Thomas Jefferson University

Alnemri, Emad

< Back



Emad Alnemri, PhD

Contact Dr. Alnemri

233 South 10th Street
BLSB 904
Philadelphia, PA 19107

(215) 503-4632
(215) 923-1098 fax

Research and Clinical Interests

Molecular mechanisms of programmed cell death (apoptosis); Pattern recognition receptors and inflammasome activation in innate immune responses to molecular danger signals; role of mitochondria in survival, cell death and aging.


Most Recent Peer-Reviewed Publications

  1. Gasdermins in apoptosis: New players in an old game
  2. Gasdermin pores permeabilize mitochondria to augment caspase-3 activation during apoptosis and inflammasome activation
  3. Gasdermins: novel mitochondrial pore-forming proteins
  4. The mitochondrial protease HtrA2 restricts the NLRP3 and AIM2 inflammasomes
  5. SUMO-mediated regulation of NLRP3 modulates inflammasome activity
  6. The NLRP6 Inflammasome Recognizes Lipoteichoic Acid and Regulates Gram-Positive Pathogen Infection
  7. Triad3a induces the degradation of early necrosome to limit RipK1-dependent cytokine production and necroptosis article
  8. Molecular mechanisms of cell death: Recommendations of the Nomenclature Committee on Cell Death 2018
  9. Cleavage of DFNA5 by caspase-3 during apoptosis mediates progression to secondary necrotic/pyroptotic cell death
  10. The Yersinia pestis Effector YopM Inhibits Pyrin Inflammasome Activation
  11. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
  12. Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356
  13. Caspase-8 scaffolding function and MLKL regulate NLRP3 inflammasome activation downstream of TLR3
  14. Non-transcriptional regulation of NLRP3 inflammasome signaling by IL-4
  15. The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease
  16. Essential versus accessory aspects of cell death: Recommendations of the NCCD 2015
  17. Inflammasome priming by lipopolysaccharide is dependent upon ERK signaling and proteasome function
  18. Inactivation of Omi/HtrA2 protease leads to the deregulation of mitochondrial Mulan E3 ubiquitin ligase and increased mitophagy
  19. IKKα negatively regulates ASC-dependent inflammasome activation
  20. Cutting edge: TLR signaling licenses IRAK1 for rapid activation of the NLRP3 inflammasome