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Tretina, Kyle; Haidar, Malak; Madsen-Bouterse, Sally A.; Sakura, Takaya; Mfarrej, Sara; Fry, Lindsay; Chaussepied, Marie; Pain, Arnab; Knowles, Donald P.; Nene, Vishvanath M.; Ginsberg, Doron; Daubenberger, Claudia A.; Bishop, Richard P.; Langsley, Gordon; Silva, Joana C.

Theileria parasites subvert E2F signaling to stimulate leukocyte proliferation

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  • Medientyp: E-Artikel
  • Titel: Theileria parasites subvert E2F signaling to stimulate leukocyte proliferation
  • Beteiligte: Tretina, Kyle; Haidar, Malak; Madsen-Bouterse, Sally A.; Sakura, Takaya; Mfarrej, Sara; Fry, Lindsay; Chaussepied, Marie; Pain, Arnab; Knowles, Donald P.; Nene, Vishvanath M.; Ginsberg, Doron; Daubenberger, Claudia A.; Bishop, Richard P.; Langsley, Gordon; Silva, Joana C.
  • Erschienen: Springer Science and Business Media LLC, 2020
  • Erschienen in: Scientific Reports, 10 (2020) 1
  • Sprache: Englisch
  • DOI: 10.1038/s41598-020-60939-x
  • ISSN: 2045-2322
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: AbstractIntracellular pathogens have evolved intricate mechanisms to subvert host cell signaling pathways and ensure their own propagation. A lineage of the protozoan parasite genus Theileria infects bovine leukocytes and induces their uncontrolled proliferation causing a leukemia-like disease. Given the importance of E2F transcription factors in mammalian cell cycle regulation, we investigated the role of E2F signaling in Theileria-induced host cell proliferation. Using comparative genomics and surface plasmon resonance, we identified parasite-derived peptides that have the sequence-specific ability to increase E2F signaling by binding E2F negative regulator Retinoblastoma-1 (RB). Using these peptides as a tool to probe host E2F signaling, we show that the disruption of RB complexes ex vivo leads to activation of E2F-driven transcription and increased leukocyte proliferation in an infection-dependent manner. This result is consistent with existing models and, together, they support a critical role of E2F signaling for Theileria-induced host cell proliferation, and its potential direct manipulation by one or more parasite proteins.
  • Zugangsstatus: Freier Zugang