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  • cAMP

    Document Type:
    Certificate of Analysis
    Lot Number:
    2884525
    Product Catalog Number:
    20-198
    Product Catalog Name:
    cAMP

  • cAMP

    Document Type:
    Certificate of Analysis
    Lot Number:
    2942741
    Product Catalog Number:
    20-198
    Product Catalog Name:
    cAMP

  • cAMP

    Document Type:
    Certificate of Analysis
    Lot Number:
    3090961
    Product Catalog Number:
    20-198
    Product Catalog Name:
    cAMP

  • Decreased cAMP response element-mediated transcription: an early event in exon 1 and full-length cell models of Huntington's disease that contributes to polyglutamine pat ... 14627700

    Huntington's disease (HD) is one of nine neurodegenerative diseases caused by an expanded polyglutamine (polyQ) tract within the disease protein. To characterize pathways induced early in HD, we have developed stable inducible PC12 cell lines expressing wild-type or mutant forms of huntingtin exon 1 fragments or the full-length huntingtin protein. Three cAMP response element-binding protein (CREB)-binding protein-dependent transcriptional pathways, regulated by cAMP response element (CRE), retinoic acid response element, and nuclear factor kappaB, show abnormalities in our exon 1 cell model. Of these, the CRE pathway shows the earliest disruption and is significantly down-regulated as early as 12 h following mutant htt transgene induction. This pathway is also the only one of the three that is similarly perturbed in our full-length HD model, where it is also down-regulated at an early time point, compatible with observations in HD brains. Reduced CRE-dependent transcription may contribute to polyQ disease pathogenesis because overexpression of transcriptionally active CREB, but not an inactive form of the protein, is able to protect against polyQ-induced cell death and reduce aggregation.
    Document Type:
    Reference
    Product Catalog Number:
    MAB2166
    Product Catalog Name:
    Anti-Huntingtin Protein Antibody, a.a. 181-810, clone 1HU-4C8

  • The cAMP effector EPAC activates Elk1 transcription factor in prostate smooth muscle, and is a minor regulator of α1-adrenergic contraction. 23815815

    Prostate smooth muscle tone is regulated by α1-adrenoceptor-induced contraction and cAMP-mediated relaxation. EPAC is an effector of cAMP, being involved in smooth muscle relaxation and cell cycle control outside the lower urinary tract. Here, we investigated the expression and function of EPAC in human prostate tissues from patients undergoing radical prostatectomy.mRNA and protein expression of EPAC was detected in all prostate tissues by RT-PCR and Western blot analysis. Immunoreactivity was observed in stromal cells, and colocalized with immunofluorescence for α-smooth muscle actin and calponin. Under normal conditions, noradrenaline- or phenylephrine-induced contraction of prostate strips in the organ bath was not affected by the EPAC activator pCPT (SP-8-pCPT-2'-O-Me-cAMPS.NA) (30 μM). However, when the cyclooxygenase inhibitor indomethacin (50 μM) was added, EPAC activators pCPT and OME (8-CPT-2'-O-Me-cAMP.Na) (30 μM) significantly reduced contractions by low concentrations of phenylephrine. These effects were not observed on noradrenaline-induced contraction. OME and pCPT caused phosphorylation of the transcription factor Elk1 in prostate tissues. Elk1 activation was confirmed by EMSA (electrophoretic mobility shift assay), where OME and pCPT incresed Elk1 binding to a specific DNA probe.EPAC activation may reduce α1-adrenergic prostate contraction in the human prostate, although this effect is masked by cyclooxygenases and β-adrenoceptors. A main EPAC function in the human prostate may be the regulation of the transcription factor Elk1.
    Document Type:
    Reference
    Product Catalog Number:
    AP124C
    Product Catalog Name:
    Goat Anti-Mouse IgG Antibody, Cy3 conjugate

  • cAMP -2722737

    Document Type:
    Certificate of Analysis
    Lot Number:
    2722737
    Product Catalog Number:
    20-198
    Product Catalog Name:
    cAMP

  • Increased cAMP in monocytes augments Notch signaling mechanisms by elevating RBP-J and transducin-like enhancer of Split (TLE). 23775085

