Author

J. Birch

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

Biology Disciplines

Click to filter author papers

Cell Biology· 3 Cancer Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cancer & tumor microenvironment· 4 Research Focus:cell signaling & trafficking· 3 Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cell type annotation· 2 Research Focus:development & morphogenesis· 2 Organism:human· 2 Assay:bulk RNA-seq· 1

Frequent Co-Authors

J. F. Passos· 3 shared F. R. Millar· 2 shared J. C. Acosta· 2 shared M. Muir· 2 shared N. Tarrats· 2 shared P. Hari· 2 shared V. G. Brunton· 2 shared A. Chalmers· 1 shared

Activity by Year

2018-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

3 shared papersCell Biology

J. F. Passos

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Glioblastoma extracellular vesicles influence glial cell hyaluronic acid deposition to promote invasiveness

J. C. Norman, D. Koessinger, D. Novo, J. Birch, L. Mitchell, M. Moore, D. Zerbst, A. Chalmers, A. Koessinger, K. Stevenson, M. Nielson

This study identifies how GBM extracellular vesicles containing podocalyxin promote astrocyte hyaluronic acid deposition, enhancing GBM invasiveness.

bioRxiv · Feb 11, 2022 · 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

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