التفاصيل البيبلوغرافية
| العنوان: |
The innate immune sensor Toll-like receptor 2 controls the senescence-associated secretory phenotype |
| المؤلفون: |
Hari P, Millar FR, Tarrats N, Birch J, Quintanilla A, Rink CJ, Fernandez-Duran I, Muir M, Finch AJ, Brunton VG, Passos JF, Morton JP, Boulter L, Acosta JC |
| المصدر: |
Science Advances, 5 June 2019 |
| بيانات النشر: |
American Association for the Advancement of Science |
| سنة النشر: |
2019 |
| المجموعة: |
Newcastle University Library ePrints Service |
| الوصف: |
© 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY).Cellular senescence is a stress response program characterized by a robust cell cycle arrest and the induction of a proinflammatory senescence-associated secretory phenotype (SASP) that is triggered through an unknown mechanism. Here, we show that, during oncogene-induced senescence (OIS), the Toll-like receptor 2 (TLR2) and its partner TLR10 are key mediators of senescence in vitro and in murine models. TLR2 promotes cell cycle arrest by regulating the tumor suppressors p53-p21CIP1, p16INK4a, and p15INK4b and regulates the SASP through the induction of the acute-phase serum amyloids A1 and A2 (A-SAAs) that, in turn, function as the damage-associated molecular patterns (DAMPs) signaling through TLR2 in OIS. Last, we found evidence that the cGAS-STING cytosolic DNA sensing pathway primes TLR2 and A-SAAs expression in OIS. In summary, we report that innate immune sensing of senescence-associated DAMPs by TLR2 controls the SASP and reinforces the cell cycle arrest program in OIS. |
| نوع الوثيقة: |
article in journal/newspaper |
| وصف الملف: |
application/pdf |
| اللغة: |
unknown |
| الإتاحة: |
https://eprint.ncl.ac.uk/fulltext.aspx?url=258340/79EB4475-31BC-46D2-90D5-17627529C76E.pdf&pub_id=258340Test |
| رقم الانضمام: |
edsbas.5783473F |
| قاعدة البيانات: |
BASE |
