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  1. AU="Georg Häcker"
  2. AU="Jain, S."
  3. AU="Alfakir, Razan"
  4. AU="Sozbilir, U."
  5. AU=Zhang Shuanghong
  6. AU="Iwama, Hisakazu"
  7. AU="Gomes, Andreia"
  8. AU="Machuca, Víctor"
  9. AU=Liu Nanyang AU=Liu Nanyang
  10. AU="Boudina, Sihem"
  11. AU="Ma, DongXue"
  12. AU="Bellucci, Margherita"
  13. AU="Prima, Musharrat Jahan"
  14. AU="Saiegh, Fadi Al"
  15. AU="Yang, Deok-Chun"
  16. AU="Arima, Hisatomi"
  17. AU=Czubak Jacek
  18. AU="de Melo, Bruna Oliveira"
  19. AU="Sokhadze, Guela"
  20. AU="Meuleman, Philip"
  21. AU=Mishra Arnab Kumar AU=Mishra Arnab Kumar
  22. AU="Linda A. Gleaves"
  23. AU="Vandelli, Maria Angela"
  24. AU="Guerrera, Luigi Pio"
  25. AU="Sabitri Lamichhane"
  26. AU="Echevarria, Marco"
  27. AU="Yanmin Li"

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Artikel: TIR‐domain‐containing adapter‐inducing interferon‐β (TRIF) forms filamentous structures, whose pro‐apoptotic signalling is terminated by autophagy

Gentle, Ian E / Arlena Metz / Arnim Weber / Dale Porter / Georg Häcker / Kevin T. McHenry / Oliver Kretz

FEBS journal. 2017 July, v. 284, no. 13

2017  

Abstract: The formation of amyloid‐like protein structures has recently emerged as a feature in signal transduction, particularly in innate immunity. These structures appear to depend on defined domains for their formation but likely also require dedicated ways ... ...

Abstract The formation of amyloid‐like protein structures has recently emerged as a feature in signal transduction, particularly in innate immunity. These structures appear to depend on defined domains for their formation but likely also require dedicated ways to terminate signalling. We, here, define the innate immunity protein/Toll‐like receptor adaptor TIR‐domain‐containing adapter‐inducing interferon‐β (TRIF) as a novel platform of fibril formation and probe signal initiation through TRIF as well as its termination in Toll‐like receptor 3 (TLR3)‐stimulated melanoma cells. A main signalling pathway triggered by TLR3 caused apoptosis, which was controlled by inhibitor of apoptosis proteins and was dependent on RIPK1 and independent of TNF. Using correlative electron/fluorescence microscopy, we visualised fibrillar structures formed through both Toll/interleukin‐1 receptor and RIP homotypic interacting motif regions of TRIF. We provide evidence that these fibrillary structures are active signalling platforms whose activity is terminated by autophagy. TRIF‐signalling enhanced autophagy, and fibrillary structures were partly contained within autophagosomes. Inhibition of autophagy increased levels of pro‐apoptotic TRIF complexes, leading to the accumulation of active caspase‐8 and enhanced apoptosis while stimulation of autophagy reduced TRIF‐dependent death. We conclude that pro‐death signals through TRIF are regulated by autophagy and propose that pro‐apoptotic signalling through TRIF/RIPK1/caspase‐8 occurs in fibrillary platforms.
Schlagwörter apoptosis ; autophagy ; caspase-8 ; fluorescence microscopy ; interferon-beta ; melanoma ; protein structure ; signal transduction ; Toll-like receptor 3 ; tumor necrosis factors
Sprache Englisch
Erscheinungsverlauf 2017-07
Umfang p. 1987-2003.
Erscheinungsort John Wiley & Sons, Ltd
Dokumenttyp Artikel
Anmerkung JOURNAL ARTICLE
ZDB-ID 2173655-8
ISSN 1742-4658 ; 1742-464X
ISSN (online) 1742-4658
ISSN 1742-464X
DOI 10.1111/febs.14091
Signatur
Z 2006/704: Hefte anzeigen
Datenquelle NAL Katalog (AGRICOLA)

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Z 2006/704: Hefte anzeigen

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