Millipore Sigma Vibrant Logo
 

166881-42-1


56 Results Gelişmiş Arama  
Showing
Products (0)
Dokümanlar (56)
Site Content (0)

Sonuçlarınızı Daraltın Use the filters below to refine your search

Aradığınızı Bulamadınız mı?
Müşteri Hizmetleri ile
İletişime Geçin

 
MilliporeSigma Documents

Doküman ararken yardıma ihtiyacınız var mı?
  • Analiz sertifikaları, Kalite Sertifikaları veya Güvenlik Bilgi Formlarını aramak için Doküman Arayıcı’yı kullanmayı deneyin.
     
  • Kullanım Kılavuzlarına erişmek için yardıma ihtiyacınız olur ise Müşteri Hizmetleri ile iletişime geçebilirsiniz.

  • Renal injury: similarities and differences in male and female rats with the metabolic syndrome. 16688121

    The metabolic syndrome is complicated by nephropathy in humans and rats, and males are more affected than females. We hypothesized that female rats had reduced expression of glomerular oxidized low-density lipoprotein (oxLDL) receptor 1 (LOX-1), attendant glomerular oxidant injury, and renal inflammation. Three groups, obese males (OM), obese females (OF), and lean males (LM) of first-generation (F(1)) hybrid rats derived from the Zucker fatty diabetic (ZDF) strain and the spontaneous hypertensive heart failure rat (SHHF/Gmi-fa) were studied from 6 to 41 weeks of age. OM had severe renal oxidant injury and renal failure. Their glomeruli expressed the LOX-1, and exhibited heavier accumulation of the lipid peroxide 4-hydroxynonenal (4-HNE). OM had compromised mitochondrial enzyme function, more renal fibrosis, and vascular leakage. Younger LM, OM, and OF ZS (ZDF/SHHF F(1) hybrid rat) rats, studied from 6 to 16 weeks of age, showed that unutilized renal lipids were comparable in OM and OF, although young OM had worse nephropathy and inflammation. In conclusion, glomerular LOX-1 expression is coupled to deposits of 4-HNE and glomerulosclerosis in OM. We presume that LOX-1 enhances glomerular uptake of oxidized lipids and renal inflammation, causing greater oxidant stress and severe glomerulosclerosis. In OF, renal protection from lipid oxidants appears to be conferred by blunted glomerular LOX-1 expression and renal inflammation.
    Document Type:
    Reference
    Product Catalog Number:
    MAB1435
    Product Catalog Name:
    Anti-Macrophages/Monocytes Antibody, clone ED-1

  • Developmental and genetic regulation of human surfactant protein B in vivo. 18776725

    Genetic and developmental disruption of surfactant protein B (SP-B) expression causes neonatal respiratory distress syndrome (RDS).To assess developmental and genetic regulation of SP-B expression in vivo.To evaluate in vivo developmental regulation of SP-B, we used immunoblotting to compare frequency of detection of mature and pro-SP-B peptides in developmentally distinct cohorts: 24 amniotic fluid samples, unfractionated tracheal aspirates from 101 infants greater than or=34 weeks' gestation with (75) and without (26) neonatal RDS, and 6 nonsmoking adults. To examine genetic regulation, we used univariate and logistic regression analyses to detect associations between common SP-B (SFTPB) genotypes and SP-B peptides in the neonatal RDS cohort.We found pro-SP-B peptides in 24/24 amniotic fluid samples and in 100/101 tracheal aspirates from newborn infants but none in bronchoalveolar lavage from normal adults (0/6) (p less than 0.001). We detected an association (p = 0.0011) between pro-SP-B peptides (M(r) 40 and 42 kDa) and genotype of a nonsynonymous single nucleotide polymorphism at genomic position 1580 that regulates amino-terminus glycosylation.Pro-SP-B peptides are more common in developmentally less mature humans. Association of genotype at genomic position 1580 with pro-SP-B peptides (M(r) 40 and 42 kDa) suggests genetic regulation of amino terminus glycosylation in vivo.
    Document Type:
    Reference
    Product Catalog Number:
    AB3430
    Product Catalog Name:
    Anti-Prosurfactant Protein B Antibody, reacts with both CT and NT

