Millipore Sigma Vibrant Logo
 

128107-47-1


199 Results Gelişmiş Arama  
Showing
Products (0)
Dokümanlar (199)
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.
  • SPARC mediates early extracellular matrix remodeling following myocardial infarction. 21602472

    Secreted protein, acidic, and rich in cysteine (SPARC) is a matricellular protein that functions in the extracellular processing of newly synthesized collagen. Collagen deposition to form a scar is a key event following a myocardial infarction (MI). Because the roles of SPARC in the early post-MI setting have not been defined, we examined age-matched wild-type (WT; n=22) and SPARC-deficient (null; n=25) mice at day 3 post-MI. Day 0 WT (n=28) and null (n=20) mice served as controls. Infarct size was 52 ± 2% for WT and 47 ± 2% for SPARC null (P=NS), indicating that the MI injury was comparable in the two groups. By echocardiography, WT mice increased end-diastolic volumes from 45 ± 2 to 83 ± 5 μl (P less than 0.05). SPARC null mice also increased end-diastolic volumes but to a lesser extent than WT (39 ± 3 to 63 ± 5 μl; P less than 0.05 vs. day 0 controls and vs. WT day 3 MI). Ejection fraction fell post-MI in WT mice from 57 ± 2 to 19 ± 1%. The decrease in ejection fraction was attenuated in the absence of SPARC (65 ± 2 to 28 ± 2%). Fibroblasts isolated from SPARC null left ventricle (LV) showed differences in the expression of 22 genes encoding extracellular matrix and adhesion molecule genes, including fibronectin, connective tissue growth factor (CTGF; CCN2), matrix metalloproteinase-3 (MMP-3), and tissue inhibitor of metalloproteinase-2 (TIMP-2). The change in fibroblast gene expression levels was mirrored in tissue protein extracts for fibronectin, CTGF, and MMP-3 but not TIMP-2. Combined, the results of this study indicate that SPARC deletion preserves LV function at day 3 post-MI but may be detrimental for the long-term response due to impaired fibroblast activation.
    Document Type:
    Reference
    Product Catalog Number:
    AB1954
    Product Catalog Name:
    Anti-Fibronectin Antibody
  • Dissociated histaminergic neuron cultures from the tuberomammillary nucleus of rats: culture methods and ghrelin effects. 14706715

    The tuberomammillary nucleus (TMN) in the hypothalamus is the sole source of histamine in the brain. This nucleus, by innervating various brain regions, plays an important role for vital functions such as arousal and appetite. We have developed dissociated primary histaminergic neuron cultures from TMN of postnatal (3 and 10-day-old) rats. More than 50% of our cultured neurons from the TMN were histaminergic as revealed by adenosine deaminase (AD) as well as histamine immunocytochemistry. Among large neurons (diameter, >22 microm), more than 88% were histaminergic. Such large neurons (mean diameter, 26.5 microm) were used for electrophysiology. Using about 2-month-old TMN cultures, we investigated the effects of ghrelin, a recently discovered appetite-stimulating endogenous peptide. In GTPgammaS-loaded neurons, ghrelin (3 microM) suppressed currents that had previously been activated by an inhibitory neuropeptide, nociceptin. The mean current suppression by ghrelin was 471+/-128 pA (S.E.M., n=7). The I-V relationship revealed that the ghrelin-suppressed current was inwardly rectifying with a reversal potential around E(K). These results suggest that ghrelin inhibits G protein-coupled inward rectifier K+ channels (Kir3, GIRK) of TMN neurons and that our TMN cultures are useful for investigating physiological properties of brain histaminergic neurons.
    Document Type:
    Reference
    Product Catalog Number:
    AB5885
  • Higher intramuscular triacylglycerol in women does not impair insulin sensitivity and proximal insulin signaling. 19574502

