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GalNAc-T14 may Contribute to Production of Galactose-Deficient Immunoglobulin A1, the Main Autoantigen in IgA Nephropathy

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F23%3A73621430" target="_blank" >RIV/61989592:15110/23:73621430 - isvavai.cz</a>

  • Alternative codes found

    RIV/00098892:_____/23:10157909

  • Result on the web

    <a href="https://www.kireports.org/article/S2468-0249(23)01169-5/fulltext" target="_blank" >https://www.kireports.org/article/S2468-0249(23)01169-5/fulltext</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.ekir.2023.02.1072" target="_blank" >10.1016/j.ekir.2023.02.1072</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    GalNAc-T14 may Contribute to Production of Galactose-Deficient Immunoglobulin A1, the Main Autoantigen in IgA Nephropathy

  • Original language description

    Introduction: Immunoglobulin A1 (IgA1) with galactose-deficient O-glycans (Gd-IgA1) play a key role in thepathogenesis of IgA nephropathy (IgAN). Mucosal-tissue infections increase IL-6 production and, in patientswith IgAN, are often associated with macroscopic hematuria. IgA1-secreting cell lines derived fromthe circulation of patients with IgAN, compared to those of healthy controls (HCs), produce more IgA1 thathas O-glycans with terminal or sialylated N-acetylgalactosamine (GalNAc). GalNAc residues are added toIgA1 hinge region by some of the 20 GalNAc transferases, the O-glycosylation-initiating enzymes.Expression of GALNT2, encoding GalNAc-T2, the main enzyme initiating IgA1 O-glycosylation, is similar incells derived from patients with IgAN and HCs. In this report, we extend our observations of GALNT14overexpression in IgA1-producing cell lines from patients with IgAN.Methods: GALNT14 expression was analyzed in peripheral blood mononuclear cells (PBMCs) from patientswith IgAN and from HCs. Moreover, the effect of GALNT14 overexpression or knock-down on Gd-IgA1production in Dakiki cells was assessed.Results: GALNT14 was overexpressed in PBMCs from patients with IgAN. IL-6 increased GALNT14expression in PBMCs from patients with IgAN and HCs. We used IgA1-producing cell line Dakiki, a previouslyreported model of Gd-IgA1-producing cells, and showed that overexpression of GalNAc-T14enhanced galactose deficiency of IgA1, whereas siRNA-mediated GalNAc-T14 knock-down reduced it.GalNAc-T14 was localized in trans-Golgi network, as expected.Conclusions: Overexpression of GALNT14 due to inflammatory signals during mucosal infections maycontribute to overproduction of Gd-IgA1 in patients with IgAN.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30102 - Immunology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2023

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Kidney International Reports

  • ISSN

    2468-0249

  • e-ISSN

  • Volume of the periodical

    2023

  • Issue of the periodical within the volume

    8

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    8

  • Pages from-to

    "1068–1075"

  • UT code for WoS article

    000999007500001

  • EID of the result in the Scopus database

    2-s2.0-85150766012