    In cells of the innate immune system, pathological increases in intracellular cAMP attenuate immune responses and contribute to infections by bacteria such as Bacillus anthracis. In this work, cAMP from B. anthracis edema toxin (ET) is found to activate the Notch signaling pathway in both mouse macrophages and human monocytes. ET as well as a cell-permeable activator of PKA induce Notch target genes (HES1, HEY1, IL2RA, and IL7R) and are able to significantly enhance the induction of these Notch target genes by a Toll-like receptor ligand. Elevated cAMP also resulted in increased levels of Groucho/transducin-like enhancer of Split (TLE) and led to increased amounts of a transcriptional repressor complex consisting of TLE and the Notch target Hes1. To address the mechanism used by ET to activate Notch signaling, components of Notch signaling were examined, and results revealed that ET increased levels of recombinant recognition sequence binding protein at the Jκ site (RBP-J), a DNA binding protein and principal transcriptional regulator of Notch signaling. Overexpression studies indicated that RBP-J was sufficient to activate Notch signaling and potentiate LPS-induced Notch signaling. Further examination of the mechanism used by ET to activate Notch signaling revealed that C/EBP β, a transcription factor activated by cAMP, helped activate Notch signaling and up-regulated RBP-J. These studies demonstrate that cAMP activates Notch signaling and increases the expression of TLE, which could be an important mechanism utilized by cAMP to suppress immune responses.
    Document Type:
    Reference
    Product Catalog Number:
    AB15470

  • cAMP differentially regulates axonal and dendritic development of dentate granule cells. 16155295

    Neurite polarity is a morphological characteristic of dentate gyrus granule cells, which extend axons to the hilar region and dendrites in the opposite direction, i.e. to the molecular layer. This remarkable polarity must require a differential system for axon and dendrite guidance. Here, we report that the axon and dendrites of a granule cell are differentially responsive to cAMP. In developing cultures of dispersed granule cells, dendritic growth cones were increased in number after pharmacological activation of cAMP signaling and decreased after blockade of cAMP signaling. Activation of cAMP signaling antagonized dendritic collapse induced by the potent repellents Sema3F and glutamate. In contrast to dendrites, axons were protected from Sema3F-induced collapse when cAMP signaling was inhibited. Axonal and dendritic growth cones both expressed type 1 adenylyl cyclase, but only axons showed a cAMP increase in response to Sema3F, and the elevated cAMP was sufficient to collapse axonal growth cones. Thus, the axons and dendrites of dentate granule cells differ in the regulation of cAMP levels as well as responsiveness to cAMP. cAMP may be crucial for shaping the information flow polarity in the dentate gyrus circuit.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • cAMP and fibroblast growth factor 2 regulate bone sialoprotein gene expression in human prostate cancer cells. 20965237

    Bone sialoprotein (BSP) is a noncollagenous protein of the extracellular matrix in mineralized connective tissues that has been implicated in the nucleation of hydroxyapatite. Forskolin (FSK), an activator of adenylate cyclase, increased the intracellular cAMP level, which stimulates the proliferation and differentiation of osteoblasts. Fibroblast growth factor 2 (FGF2) is a potent mitogen in many cell types, including osteoblasts. In human prostate cancer DU145 cells, FSK (1μM) and FGF2 (10ng/ml) increased BSP and Runx2 mRNA and protein levels at 3 and 12h, respectively. Transient transfection analyses were performed using chimeric constructs of the human BSP gene promoter linked to a luciferase reporter gene. Treatment of DU145 cells with FSK (1μM) and FGF2 (10ng/ml) increased the luciferase activities of constructs between -60LUC to -927LUC and -108LUC to -927LUC, including the human BSP gene promoter. Effects of FSK and FGF2 abrogated in constructs included 2bp mutations in the two cAMP response elements (CRE1 and CRE2). Luciferase activities induced by FSK and FGF2 were blocked by protein kinase A and tyrosine kinase inhibitors. Gel mobility shift analyses showed that FSK and FGF2 increased the binding of CRE1 and CRE2. CRE1-protein complexes were supershifted by phospho-CREB1 and c-Fos antibodies, and disrupted by CREB1, c-Jun, JunD, Fra2, p300, Runx2, Dlx5 and Smad1 antibodies. CRE2-protein complexes were disrupted by CREB1, phospho-CREB1, c-Fos, c-Jun, JunD, Fra2, p300, Runx2, Dlx5 and Smad1 antibodies. These studies demonstrate that FSK and FGF2 stimulate BSP transcription in DU145 human prostate cancer cells by targeting the CRE1 and CRE2 elements in the human BSP gene promoter.
    Document Type:
    Reference
    Product Catalog Number:
    AB5728

  • cAMP - 2453657

    Document Type:
    Certificate of Analysis
    Lot Number:
    2453657
    Product Catalog Number:
    20-198
    Product Catalog Name:
    cAMP