad activation (termed crosstalk signaling), which follows a similar chronological sequence and R-Smad specificity as induced by transforming growth factor (TGF)-beta1. Smad4 nuclear translocation occurred in response to collagen binding, indicating downstream signal propagation. TGF-beta scavenging antibody affected only TGF-beta1, but not crosstalk-induced responses. TGF-beta type II receptor mutation (DR26Delta25), which is deficient in TGF-beta type I receptor recruitment to the ligand, induced a heterotetramer signaling complex, and propagated Smad2 activation only through collagen induction and not TGF-beta signaling. Consequentially, TGF-beta ligand participation is not required for crosstalk signaling. This signaling requires a functional integrin beta1 receptor as showed by RNA interference. Co-immunoprecipitation (co-IP) and fluorescent microscopy indicate the involvement of focal adhesion kinase (FAK) and Src activity in collagen-induced signal propagation, and suggest a membrane signaling complex formation that includes both TGF-beta receptors and integrins. The related gene expressional responses are distinct from that evoked by TGF-beta1, supporting its separate function. This signaling mechanism expands and partially explains TGF-beta receptor dynamics and consequential signaling diversity-related gene expressional plasticity.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB1965
    Nombre del producto:
    Anti-Integrin β1 Antibody, a.a. 82-87, clone JB1A (a.k.a. J10)

  • 14-3-3zeta contributes to tyrosine hydroxylase activity in MN9D cells: localization of dopamine regulatory proteins to mitochondria. 19289463

    The 14-3-3 proteins stimulate the activation of tyrosine hydroxylase (TH), the rate-limiting catecholamine biosynthetic enzyme. To explore if particular endogenous 14-3-3 isoforms specifically affected TH activity and dopamine synthesis, we utilized rodent nigrostriatal tissues and midbrain-derived MN9D dopaminergic cells. Extracts from ventral midbrain and MN9D cells contained similar pools of 14-3-3 mRNAs, with 14-3-3zeta being relatively abundant in both. Protein levels of 14-3-3zeta were also abundant. [(32)P]Orthophosphate labeling of MN9D cells, followed by co-immunoprecipitation with pan-TH and pan-14-3-3 antibodies brought down similar amounts of phosphorylated TH in each, confirming that 14-3-3-bound phosphorylated TH in our cells. Co-immunoprecipitation of striatal tissues with a pan-TH antibody precipitated 14-3-3zeta but not another potential TH regulatory isoform, 14-3-3eta. In whole cell extracts from MN9D cells after 14-3-3 small interfering RNA treatments, we found that 14-3-3zeta knockdown significantly reduced TH activity and dopamine synthesis whereas knockdown of 14-3-3eta had no effect. 14-3-3zeta was found co-localized on mitochondria with TH, and its knockdown by small interfering RNA reduced TH phosphorylation and TH activity in the mitochondrial pool. Together the data support a role for 14-3-3zeta as an endogenous activator of TH in midbrain dopaminergic neurons and furthermore, identify mitochondria as a potential novel site for dopamine synthesis, with implications for Parkinson disease.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo

  • Nuclear expression of a group II intron is consistent with spliceosomal intron ancestry. 20351053

    Group II introns are self-splicing RNAs found in eubacteria, archaea, and eukaryotic organelles. They are mechanistically similar to the metazoan nuclear spliceosomal introns; therefore, group II introns have been invoked as the progenitors of the eukaryotic pre-mRNA introns. However, the ability of group II introns to function outside of the bacteria-derived organelles is debatable, since they are not found in the nuclear genomes of eukaryotes. Here, we show that the Lactococcus lactis Ll.LtrB group II intron splices accurately and efficiently from different pre-mRNAs in a eukaryote, Saccharomyces cerevisiae. However, a pre-mRNA harboring a group II intron is spliced predominantly in the cytoplasm and is subject to nonsense-mediated mRNA decay (NMD), and the mature mRNA from which the group II intron is spliced is poorly translated. In contrast, a pre-mRNA bearing the Tetrahymena group I intron or the yeast spliceosomal ACT1 intron at the same location is not subject to NMD, and the mature mRNA is translated efficiently. Thus, a group II intron can splice from a nuclear transcript, but RNA instability and translation defects would have favored intron loss or evolution into protein-dependent spliceosomal introns, consistent with the bacterial group II intron ancestry hypothesis.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo

  • Characterisation of a novel model of Parkinson\'s disease by intra-striatal infusion of the pesticide rotenone. 21277943

    One of the most promising models of Parkinson\'s disease to have emerged in recent years is one in which the pesticide, rotenone, is administered systemically to laboratory rats. However, this model is associated with peripheral toxicity and high mortality rates which impede its widespread application in preclinical drug discovery research. This study sought to determine if administration of rotenone directly into the rat striatum could also mimic the motor dysfunction and neuropathological features of the human condition while overcoming the toxicity associated with systemic administration. Male Sprague-Dawley rats were infused with control or rotenone solutions into the striatum. The effect of the pesticide on body weight and spontaneous motor function (Corridor, Stepping and Whisker Tests) was assessed ante mortem, and its effect on nigrostriatal integrity (quantitative tyrosine hydroxylase immunohistochemistry), α-synuclein expression (quantitative α-synuclein immunohistochemistry), and striatal neurotransmitter content (HLPC for dopamine, GABA and noradrenaline) was assessed post mortem. Intra-striatal infusion of rotenone had no detrimental effect on the rats\' body weight but caused significant impairments in contralateral motor function. Neuropathologically, rotenone caused significant nigrostriatal degeneration and selective loss of dopamine from the striatum but there was no evidence of any change in α-synuclein expression in the rotenone-infused rats. This study shows intra-striatal rotenone to be capable of modelling some of the main behavioural and neuropathological features of human Parkinsonism, while being less toxic than its systemic counterpart. Thus, this model may prove to be useful in future Parkinson\'s disease drug discovery programmes.Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB318
    Nombre del producto:
    Anti-Tyrosine Hydroxylase Antibody, clone LNC1