    Women have been shown to have higher muscle triacylglycerol (IMTG) levels than men and could therefore be expected to have lower insulin sensitivity than men, since previous studies have linked high IMTG to decreased insulin sensitivity. Therefore, insulin sensitivity of whole body and leg glucose uptake was studied in 9 women in the follicular phase and 8 men on a controlled diet and matched for maximal oxygen uptake per kilogram of lean body mass and habitual activity level. A 47% higher (P 0.05) IMTG level was found in women than in men, and, at the same time, women also displayed 22% higher whole body insulin sensitivity (P 0.05) and 29% higher insulin-stimulated leg glucose uptake (P = 0.05) during an euglycemic-hyperinsulinemic ( approximately 70 muU/ml) clamp compared with matched male subjects. The higher insulin sensitivity in women could not be explained by higher expression of muscle glucose transporter GLUT4, insulin receptor, or Akt expression or by the ability of insulin to stimulate Akt Thr(308) or Akt Ser(473) phosphorylation. However, a 30% higher (P 0.05) capillary density and 31% more type 1 muscle fiber expressed per area in the vastus lateralis muscle were noted in women than in matched men. It is concluded that despite 47% higher IMTG levels in women in the follicular phase, whole body as well as leg insulin sensitivity are higher than in matched men. This was not explained by sex differences in proximal insulin signaling in women. In women, it seems that a high capillary density and type 1 muscle fiber expression may be important for insulin action.
    Document Type:
    Reference
    Product Catalog Number:
    05-802
  • FITTING KITS - 12710-1

    Document Type:
    Certificate of Quality
    Lot Number:
    12710-1
    Product Catalog Number:
    VPMHADAPSK
    Product Catalog Name:
    Fittings Kit
  • Measles virus V protein blocks interferon (IFN)-alpha/beta but not IFN-gamma signaling by inhibiting STAT1 and STAT2 phosphorylation. 12804771

    Measles virus (MV), a member of the family Paramyxoviridae, encodes C and V non-structural proteins. To clarify the functions of MV C and V proteins, HeLa cell lines constitutively expressing C or V protein were established. We found that expression of V protein inhibited interferon (IFN)-alpha/beta signaling but not IFN-gamma signaling. C protein had no inhibitory effect on IFN signaling in our experimental condition. Degradation of selective signal transducers and activators of transcription (STAT) proteins was not observed in HeLa cells expressing V protein. In contrast, tyrosine phosphorylation of both STAT1 and STAT2 was inhibited in these cells after IFN-beta stimulation.
    Document Type:
    Reference
    Product Catalog Number:
    07-224
    Product Catalog Name:
    Anti-phospho-STAT2 (Tyr689) Antibody
  • SynCAM 1 participates in axo-dendritic contact assembly and shapes neuronal growth cones. 20368431

    Neuronal growth cones are highly motile structures that tip developing neurites and explore their surroundings before axo-dendritic contact and synaptogenesis. However, the membrane proteins organizing these processes remain insufficiently understood. Here we identify that the synaptic cell adhesion molecule 1 (SynCAM 1), an immunoglobulin superfamily member, is already expressed in developing neurons and localizes to their growth cones. Upon interaction of growth cones with target neurites, SynCAM 1 rapidly assembles at these contacts to form stable adhesive clusters. Synaptic markers can also be detected at these sites. Addressing the functions of SynCAM 1 in growth cones preceding contact, we determine that it is required and sufficient to restrict the number of active filopodia. Further, SynCAM 1 negatively regulates the morphological complexity of migrating growth cones. Focal adhesion kinase, a binding partner of SynCAM 1, is implicated in its morphogenetic activities. These results reveal that SynCAM 1 acts in developing neurons to shape migrating growth cones and contributes to the adhesive differentiation of their axo-dendritic contacts.
    Document Type:
    Reference
    Product Catalog Number:
    MAB3420
    Product Catalog Name:
    Anti-Tau-1 Antibody, clone PC1C6
  • Anti-Daxx - 24496

