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    Wyświetlanie 1-4 z 4
    Tytuł:
    Novel properties of antimicrobial peptides.
    Autorzy:
    Kamysz, Wojciech
    Okrój, Marcin
    Łukasiak, Jerzy
    Powiązania:
    https://bibliotekanauki.pl/articles/1043622.pdf
    Data publikacji:
    2003
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    tumour
    cells
    mitogen
    immunity
    signalling pathways
    antimicrobial peptides
    Opis:
    Endogenous peptide antibiotics are known as evolutionarily old components of innate immunity. Due to interaction with cell membrane these peptides cause permeabilization of the membrane and lysis of invading microbes. However, some studies proved that antimicrobial peptides are universal multifunctional molecules and their functions extend far beyond simple antibiotics. In this review we present an overview of the general mechanism of action of antimicrobial peptides and discuss some of their additional properties, like antitumour activity, mitogenic activity, role in signal transduction pathways and adaptive immune response.
    Źródło:
    Acta Biochimica Polonica; 2003, 50, 2; 461-469
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    The bystander effect: is reactive oxygen species the driver?
    Autorzy:
    Szumiel, I.
    Powiązania:
    https://bibliotekanauki.pl/articles/148463.pdf
    Data publikacji:
    2003
    Wydawca:
    Instytut Chemii i Techniki Jądrowej
    Tematy:
    bystander effect
    reactive oxygen species
    ionising radiation
    DNA repair
    signalling pathways
    Opis:
    The paper reviews selected examples of the bystander effect, such as clonogenic survival decrease, chromosomal aberrations and mutations. The similarities and differences between the biological effects in directly targeted and bystander cells are briefly discussed. Also reviewed are the experimental data which support the role of reactive oxygen species (ROS), especially *O2-, as mediators of the bystander effect. Endogenously generated ROS, due to activation of NAD(P)H oxidases, play a key role in the induction of DNA damage in bystander cells. All the observed effects in bystander cells, such as alterations in gene expression patterns, chromosomal aberrations, sister chromatid exchanges, mutations, genome instability, and neoplastic transformation are the consequence of DNA damage.
    Źródło:
    Nukleonika; 2003, 48, 3; 113-120
    0029-5922
    1508-5791
    Pojawia się w:
    Nukleonika
    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
    Tytuł:
    Cross-talk between the ATP and ADP nucleotide receptor signalling pathways in glioma C6 cells.
    Autorzy:
    Czajkowski, Rafał
    Barańska, Jolanta
    Powiązania:
    https://bibliotekanauki.pl/articles/1043690.pdf
    Data publikacji:
    2002
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    ATP
    cross-talk
    glioma C6 cells
    ADP
    phospholipase C
    nucleotide receptors
    adenylyl cyclase
    signalling pathways
    adenosine
    Opis:
    In this review we summarize the present status of our knowledge on the enzymes involved in the extracellular metabolism of nucleotides and the receptors involved in nucleotide signalling. We focus on the mechanism of the ATP and ADP signalling pathways in glioma C6, representative of the type of nonexcitable cells. In these cells, ATP acts on the P2Y2 receptor coupled to phospholipase C, whereas ADP on two distinct P2Y receptors: P2Y1 and P2Y12. The former is linked to phospholipase C and the latter is negatively coupled to adenylyl cyclase. The possible cross-talk between the ATP-, ADP- and adenosine-induced pathways, leading to simultaneous regulation of inositol 1,4,5-trisphosphate and cAMP mediated signalling, is discussed.
    Źródło:
    Acta Biochimica Polonica; 2002, 49, 4; 877-889
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-4 z 4

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