  • Identification and characterization of uncoupling protein in heart and muscle mitochondria of canary birds. 20686918

    An uncoupling protein (cUCP) was identified in heart and skeletal muscle mitochondria of canary birds. cUCP was immunodetected using polyclonal antibodies raised against murine UCP2. Its molecular mass was similar to those of mammalian UCPs (32 kDa). The activity of cUCP was stimulated by palmitic acid (PA) and inhibited by GTP mainly in state 3 respiration. Additions of PA augmented state 4 respiration and lowered the ADP/O ratio. Thus, the activity of cUCP diverted energy from oxidative phosphorylation in state 3 respiration. cUCP in heart and skeletal muscles of canary birds might have implications in thermogenesis as well as protection against free radical production.
    Document Type:
    Reference
    Product Catalog Number:
    AB3046
    Product Catalog Name:
    Anti-Uncoupling Protein 3 Antibody

  • Post-receptor IGF1 insensitivity restricted to the MAPK pathway in a Silver-Russell syndrome patient with hypomethylation at the imprinting control region on chromosome 1 ... 22170793

    Hypomethylation of the paternal imprinting center region 1 (ICR1) is the most frequent molecular cause of Silver-Russell syndrome (SRS). Clinical evidence suggests that patients with this epimutation have mild IGF1 insensitivity.To assess in vitro IGF1 action in fibroblast culture from a patient with SRS and IGF1 insensitivity.Fibroblast cultures from one patient with SRS due to ICR1 demethylation and controls were established. The SRS patient has severe growth failure, elevated IGF1 level, and poor growth rate during human recombinant GH treatment. IGF1 action was assessed by cell proliferation, AKT, and p42/44-MAPK phosphorylation. Gene expression was determined by real-time PCR.Despite normal IGF1R sequence and expression, fibroblast proliferation induced by IGF1 was 50% lower in SRS fibroblasts in comparison with controls. IGF1 and insulin promoted a p42/44-MAPK activation in SRS fibroblasts 40 and 36%, respectively, lower than that in control fibroblasts. On the other hand, p42/44-MAPK activation induced by EGF stimulation was only slightly reduced (75% in SRS fibroblasts in comparison with control), suggesting a general impairment in MAPK pathway with a greater impairment of the stimulation induced by insulin and IGF1 than by EGF. A PCR array analysis disclosed a defect in MAPK pathway characterized by an increase in DUSP4 and MEF2C gene expressions in patient fibroblasts.A post-receptor IGF1 insensitivity was characterized in one patient with SRS and ICR1 hypomethylation. Although based on one unique severely affected patient, these results raise an intriguing mechanism to explain the postnatal growth impairment observed in SRS patients that needs confirmation in larger cohorts.
    Document Type:
    Reference
    Product Catalog Number:
    06-108

  • 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.
    Document Type:
    Reference
    Product Catalog Number:
    MAB318
    Product Catalog Name:
    Anti-Tyrosine Hydroxylase Antibody, clone LNC1

  • Slit protein-mediated inhibition of CXCR4-induced chemotactic and chemoinvasive signaling pathways in breast cancer cells. 14645233