    Document Type:
    Certificate of Analysis
    Lot Number:
    24496
    Product Catalog Number:
    07-471
    Product Catalog Name:
    Anti-Daxx Antibody
  • Subacute oral toxicity investigation of nanoparticulate and ionic silver in rats. 21969074

    Subacute toxicity of 14 nm nanoparticulate silver (Ag-NP) stabilised with polyvinylpyrrolidone and ionic silver in the form of silver acetate (Ag-acetate) was investigated in four-week-old Wistar rats. Animals received orally by gavage the following: vehicle control (10 ♀, 6 ♂); Ag-NP at doses: 2.25 (8 ♀), 4.5 (8 ♀) or 9 mg/kg bw/day (10 ♀, 6 ♂); or Ag-acetate 9 mg silver/kg bw/day (8 ♀) for 28 days. Clinical, haematolological and biochemical parameters, organ weights, macro- and microscopic pathological changes were investigated. Caecal bacterial phyla and their silver resistance genes were quantified. For the Ag-NP groups, no toxicological effects were recorded. For Ag-acetate, lower body weight gain (day 4-7, 11-14, 14-16, P < 0.05; overall, day 1-28, P < 0.01), increased plasma alkaline phosphatase (P < 0.05), decreased plasma urea (P < 0.05) and lower absolute (P < 0.01) and relative (P < 0.05) thymus weight were recorded. In conclusion, these findings indicate toxicity of 9 mg/kg bw/day ionic silver but not of an equimolar Ag-NP dose. This is in accordance with previously reported data showing that oral Ag-acetate, in comparison with an equimolar dose of Ag-NP, resulted in higher silver plasma and organ concentrations.
    Document Type:
    Reference
    Product Catalog Number:
    S7100
    Product Catalog Name:
    ApopTag® Peroxidase In Situ Apoptosis Detection Kit
  • Identification of a functional TPH1 polymorphism associated with irritable bowel syndrome bowel habit subtypes. 24060757

    Alterations in 5-hydroxytryptamine (5-HT) signaling have been implicated as a factor contributing to the altered bowel habit of irritable bowel syndrome (IBS) patients. Tryptophan hydroxylase 1 (TPH1) is the rate-limiting enzyme in enterochromaffin cell 5-HT biosynthesis. We hypothesized that genetic variants affecting TPH1 gene expression might alter intestinal 5-HT bioavailability and subsequently the propensity for distinct bowel habit subtypes in IBS. In this study, we assessed the only common TPH1 proximal promoter variant (-347C/A; rs7130929) and its association with bowel habit predominance in IBS.Electrophoretic mobility shift assays were performed to assess whether the -347C/A-allele variant affects the DNA binding of nuclear factors. Genotype distribution was determined for 422 IBS patients subtyped using the Rome III criteria and for 495 healthy controls recruited from two university medical centers. Association with bowel habit was tested using a multinomial logistic regression model controlling for race, anxiety, depression, and study site.Early growth response factor 1 (EGR-1) bound with higher affinity to a site comprising the minor A-allele of single-nucleotide polymorphism (SNP) -347C/A. TPH1 genotype frequencies did not differ between IBS patients and controls overall. The CC genotype was more prevalent in the IBS-D subtype (47%) than in the IBS-C (25%) and IBS-M (37%) subtypes (P=0.039) after adjusting for race and other covariates. Colonic biopsies from a small cohort of IBS patients from one center were tested for higher TPH1 mRNA expression in samples with CC compared with the CA genotype, but the results did not reach statistical significance.The TPH1 promoter SNP -347C/A differentially binds EGR-1 and correlates with IBS bowel habit subtypes and possibly colonic TPH1 expression consistent with its role in modulating intestinal 5-HT signaling.
    Document Type:
    Reference
    Product Catalog Number:
    MAB374
    Product Catalog Name:
    Anti-Glyceraldehyde-3-Phosphate Dehydrogenase Antibody, clone 6C5