Author

J. F. Passos

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cell Biology· 5 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell signaling & trafficking· 6 Approach:experimental assay· 6 Organism:mouse· 5 Research Focus:cancer & tumor microenvironment· 4 Research Focus:development & morphogenesis· 4 Research Focus:cell type annotation· 2 Organism:human· 2 Research Focus:metabolism & bioenergetics· 2

Frequent Co-Authors

J. Birch· 3 shared A. Walaszczyk· 2 shared D. Jurk· 2 shared E. Dookun· 2 shared E. Fielder· 2 shared F. R. Millar· 2 shared G. D. Richardson· 2 shared H. Arthur· 2 shared

Activity by Year

2018-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 31 mutual co-author links

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3 shared papersCell Biology

J. Birch

Mutual co-authors in cluster

Author profile →

6 papers

Recent·Most cited

Linked regulation of genome integrity and senescence-associated inflammation by p53

K. N. Miller, B. Li, H. R. Pierce-Hoffman, S. Patel, X. Lei, A. Rajesh, M. G. Teneche, A. P. Havas, A. Gandhi, C. Cano Macip, J. Lyu, S. G. Victorelli, S.-H. Woo, A. B. Lagnado, M. A. LaPorta, , P. D. Adams

This study identifies a mitochondria-regulated p53 circuit that links genomic instability and inflammation in senescent cells, showing p53 suppresses inflammation without affecting cell cycle arrest.

bioRxiv · Nov 20, 2023 · PreprintCell Biology

Cytoplasmic innate immune sensing by the caspase-4 non-canonical inflammasome promotes cellular senescence.

I. Fernandez Duran, N. Tarrats, J. Birch, P. Hari, F. R. Millar, M. Muir, A. Quintanilla, V. G. Brunton, J. F. Passos, J. C. Acosta

This study shows that caspase-4 non-canonical inflammasome activation by LPS induces cellular senescence and contributes to oncogene-induced senescence and tumour suppression.

bioRxiv · Oct 16, 2020Cell Biology

Clearance of senescent cells during cardiac ischemia-reperfusion injury improves heart recovery following myocardial infarction

E. Dookun, A. Walaszczyk, R. Redgrave, P. Palmowski, S. Tual-Chalot, A. Suwana, J. Chapman, E. Jirkovsky, L. Donastorg, E. Gill, Y. Santin, o. E. Yausep, J. Mialet-Perez, W. A. Owens, D. G. Grieve, , G. D. Richardson

This study shows that clearing senescent cells after cardiac ischemia-reperfusion injury improves heart function, reduces scar size, and decreases inflammation.

bioRxiv · Apr 28, 2020 · PreprintCell Biology

The innate immune sensor Toll-like receptor 2 controls the senescence-associated secretory phenotype.

P. Hari, F. R. Millar, N. Tarrats, J. Birch, C. J. Rink, I. Fernandez-Duran, M. Muir, A. J. Finch, V. G. Brunton, J. F. Passos, J. P. Morton, L. Boulter, J. C. Acosta

This study identifies TLR2 as a key mediator of oncogene-induced senescence by promoting cell cycle arrest and regulating the senescence-associated secretory phenotype through DAMPs.

Science Advances · Jun 1, 2019Peer-reviewedCell Biology

Temporal inhibition of autophagy reveals segmental reversal of aging with increased cancer risk

L. Cassidy, A. R. Young, C. N. Young, E. J. Soilleux, E. Fielder, B. M. Weigand, R. Brais, K. A. Wiggins, M. C. Clarke, D. Jurk, J. F. Passos, M. Narita

This study shows that inhibiting autophagy in mammals accelerates aging and increases cancer risk, while restoring autophagy extends lifespan but does not fully prevent cancer.

bioRxiv · Jan 23, 2019 · PreprintCancer Biology

Length-independent telomere damage drives cardiomyocyte senescence

R. Anderson, A. Lagnado, D. Maggiorani, A. Walaszczyk, E. Dookun, J. Chapman, J. Birch, H. Salmonowicz, M. Ogrodnik, D. Jurk, C. Proctor, C. Correia-Melo, S. Victorelli, E. Fielder, R. Berlinguer-Palmini, , J. F. Passos

This study shows that telomere damage independent of length causes cardiomyocyte senescence, leading to cardiac dysfunction, and that clearing senescent cells improves cardiac health.

bioRxiv · Aug 17, 2018Cell Biology