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Tytuł oryginału: Unstable receptors disappear from cell surface during poliovirus infection.
Autorzy: Neznanov Nickolay, Chumakov Konstantin P., Ullrich Axel, Agol Vadim I., Gudkov Andrei V.
Źródło: Med. Sci. Monitor 2002: 8 (10) s.BR391-BR396, il., bibliogr. 24 poz.
Sygnatura GBL: 313,278

Hasła klasyfikacyjne GBL:
  • mikrobiologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • in vitro

    Streszczenie angielskie: Background: Cellular recptors play a significant role in pathogenesis of viral infections. Previously, we demonstrated that TNFŕ receptor (TNFR1) rapidly disappeared from the cell surface upon poliovirus infection, whereas FAS was much more stable [1]. We suggested what the rate of decrease in receptor presentation on the surface of infected cells might reflect its turnover rate on uninfected cells. Material/Methods: To test this hypothesis, we estimated by FACS analysis the turnover rates of receptors for TRAIL (TRAILR1 and TRAILR2), signal regulatory protien SIRPŕ, receptor for ŕ/á interferon (INFR1), and poliovirus receptor (CD155) on the surface of HeLa cells after the treatment with brefeldin A (to stop receptor replenishment through the Golgi-mediated trafficking) or polivirus infection. Results: A good correlation between turnover rates caused by the two interventions was observed, with the stability of receptor presentation changing in the following order: TRAILR1, TRAILR2, SIRPŕ (half-life on infected cells between 2-4 h) INFR1 (4-6 h) CD155 ( 8 h, besides some early masking of the receptor by its binding of the virus). Conclusion: Our results suggest that disruption of the protein trafficking pathway during polivirus infection leads to the diminished sensitivity of infected cells to pro-apoptotic factors, and thus represents one of the mechanisms by which virus modulates the host defense reactions.

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