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  • Anti-GLUT-5, a.a. 490-502 -2891899

    Document Type:
    Certificate of Analysis
    Lot Number:
    2891899
    Product Catalog Number:
    07-1406
    Product Catalog Name:
    Anti-GLUT-5 Antibody, a.a. 490-502

  • Evidence for differential cortical input to direct pathway versus indirect pathway striatal projection neurons in rats. 15385612

    The two main types of corticostriatal neurons are those that project only intratelencephalically (IT-type), the intrastriatal terminals of which are 0.41 microm in mean diameter, and those that send their main axon into pyramidal tract and have a collateral projection to striatum (PT-type), the intrastriatal terminals of which are 0.82 microm in mean diameter. We used three approaches to examine whether the two striatal projection neuron types (striatonigral direct pathway vs striatopallidal indirect pathway) differ in their input from IT-type and PT-type neurons. First, we retrogradely labeled one striatal projection neuron type or the other with biotinylated dextran amine (BDA)-3000 molecular weight. We found that terminals making asymmetric axospinous contact with striatonigral neurons were 0.43 microm in mean diameter, whereas those making asymmetric axospinous contact with striatopallidal neurons were 0.69 microm. Second, we preferentially immunolabeled striatonigral neurons for D1 dopamine receptors or striatopallidal neurons for D2 dopamine receptors and found that axospinous terminals had a smaller mean size (0.45 microm) on D1+ spines than on D2+ spines (0.61 microm). Finally, we combined selective BDA labeling of IT-type or PT-type terminals with immunolabeling for D1 or D2, and found that IT-type terminals were twice as common as PT-type on D1+ spines, whereas PT-type terminals were four times as common as IT-type on D2+ spines. These various results suggest that striatonigral neurons preferentially receive input from IT-type cortical neurons, whereas striatopallidal neurons receive greater input from PT-type cortical neurons. This differential cortical connectivity may further the roles of the direct and indirect pathways in promoting desired movements and suppressing unwanted movements, respectively.
    Document Type:
    Reference
    Product Catalog Number:
    AB5084P
    Product Catalog Name:
    Anti-Dopamine D2 Receptor Antibody

  • Estrogen and cytochrome P450 1B1 contribute to both early- and late-stage head and neck carcinogenesis. 21205741

    Squamous cell carcinoma of the head and neck (HNSCC) is the sixth most common type of cancer in the United States. The goal of this study was to evaluate the contribution of estrogens to the development of HNSCCs. Various cell lines derived from early- and late-stage head and neck lesions were used to characterize the expression of estrogen synthesis and metabolism genes, including cytochrome P450 (CYP) 1B1, examine the effect of estrogen on gene expression, and evaluate the role of CYP1B1 and/or estrogen in cell motility, proliferation, and apoptosis. Estrogen metabolism genes (CYP1B1, CYP1A1, catechol-o-methyltransferase, UDP-glucuronosyltransferase 1A1, and glutathione-S-transferase P1) and estrogen receptor (ER) β were expressed in cell lines derived from both premalignant (MSK-Leuk1) and malignant (HNSCC) lesions. Exposure to estrogen induced CYP1B1 2.3- to 3.6-fold relative to vehicle-treated controls (P = 0.0004) in MSK-Leuk1 cells but not in HNSCC cells. CYP1B1 knockdown by shRNA reduced the migration and proliferation of MSK-Leuk1 cells by 57% and 45%, respectively. Exposure of MSK-Leuk1 cells to estrogen inhibited apoptosis by 26%, whereas supplementation with the antiestrogen fulvestrant restored estrogen-dependent apoptosis. Representation of the estrogen pathway in human head and neck tissues from 128 patients was examined using tissue microarrays. The majority of the samples exhibited immunohistochemical staining for ERβ (91.9%), CYP1B1 (99.4%), and 17β-estradiol (88.4%). CYP1B1 and ERβ were elevated in HNSCCs relative to normal epithelium (P = 0.024 and 0.008, respectively). These data provide novel insight into the mechanisms underlying head and neck carcinogenesis and facilitate the identification of new targets for chemopreventive intervention.
    Document Type:
    Reference
    Product Catalog Number:
    05-824
    Product Catalog Name:
    Anti-Estrogen Receptor β Antibody, clone 68-4, rabbit monoclonal

  • Detection of human influenza virus in Yucatan, Mexico. 12587415

    OBJECTIVE: Influenza virus is the most common cause of Acute Respiratory Infections (ARI) world wide. In patients with chronic condition, infection by the influenza virus can cause complications such as pneumonia which may have fatal outcome. The aim of this work was to determine the frequency of human influenza virus in outpatients with influenza-like illness (ILI) and in those patients admitted to hospital with community acquired pneumonia (CAP) in Yucatan, Mexico (October 1998-July 1999). MATERIALS AND METHODS: Throat swabs were collected from ILI and CAP patients and processed to detect respiratory viruses. All clinical samples were tested for seven respiratory viruses using a rapid indirect immunofluorescence test (IFI). Clinical samples with positive results for influenza virus by IFI were inoculated into chick embryo eggs and/or MDCK cells for viral isolation. All influenza virus isolates were typed using the WHO influenza Kit 1998-1999. RESULTS: A total of 288 clinical samples were collected. Influenza virus type A was diagnosed in 29 clinical samples (10%), no other respiratory viruses were identified. Influenza virus was present with 8.9% (17 out of 189) in ILI patients, whereas with 12.12% (12 out of 99) in CAP patients. Influenza virus was detected from December to July. Six viral isolates were obtained and identified as influenza A (H3N2). CONCLUSION: Human influenza virus is certainly a cause of ARI and pneumonia in Yucatan, Mexico. The results showed that influenza virus contributes to at least 8.9% of the ARI, and more importantly to 12% of CAP patients. Positive cases were present in a different pattern to temperate zones where the peak of incidence occurs during autumn and winter.
    Document Type:
    Reference
    Product Catalog Number:
    3105

