Author

P. Hari

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· 3 Cancer Biology· 2 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 6 Research Focus:cancer & tumor microenvironment· 4 Research Focus:cell signaling & trafficking· 3 Research Focus:development & morphogenesis· 3 Organism:human· 3 Research Focus:cell type annotation· 2 Research Focus:host-pathogen & immune response· 2 Organism:mouse· 2

Frequent Co-Authors

J. C. Acosta· 4 shared A. Quintanilla· 3 shared F. R. Millar· 3 shared M. Muir· 3 shared N. Tarrats· 3 shared J. Birch· 2 shared J. F. Passos· 2 shared L. Boulter· 2 shared

Activity by Year

2018-2021 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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4 shared papersCancer Biology

J. C. Acosta

Mutual co-authors in cluster

Author profile →

6 papers

Recent·Most cited

Toll-like receptor 2 orchestrates a potent anti-tumor response in non-small cell lung cancer

F. R. Millar, A. Pennycuick, M. Muir, A. Quintanilla, P. Hari, E. Freyer, P. Gautier, A. Meynert, V. H. Teixeira, J. Connelly, W. A. Wallace, A. H. Sims, M. C. Frame, L. Boulter, S. M. Janes, , J. C. Acosta

This study identifies TLR2 as a tumor suppressor in early-stage lung cancer, showing its role in immune surveillance and tumor growth reduction through synthetic agonist administration.

bioRxiv · Jun 4, 2021 · PreprintCancer 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

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

Inhibition of the 60S ribosome biogenesis GTPase LSG1 causes endoplasmic reticular disruption and cellular senescence

A. Pantazi, A. Quintanilla, P. Hari, N. Tarrats, E. Parasyraki, F. L. Dix, J. Patel, T. Chandra, J. C. Acosta, A. Finch

This study shows that inhibiting LSG1, a GTPase involved in 60S ribosome biogenesis, induces cellular senescence through ER disruption and cholesterol biosynthesis upregulation, with potential therapeutic implications.

bioRxiv · Nov 8, 2018Cancer Biology

Versican Proteolysis Predicts Immune Effector Infiltration And Post-Transplant Survival In Myeloma

B. Dhakal, A. Pagenkopf, M. U. Mushtaq, A. M. Cunningham, E. Flietner, Z. Morrow, A. Papadas, C. Hope, C. Leith, P. Hematti, P. Hari, N. S. Callander, F. Asimakopoulos

This study shows that VCAN proteolysis predicts CD8+ T cell infiltration and poor survival after myeloma transplantation, suggesting it as a biomarker for relapse risk.

bioRxiv · Sep 12, 2018Immunology

Nuclear pore density controls heterochromatin reorganization during senescence

W. Bickmore, C. Boumendil, P. Hari, K. Olsen, J.-C. Acosta

This study shows that increased nuclear pore density during oncogene-induced senescence drives SAHF formation, which is essential for SASP expression but not cell cycle arrest.

bioRxiv · Jul 21, 2018Cell Biology