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  • Anti-GLUT-4 - 3330205

    Document Type:
    Certificate of Analysis
    Lot Number:
    3330205
    Product Catalog Number:
    07-1404
    Product Catalog Name:
    Anti-GLUT-4 Antibody, C-terminus

  • Anti-KLF11 - NRG1672069

    Document Type:
    Certificate of Analysis
    Lot Number:
    NRG1672069
    Product Catalog Number:
    06-1404
    Product Catalog Name:
    Anti-KLF11 Antibody

  • Anti-GLUT-4 -2639369

    Document Type:
    Certificate of Analysis
    Lot Number:
    2639369
    Product Catalog Number:
    07-1404
    Product Catalog Name:
    Anti-GLUT-4 Antibody, C-terminus

  • Anti-GLUT-4 Polyclonal Antibody

    Document Type:
    Certificate of Analysis
    Lot Number:
    2972852
    Product Catalog Number:
    07-1404
    Product Catalog Name:
    Anti-GLUT-4 Antibody, C-terminus

  • Intrahippocampal administration of amyloid-β(1-42) oligomers acutely impairs spatial working memory, insulin signaling, and hippocampal metabolism. 22430529

    Increasing evidence suggests that abnormal brain accumulation of amyloid-β(1-42) (Aβ(1-42)) oligomers plays a causal role in Alzheimer's disease (AD), and in particular may cause the cognitive deficits that are the hallmark of AD. In vitro, Aβ(1-42) oligomers impair insulin signaling and suppress neural functioning. We previously showed that endogenous insulin signaling is an obligatory component of normal hippocampal function, and that disrupting this signaling led to a rapid impairment of spatial working memory, while delivery of exogenous insulin to the hippocampus enhanced both memory and metabolism; diet-induced insulin resistance both impaired spatial memory and prevented insulin from increasing metabolism or cognitive function. Hence, we tested the hypothesis that Aβ(1-42) oligomers could acutely impair hippocampal metabolic and cognitive processes in vivo in the rat. Our findings support this hypothesis: Aβ(1-42) oligomers impaired spontaneous alternation behavior while preventing the task-associated dip in hippocampal ECF glucose observed in control animals. In addition, Aβ(1-42) oligomers decreased plasma membrane translocation of the insulin-sensitive glucose transporter 4 (GluT4), and impaired insulin signaling as measured by phosphorylation of Akt. These data show in vivo that Aβ(1-42) oligomers can rapidly impair hippocampal cognitive and metabolic processes, and provide support for the hypothesis that elevated Aβ(1-42) leads to cognitive impairment via interference with hippocampal insulin signaling.
    Document Type:
    Reference
    Product Catalog Number:
    07-1404
    Product Catalog Name:
    Anti-GLUT-4 Antibody, C-terminus

  • ChREBP, a glucose-responsive transcriptional factor, enhances glucose metabolism to support biosynthesis in human cytomegalovirus-infected cells. 24449882

    Carbohydrate-response element binding protein (ChREBP) plays a key role in regulating glucose metabolism and de novo lipogenesis in metabolic tissues and cancer cells. Here we report that ChREBP is also a critical regulator of the metabolic alterations induced during human cytomegalovirus (HCMV) infection. The expression of both ChREBP-α and ChREBP-β is robustly induced in HCMV-infected human fibroblasts; this induction is required for efficient HCMV infection. Depletion of ChREBP in HCMV-infected cells results in reduction of HCMV-induced glucose transporter 4 and glucose transporter 2 expression, leading to inhibition of glucose uptake, lactate production, nucleotide biosynthesis, and NADPH generation. We previously reported that HCMV infection induces lipogenesis through the activation of sterol regulatory element binding protein 1, which is mediated by the induction of PKR-like endoplasmic reticulum kinase. Data from the present study show that HCMV-induced lipogenesis is also controlled by the induction of ChREBP, in a second mechanism involved in the regulation of HCMV-induced de novo lipogenesis. These results suggest that ChREBP plays a key role in reprogramming glucose and lipid metabolism in HCMV infection.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Anti-GLUT-4 - 3175963

    Document Type:
    Certificate of Analysis
    Lot Number:
    3175963
    Product Catalog Number:
    07-1404
    Product Catalog Name:
    Anti-GLUT-4 Antibody, C-terminus

  • Anti-GLUT-4 - 3829399

    Document Type:
    Certificate of Analysis
    Lot Number:
    3829399
    Product Catalog Number:
    07-1404
    Product Catalog Name:
    Anti-GLUT-4 Antibody, C-terminus

  • Clk/STY (cdc2-like kinase 1) and Akt regulate alternative splicing and adipogenesis in 3T3-L1 pre-adipocytes. 23308182

    The development of adipocytes from their progenitor cells requires the action of growth factors signaling to transcription factors to induce the expression of adipogenic proteins leading to the accumulation of lipid droplets, induction of glucose transport, and secretion of adipokines signaling metabolic events throughout the body. Murine 3T3-L1 pre-adipocytes sequentially express all the proteins necessary to become mature adipocytes throughout an 8-10 day process initiated by a cocktail of hormones. We examined the role of Clk/STY or Clk1, a cdc2-like kinase, in adipogenesis since it is known to be regulated by Akt, a pivotal kinase in development. Inhibition of Clk1 by a specific inhibitor, TG003, blocked alternative splicing of PKCβII and expression of PPARγ1 and PPARγ2. SiRNA depletion of Clk1 resulted in early expression of PKCβII and sustained PKCβI expression. Since Clk1 is a preferred Akt substrate, required for phosphorylation of splicing factors, mutation of Clk1 Akt phosphorylation sites was undertaken. Akt sites on Clk1 are in the serine/arginine-rich domain and not the kinase domain. Mutation of single and multiple sites resulted in dysregulation of PKCβII, PKCβI, and PPARγ1&2 expression. Additionally, adipogenesis was blocked as assessed by Oil Red O staining, adiponectin, and Glut1 and 4 expression. Immunofluorescence microscopy revealed that Clk1 triple mutant cDNA, transfected into pre-adipocytes, resulted in excluding SRp40 (SFSR6) from co-localizing to the nucleus with PFS, a perispeckle specific protein. This study demonstrates the role of Akt and Clk1 kinases in the early differentiation of 3T3-L1 cells to adipocytes.
    Document Type:
    Reference
    Product Catalog Number:
    07-1404
    Product Catalog Name:
    Anti-GLUT-4 Antibody, C-terminus

  • Anti-GLUT-4 - NG1757996

    Document Type:
    Certificate of Analysis
    Lot Number:
    NG1757996
    Product Catalog Number:
    07-1404
    Product Catalog Name:
    Anti-GLUT-4 Antibody, C-terminus