S J Martin

Summary

Affiliation: Trinity College
Country: Ireland

Publications

  1. Cullen S, Kearney C, Clancy D, Martin S. Diverse Activators of the NLRP3 Inflammasome Promote IL-1β Secretion by Triggering Necrosis. Cell Rep. 2015;11:1535-48 pubmed publisher
    ..Thus, signal II agents initiate inflammation by promoting necrosis-driven IL-1β release, suggesting that IL-1β represents an inducible danger signal. ..
  2. Sullivan G, Henry C, Clancy D, Mametnabiev T, Belotcerkovskaya E, Davidovich P, et al. Suppressing IL-36-driven inflammation using peptide pseudosubstrates for neutrophil proteases. Cell Death Dis. 2018;9:378 pubmed publisher
    ..Thus, antagonists of neutrophil-derived proteases may have therapeutic potential for blocking activation of IL-36 family cytokines in inflammatory conditions such as psoriasis. ..
  3. Clancy D, Sullivan G, Moran H, Henry C, Reeves E, McElvaney N, et al. Extracellular Neutrophil Proteases Are Efficient Regulators of IL-1, IL-33, and IL-36 Cytokine Activity but Poor Effectors of Microbial Killing. Cell Rep. 2018;22:2937-2950 pubmed publisher
    ..Thus, in addition to their classical role as phagocytes, neutrophils play an important immunoregulatory role through deployment of their granule proteases into the extracellular space to process multiple IL-1 family cytokines. ..
  4. Carroll R, Hollville E, Martin S. Parkin sensitizes toward apoptosis induced by mitochondrial depolarization through promoting degradation of Mcl-1. Cell Rep. 2014;9:1538-53 pubmed publisher
    ..These data suggest that similar to other sensors of cell stress, such as p53, Parkin has cytoprotective (mitophagy) or cytotoxic modes (apoptosis), depending on the degree of mitochondrial damage. ..
  5. Cullen S, Martin S. Fas and TRAIL 'death receptors' as initiators of inflammation: Implications for cancer. Semin Cell Dev Biol. 2015;39:26-34 pubmed publisher
    ..Here we will discuss death-independent outcomes of Fas and TRAIL signaling and their implications for cancer. ..
  6. Henry C, Sullivan G, Clancy D, Afonina I, Kulms D, Martin S. Neutrophil-Derived Proteases Escalate Inflammation through Activation of IL-36 Family Cytokines. Cell Rep. 2016;14:708-722 pubmed publisher
    ..Inhibition of neutrophil-derived proteases may therefore have therapeutic benefits in psoriasis. ..
  7. Clancy D, Martin S. Getting a gRIP on Flu by Casting the DAI. Cell Host Microbe. 2016;20:552-554 pubmed publisher
    ..2016), indicate that this virus provokes divergent modes of cell death, including apoptosis and necroptosis, via the nucleic acid sensor, DAI. ..
  8. Kearney C, Martin S. An Inflammatory Perspective on Necroptosis. Mol Cell. 2017;65:965-973 pubmed publisher
    ..Here, we suggest that necroptosis might have anti-inflammatory effects in certain settings, through curbing excessive TNF- or TLR-induced inflammatory cytokine production. ..
  9. Hollville E, Carroll R, Cullen S, Martin S. Bcl-2 family proteins participate in mitochondrial quality control by regulating Parkin/PINK1-dependent mitophagy. Mol Cell. 2014;55:451-66 pubmed publisher

More Information

Publications12

  1. request reprint
    Martin S. Destabilizing influences in apoptosis: sowing the seeds of IAP destruction. Cell. 2002;109:793-6 pubmed
    ..Recent developments suggest that ubiquitin-proteasome mediated destruction of the Drosophila IAP, DIAP1, is a key event during the initiation of programmed cell death in the fly. ..
  2. Chipuk J, Martin S. Special Issue on Cell Death: Murder, mystery (and a little bit of mayhem) in Manhattan. FEBS J. 2016;283:2565-7 pubmed publisher
    ..We hope that you will find these pieces to be of interest; we certainly found them to be fresh and engaging and we are grateful to their authors for taking the time to write for The FEBS Journal. ..
  3. Henry C, Martin S. Caspase-8 Acts in a Non-enzymatic Role as a Scaffold for Assembly of a Pro-inflammatory "FADDosome" Complex upon TRAIL Stimulation. Mol Cell. 2017;65:715-729.e5 pubmed publisher