Graeme P. Sullivan

发表

Suppressing IL-36-driven inflammation using peptide pseudosubstrates for neutrophil proteases

Seamus J. Martin, P. Davidovich, Tazhir Mametnabiev, 2018, Cell Death & Disease.

TRAIL Receptors Serve as Stress-Associated Molecular Patterns to Promote ER-Stress-Induced Inflammation.

S. Cullen, Seamus J. Martin, P. Davidovich, 2020, Developmental cell.

Neutrophil-Derived Proteases Escalate Inflammation through Activation of IL-36 Family Cytokines.

Seamus J. Martin, Graeme P. Sullivan, C. M. Henry, 2016, Cell reports.

Neutrophil extracellular traps can serve as platforms for processing and activation of IL‐1 family cytokines

Seamus J. Martin, Graeme P. Sullivan, C. M. Henry, 2017, The FEBS journal.

Identification of small‐molecule elastase inhibitors as antagonists of IL‐36 cytokine activation

Seamus J. Martin, P. Davidovich, A. Garabadzhiu, 2018, FEBS open bio.

IL-1α and IL-36 Family Cytokines Can Undergo Processing and Activation by Diverse Allergen-Associated Proteases

Seamus J. Martin, P. Davidovich, Graeme P. Sullivan, 2022, Frontiers in Immunology.

Extracellular Neutrophil Proteases Are Efficient Regulators of IL-1, IL-33, and IL-36 Cytokine Activity but Poor Effectors of Microbial Killing.

Seamus J. Martin, N. McElvaney, E. Lavelle, 2018, Cell reports.

Extracellular Neutrophil P roteases Are Efficient Regulators of IL-1 , IL-33 , and IL-36 Cytokine Activity but Poor Effectors of Microbial Killing Graphical

Seamus J. Martin, N. McElvaney, E. Lavelle, 2018 .

The path to venetoclax resistance is paved with mutations, metabolism, and more

D. A. Rodrigues, T. Ní Chonghaile, Graeme P. Sullivan, 2022, Science Translational Medicine.

iTAP, a novel iRhom interactor, controls TNF secretion by policing the stability of iRhom/TACE

Seamus J. Martin, A. von Kriegsheim, J. Březinová, 2018, bioRxiv.

Production of biologically active IL‐36 family cytokines through insertion of N‐terminal caspase cleavage motifs

Seamus J. Martin, P. Davidovich, Graeme P. Sullivan, 2016, FEBS open bio.

Suppressing IL-36-driven inflammation using peptide pseudosubstrates for neutrophil proteases

Seamus J. Martin, P. Davidovich, A. Garabadzhiu, 2018, Cell Death & Disease.

Myeloid cell–derived proteases produce a proinflammatory form of IL-37 that signals via IL-36 receptor engagement

Seamus J. Martin, P. Davidovich, B. Turk, 2022, Science Immunology.