    Slit, which mediates its function by binding to the Roundabout (Robo) receptor, has been shown to regulate neuronal and CXCR4-mediated leukocyte migration. Slit-2 was shown to be frequently inactivated in lung and breast cancers because of hypermethylation of its promoter region. Furthermore, the CXCR4/CXCL12 axis has been reported recently to be actively involved in breast cancer metastasis to target organs such as lymph nodes, lung, and bone. In this study, we sought to characterize the effect of Slit (=Slit-2) on the CXCL12/CXCR4-mediated metastatic properties of breast cancer cells. We demonstrate here that breast cancer cells and tissues derived from breast cancer patients express Robo 1 and 2 receptors. We also show that Slit treatment inhibits CXCL12/CXCR4-induced breast cancer cell chemotaxis, chemoinvasion, and adhesion, the fundamental components that promote metastasis. Slit had no significant effect on the CXCL12-induced internalization process of CXCR4. In addition, characterization of signaling events revealed that Slit inhibits CXCL12-induced tyrosine phosphorylation of focal adhesion components such as RAFTK/Pyk2 at residues 580 and 881, focal adhesion kinase at residue 576, and paxillin. We found that Slit also inhibits CXCL12-induced phosphatidylinositol 3-kinase, p44/42 MAP kinase, and metalloproteinase 2 and 9 activities. However, it showed no effect on JNK and p38 MAP kinase activities. To our knowledge, this is the first report to analyze in detail the effect of Slit on breast cancer cell motility as well as its effect on the critical components of the cancer cell chemotactic machinery. Studies of the Slit-Robo complex may foster new anti-chemotactic approaches to block cancer cell metastasis.
    Document Type:
    Reference
    Product Catalog Number:
    13-104
    Product Catalog Name:
    MBP (myelin basic protein), bovine, purified

  • Genome-wide mapping of estrogen receptor α binding sites by ChIP-seq to identify genes related to sexual maturity in hens. 29128632

    In ovarian follicle development, estrogen acts as a regulatory molecule to mediate proliferation and differentiation of follicular cells. ERα (estrogen receptor α) exerts regulatory function classically by binding directly to the estrogen response element, recruiting co-factors and activating or repressing transcription in response to E2. In this study, we used ChIP-seq to map ERα-binding sites in ovaries of Hy-line Brown commercial hens at 45d, 90d and 160d. In total, 24,886, 21,680 and 23,348 binding sites were identified in the ovaries of hens at 45d, 90d and 160d, which are linked to 86, 83 and 74 genes, respectively. The PPI network contains 47 protein nodes and 164 interaction edges, among which, AKT1 (V-Akt Murine Thymoma Viral Oncogene Homolog 1) and ACTN2 (Actinin Alpha 2) with the highest weight in the network, followed by CREB1 (CAMP Responsive Element Binding Protein 1), and EPHA5 (EPH Receptor A5) were identified. These genes are likely related to sexual maturity in hens. This study also provides insight into the regulation of the ERα target gene networks and a reference for understanding ERα-regulated transcription.
    Document Type:
    Reference
    Product Catalog Number:
    17-20000
    Product Catalog Name:
    Magna ChIP™ G Tissue Kit

  • The transcription factor Erg controls endothelial cell quiescence by repressing activity of nuclear factor (NF)-κB p65. 22337883

    The interaction of transcription factors with specific DNA sequences is critical for activation of gene expression programs. In endothelial cells (EC), the transcription factor NF-κB is important in the switch from quiescence to activation, and is tightly controlled to avoid excessive inflammation and organ damage. Here we describe a novel mechanism that controls the activation of NF-κB in EC. The transcription factor Erg, the most highly expressed ETS member in resting EC, controls quiescence by repressing proinflammatory gene expression. Focusing on intercellular adhesion molecule 1(ICAM)-1 as a model, we identify two ETS binding sites (EBS -118 and -181) within the ICAM-1 promoter required for Erg-mediated repression. We show that Erg binds to both EBS -118 and EBS -181, the latter located within the NF-κB binding site. Interestingly, inhibition of Erg expression in quiescent EC results in increased NF-κB-dependent ICAM-1 expression, indicating that Erg represses basal NF-κB activity. Erg prevents NF-κB p65 from binding to the ICAM-1 promoter, suggesting a direct mechanism of interference. Gene set enrichment analysis of transcriptome profiles of Erg and NF-κB-dependent genes, together with chromatin immunoprecipitation (ChIP) studies, reveals that this mechanism is common to other proinflammatory genes, including cIAP-2 and IL-8. These results identify a role for Erg as a gatekeeper controlling vascular inflammation, thus providing an important barrier to protect against inappropriate endothelial activation.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple