Photo of Bruce Magun, Ph.D

Bruce Magun Ph.D

  • 5034947811
My major fields of interest involve cellular mechanisms of inflammatory signaling cascades that control the responses to environmental toxic agents.In some studies, the laboratory investigates how proinflammatory signals (cytokines, toxins, and other stressors) interact with surface receptors to activate the stress-activated protein kinases and NF-kappaB and how activation of these pathways leads to transcriptional regulation of genes. Some projects involve the effects of ricin, a potential bioterrorist agent, on activating proinflammatory pathways in vitro and in mouse models.In other studies we are investigating the mechanisms that control the responses keratinocytes to environmental agents such as ultraviolet radiation and xenobiotic toxic agents.

Memberships and associations

  • Cell &Developmental Biology Neuroscience Graduate Program Program in Molecular &Cellular Biosciences Cancer Biology


  • "Production of IL-1β by bone marrow-derived macrophages in response to chemotherapeutic drugs : Synergistic effects of doxorubicin and vincristine." Cancer Biology and Therapy In: , Vol. 15, No. 10, 01.10.2014, p. 1395-1403.
  • "Small molecule kinase inhibitors block the ZAK-dependent inflammatory effects of Doxorubicin." Cancer Biology and Therapy In: , Vol. 14, No. 1, 01.2013, p. 56-63.
  • "Suppression of ribosomal function triggers innate immune signaling through activation of the NLRP3 inflammasome." PLoS One In: , Vol. 7, No. 5, e36044, 14.05.2012.
  • "Shiga toxin 2-induced intestinal pathology in infant rabbits is A-subunit dependent and responsive to the tyrosine kinase and potential ZAK inhibitor imatinib." Frontiers in cellular and infection microbiology In: , Vol. 2, 2012, p. 135.
  • "Ricin and Shiga toxins : Effects on host cell Signal transduction." Current Topics in Microbiology and Immunology  In: , Vol. 357, 2012, p. 41-65.
  • "Doxorubicin and daunorubicin induce processing and release of interleukin-1β through activation of the NLRP3 inflammasome." Cancer Biology and Therapy In: , Vol. 11, No. 12, 15.06.2011, p. 1008-1016.
  • "ZAK is required for doxorubicin, a novel ribotoxic stressor, to induce SAPK activation and apoptosis in HaCaT cells." Cancer Biology and Therapy In: , Vol. 10, No. 3, 01.08.2010, p. 258-266.
  • "Ricin toxin activates the NALP3 inflammasome." Toxins  In: , Vol. 2, No. 6, 06.2010, p. 1500-1514.
  • "Pulmonary inflammation triggered by ricin toxin requires macrophages and IL-1 signaling." Journal of Immunology In: , Vol. 183, No. 2, 15.07.2009, p. 1419-1426.
  • "Mouse model of hemolytic-uremic syndrome caused by endotoxin-free Shiga toxin 2 (Stx2) and protection from lethal outcome by anti-Stx2 antibody." Infection and Immunity In: , Vol. 76, No. 10, 10.2008, p. 4469-4478.
  • "Fas ligand-induced proinflammatory transcriptional responses in reconstructed human epidermis : Recruitment of the epidermal growth factor receptor and activation of MAP kinases." Journal of Biological Chemistry In: , Vol. 283, No. 2, 11.01.2008, p. 919-928.
  • "Proinflammatory responses of human airway cells to ricin involve stress-activated protein kinases and NF-κB." American Journal of Physiology - Lung Cellular and Molecular Physiology In: , Vol. 293, No. 6, 12.2007.
  • "Intrapulmonary delivery of ricin at high dosage triggers a systemic inflammatory response and glomerular damage." American Journal of Pathology  In: , Vol. 170, No. 5, 05.2007, p. 1497-1510.
  • "Role of apoptotic signaling pathways in regulation of inflammatory responses to ricin in primary murine macrophages." Molecular Immunology  In: , Vol. 44, No. 10, 04.2007, p. 2761-2771.
  • "Fas ligand elicits a caspase-independent proinflammatory response in human keratinocytes : Implications for Dermatitis." Journal of Investigative Dermatology In: , Vol. 126, No. 11, 15.11.2006, p. 2438-2451.
  • "Human cytomegalovirus attenuates interleukin-1β and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-κB activation." Journal of Virology In: , Vol. 80, No. 11, 06.2006, p. 5588-5598.
  • "Cell death-induced activation of epidermal growth factor receptor in keratinocytes : Implications for restricting epidermal damage in dermatitis." Journal of Investigative Dermatology In: , Vol. 125, No. 1, 07.2005, p. 134-142.
  • "Administration of ricin induces a severe inflammatory response via nonredundant stimulation of ERK, JNK, and p38 MAPK and provides a mouse model of hemolytic uremic syndrome." American Journal of Pathology  In: , Vol. 166, No. 1, 01.2005, p. 323-339.
  • "Two mechanisms of caspase 9 processing in double-stranded RNA- and virus-triggered apoptosis." Apoptosis In: , Vol. 10, No. 1, 01.2005, p. 153-166.
  • "Recruitment of TRADD, FADD, and caspase 8 to double-stranded RNA-triggered death inducing signaling complexes (dsRNA-DISCs)." Apoptosis In: , Vol. 10, No. 1, 01.2005, p. 167-176.
  • "The UV (ribotoxic) stress response of human keratinocytes involves the unexpected uncoupling of the Ras-extracellular signal-regulated kinase signaling cascade from the activated epidermal growth factor receptor." Molecular and Cellular Biology In: , Vol. 22, No. 15, 2002, p. 5380-5394.
  • "Specifically targeting the CD22 receptor of human B-cell lymphomas with RNA damaging agents." Critical Reviews in Oncology/Hematology In: , Vol. 39, No. 1-2, 2001, p. 79-86.
  • "Activation of NF-κB by double-stranded RNA (dsRNA) in the absence of protein kinase R and RNase L demonstrates the existence of two separate dsRNA-triggered antiviral programs." Molecular and Cellular Biology In: , Vol. 21, No. 1, 2001, p. 61-72.
  • "Molecular determinants of apoptosis induced by the cytotoxic ribonuclease onconase : Evidence for cytotoxic mechanisms different from inhibition of protein synthesis." Cancer Research In: , Vol. 60, No. 7, 01.04.2000, p. 1983-1994.
  • "Activation of p38 mitogen-activated protein kinase and c-Jun NH2- terminal kinase by double-stranded RNA and encephalomyocarditis virus : Involvement of RNase L, protein kinase R, and alternative pathways." Molecular and Cellular Biology In: , Vol. 20, No. 2, 01.2000, p. 617-627.
  • "Differential requirement for the stress-activated protein kinase/c-Jun NH2-terminal kinase in RNA damage-induced apoptosis in primary and in immortalized fibroblasts." Molecular Cell Biology Research Communications In: , Vol. 4, No. 2, 2000, p. 122-128.
  • "Different mechanisms of c-Jun NH2-terminal kinase-1 (JNK1) activation by ultraviolet-B radiation and by oxidative stressors." Journal of Biological Chemistry In: , Vol. 274, No. 36, 03.09.1999, p. 25801-25806.
  • "The p38MAPK inhibitor SB203580 alleviates ultraviolet-induced phosphorylation at serine 389 but not serine 15 and activation of p53." Biochemical and Biophysical Research Communications  In: , Vol. 261, No. 2, 02.08.1999, p. 464-471.
  • "Ultraviolet radiation triggers the ribotoxic stress response in mammalian cells." Journal of Biological Chemistry In: , Vol. 273, No. 25, 19.06.1998, p. 15794-15803.
  • "Loss of cellular K+ mimics ribotoxic stress. Inhibition of protein synthesis and activation of the stress kinases SEK1/MKK4, stress-activated protein kinase/c-Jun NH2-terminal kinase 1, and p38/HOG1 by palytoxin." Journal of Biological Chemistry In: , Vol. 273, No. 6, 06.02.1998, p. 3528-3534.

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