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Francisella tularensis Glyceraldehyde-3-Phosphate Dehydrogenase Is Relocalized during Intracellular Infection and Reveals Effect on Cytokine Gene Expression and Signaling

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F23%3A00570267" target="_blank" >RIV/68378050:_____/23:00570267 - isvavai.cz</a>

  • Alternative codes found

    RIV/60162694:G44__/24:00560591 RIV/00216208:11160/23:10471847

  • Result on the web

    <a href="https://www.mdpi.com/2073-4409/12/4/607" target="_blank" >https://www.mdpi.com/2073-4409/12/4/607</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3390/cells12040607" target="_blank" >10.3390/cells12040607</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Francisella tularensis Glyceraldehyde-3-Phosphate Dehydrogenase Is Relocalized during Intracellular Infection and Reveals Effect on Cytokine Gene Expression and Signaling

  • Original language description

    Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is known for its multifunctionality in several pathogenic bacteria. Our previously reported data suggest that the GAPDH homologue of Francisella tularensis, GapA, might also be involved in other processes beyond metabolism. In the present study, we explored GapA's potential implication in pathogenic processes at the host cell level. Using immunoelectron microscopy, we demonstrated the localization of this bacterial protein inside infected macrophages and its peripheral distribution in bacterial cells increasing with infection time. A quantitative proteomic approach based on stable isotope labeling of amino acids in cell culture (SILAC) combined with pull-down assay enabled the identification of several of GapA's potential interacting partners within the host cell proteome. Two of these partners were further confirmed by alternative methods. We also investigated the impact of gapA deletion on the transcription of selected cytokine genes and the activation of the main signaling pathways. Our results show that increment gapA-induced transcription of genes encoding several cytokines whose expressions were not affected in cells infected with a fully virulent wild-type strain. That might be caused, at least in part, by the detected differences in ERK/MAPK signaling activation. The experimental observations together demonstrate that the F. tularensis GAPDH homologue is directly implicated in multiple host cellular processes and, thereby, that it participates in several molecular mechanisms of pathogenesis.

  • 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

    10601 - Cell biology

Result continuities

  • Project

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

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

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

    Cells

  • ISSN

    2073-4409

  • e-ISSN

    2073-4409

  • Volume of the periodical

    12

  • Issue of the periodical within the volume

    4

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    22

  • Pages from-to

    607

  • UT code for WoS article

    000939293900001

  • EID of the result in the Scopus database

    2-s2.0-85148965551