0B68 Alnemri, Emad - Thomas Jefferson University - Thomas Jefferson University
esa101

Emad Alnemri, PhD

Contact Dr. Alnemri

233 S. 10th Street
904 BLSB
Philadelphia, PA 19107

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

Most Recent Peer-reviewed Publications

  1. Inflammasome priming by lipopolysaccharide is dependent upon ERK signaling and proteasome function
  2. Cutting edge: TLR signaling licenses IRAK1 for rapid activation of the NLRP3 inflammasome
  3. The mitochondrial antiviral protein MAVS associates with NLRP3 and regulates its inflammasome activity
  4. Restoration of ASC expression sensitizes colorectal cancer cells to genotoxic stress-induced caspase-independent cell death
  5. Ribotoxic stress through p38 mitogen-activated protein kinase activates in Vitro the human pyrin inflammasome
  6. A novel role for the mitochondrial HTRA2/OMI protease in aging
  7. Loss of HtrA2/Omi activity in non-neuronal tissues of adult mice causes premature aging
  8. Translation termination factor eRF3 is targeted for caspase-mediated proteolytic cleavage and degradation during DNA damage-induced apoptosis
  9. Non-transcriptional priming and deubiquitination regulate NLRP3 inflammasome activation
  10. Molecular definitions of cell death subroutines: Recommendations of the Nomenclature Committee on Cell Death 2012
  11. Critical roles of ASC inflammasomes in caspase-1 activation and host innate resistance to Streptococcus pneumoniae infection
  12. Cutting edge: Mutation of Francisella tularensis mviN leads to increased macrophage absent in melanoma 2 inflammasome activation and a loss of virulence
  13. Involvement of the AIM2, NLRC4, and NLRP3 inflammasomes in caspase-1 activation by Listeria monocytogenes
  14. Sensing cytoplasmic danger signals by the inflammasome
  15. The AIM2 inflammasome is critical for innate immunity to Francisella tularensis
  16. Functional consequences of a germline mutation in the leucine-rich repeat domain of NLRP3 Identified in an atypical autoinflammatory disorder
  17. Anti-inflammatory compounds parthenolide and bay 11-7082 are direct inhibitors of the inflammasome
  18. THAP5 is a human cardiac-specific inhibitor of cell cycle that is cleaved by the proapoptotic Omi/HtrA2 protease during cell death
  19. Cutting edge: NF-κB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression
  20. Guide 0176 lines for the use and interpretation of assays for monitoring cell death in higher eukaryotes
0