  • Direct inhibition of RNAse T2 expression by the HTLV-1 viral protein Tax. 21994792

    Adult T-cell leukemia (ATL) is one of the primary diseases caused by Human T-cell Leukemia Virus type 1 (HTLV-1) infection. The virally-encoded Tax protein is believed to initiate early events in the development of this disease, as it is able to promote immortalization of T-cells and transformation of other cell types. These processes may be aided by the ability of the viral protein to directly deregulate expression of specific cellular genes through interactions with numerous transcriptional regulators. To identify gene promoters where Tax is localized, we isolated Tax-DNA complexes from an HTLV-1-infected T-cell line through a chromatin immunoprecipitation (ChIP) assay and used the DNA to probe a CpG island microarray. A site within the RNASET2 gene was found to be occupied by Tax. Real-time PCR analysis confirmed this result, and transient expression of Tax in uninfected cells led to the recruitment of the viral protein to the promoter. This event correlated with a decrease in the level of RNase T2 mRNA and protein, suggesting that Tax represses expression of this gene. Loss of RNase T2 expression occurs in certain hematological malignancies and other forms of cancer, and RNase T2 was recently reported to function as a tumor suppressor. Consequently, a reduction in the level of RNase T2 by Tax may play a role in ATL development.
    Document Type:
    Reference
    Product Catalog Number:
    06-863
    Product Catalog Name:
    Anti-CREB Antibody

  • Glycoprotein gp110 of Epstein-Barr virus determines viral tropism and efficiency of infection. 12409611

    The Epstein-Barr virus (EBV) genome has been detected in lymphomas and in tumors of epithelial or mesenchymal origin such as nasopharyngeal carcinoma or leiomyosarcoma. Thus, there is little doubt that EBV can infect cells of numerous lineages in vivo, in contrast to its in vitro infectious spectrum, which appears restricted predominantly to B lymphocytes. We show here that the EBV BALF4 gene product, the glycoprotein gp110, dramatically enhances the ability of EBV to infect human cells. gp110(high) viruses were up to 100 times more efficient than their gp110(low) counterparts in infecting lymphoid or epithelial cells. In addition, gp110(high) viruses infected the carcinoma cell line HeLa and the T cell lymphoma cell line Molt-4, both previously thought to be refractory to EBV infection. Analysis of several virus isolates showed that the amount of BALF4 present within mature virions markedly differed among these strains. In some strains, gp110 was found expressed during lytic replication not only at the nuclear but also at the cellular membrane. Heterologous expression of gp110 during the virus lytic phase neither altered virus concentration nor affected virus binding to cells. It appears that gp110 plays a crucial role after the virus has adhered to its cellular target. gp110 constitutes an important virulence factor that determines infection of non-B cells by EBV. Therefore, the use of gp110(high) viruses will help to determine the range of the target cells of EBV beyond B lymphocytes and provide a useful in vitro model to assess the oncogenic potential of EBV in these cells.
    Document Type:
    Reference
    Product Catalog Number:
    MAB8184
    Product Catalog Name:
    Anti-EBV VCA gp125 Antibody, clone L2

  • Hematopoietic-specific activators establish an overlapping pattern of histone acetylation and methylation within a mammalian chromatin domain. 12379744

    Posttranslational modification of histones through acetylation, methylation, and phosphorylation is a common mode of regulating chromatin structure and, therefore, diverse nuclear processes. One such modification, methylated histone H3 at lysine-4 (H3-meK4), colocalizes with hyperacetylated histones H3 and H4 in mammalian chromatin. Whereas activators directly recruit acetyltransferases, the process whereby H3-meK4 is established is unknown. We tested whether the hematopoietic-specific activators NF-E2 and GATA-1, which mediate transactivation of the beta-globin genes, induce both histone acetylation and H3-meK4. Through the use of NF-E2- and GATA-1-null cell lines, we show that both activators induce H3 acetylation at the promoter upon transcriptional activation. However, analysis of H3-mek4 revealed that NF-E2 and GATA-1 differentially regulate chromatin modifications at the betamajor promoter. NF-E2, but not GATA-1, induces H3-meK4 at the promoter. Thus, under conditions in which NF-E2 and GATA-1 activate the transcription of an endogenous gene at least 570-fold, these activators differ in their capacity to induce H3-meK4. Despite strong H3-meK4 at hypersensitive site 2 of the upstream locus control region, neither factor was required to establish H3-meK4 at this site. These results support a model in which multiple tissue-specific activators collectively function to assemble a composite histone modification pattern, consisting of overlapping histone acetylation and methylation. As GATA-1 induced H3 acetylation, but not H3-meK4, at the promoter, H3 acetylation and H3-meK4 components of a composite histone modification pattern can be established independently.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple