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    Tytuł:
    Isolation and characterization of novel human short-chain dehydrogenase/reductase SCDR10B which is highly expressed in the brain and acts as hydroxysteroid dehydrogenase*
    Autorzy:
    Huang, Chaoqun
    Wan, Bo
    Gao, Bo
    Hexige, Saiyin
    Yu, Long
    Powiązania:
    https://bibliotekanauki.pl/articles/1040586.pdf
    Data publikacji:
    2009
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    expression pattern
    clone
    brain
    hydroxysteroid dehydrogenase
    Opis:
    Hydroxysteroid dehydrogenase belongs to the subfamily of short-chain dehydrogenases/reductases (SDR), and 11-β-hydroxysteroid dehydrogenase catalyzes the interconversion of inactive glucocorticoids (cortisone in human, dehydrocorticosterone in rodents) and active glucocorticoids (cortisol in human, corticosterone in rodents). We report here the cloning and characterization of a novel human SDR gene SCDR10B which encodes a protein with similarity to 11β-hydroxysteroid dehydrogenase 1. SCDR10B was isolated from a human brain cDNA library, and was mapped to chromosome 19p13.3 by browsing the UCSC genomic database. It contains an ORF with a length of 858 bp, encoding a protein with a transmembrane helix and SDR domain. Its molecular mass and isoelectric point are predicted to be 30.8 kDa and 10.3 kDa, respectively. SCDR10B protein is highly conserved in mammals and fish. Phylogenetic tree analysis indicated that SCDR10B stands for a new subgroup in the 11β-hydroxysteroid dehydrogenase family. Northern blot analysis showed that SCDR10B was highly expressed in brain, and a strong expression signal was detected in hippocampal neurons by immunohistochemical analysis. RT-PCR and immunohistochemical analysis showed that SCDR10B was up-regulated in lung-cancer cell lines and human lung cancer. SCDR10B can catalyze the dehydrogenation of cortisol in the presence of NADP+, and therefore it is a hydroxysteroid dehydrogenase.
    Źródło:
    Acta Biochimica Polonica; 2009, 56, 2; 279-289
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Contribution of protein kinase A and protein kinase C signalling pathways to the regulation of HSD11B2 expression and proliferation of MCF-7 cells.
    Autorzy:
    Rubiś, Błażej
    Grodecka-Gazdecka, Sylwia
    Lecybył, Remigiusz
    Ociepa, Marta
    Krozowski, Zygmunt
    Trzeciak, Wiesław
    Powiązania:
    https://bibliotekanauki.pl/articles/1041503.pdf
    Data publikacji:
    2004
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    MCF-7 proliferation
    HSD11B2 gene expression
    11β-hydroxysteroid dehydrogenase type II
    signalling pathways
    Opis:
    Contribution of the protein kinase A (PKA) and protein kinase C (PKC) signalling pathways to the regulation of 11β-hydroxysteroid dehydrogenase type II (HSD11B2) gene expression was investigated in human breast cancer cell line MCF-7. Treatment of the cells with an adenylyl cyclase activator, forskolin, known to stimulate the PKA pathway, resulted in an increase in HSD11B2 mRNA content. Semi-quantitative RT-PCR revealed attenuation of the effect of forskolin by phorbol ester, tetradecanoyl phorbol acetate (TPA), an activator of the PKC pathway. It was also demonstrated that specific inhibitors significantly reduced the effect of activators of the two pathways. Stimulation of the PKA pathway did not affect, whereas stimulation of the PKC pathway significantly reduced MCF-7 cell proliferation in a time-dependent manner. A cell growth inhibitor, dexamethasone, at high concentrations, caused a 40% decrease in proliferation of MCF-7 cells and this effect was abolished under conditions of increased HSD11B2 expression. It was concluded that in MCF-7 cells, stimulation of the PKA signal transduction pathway results in the induction of HSD11B2 expression and that this effect is markedly reduced by activation of the PKC pathway. Activation of the PKC pathway also resulted in inhibition of cell proliferation, while activation of the PKA pathway abolished the antiproliferative effect of dexamethasone. These effects might be due to oxidation of dexamethasone by the PKA-inducible HSD11B2g.
    Źródło:
    Acta Biochimica Polonica; 2004, 51, 4; 919-924
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-2 z 2

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