Stefan Riedl

Summary

Affiliation: The Burnham Institute
Country: USA

Publications

  1. ncbi The apoptosome: signalling platform of cell death
    Stefan J Riedl
    Program in Apoptosis and Cell Death Research, The Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Nat Rev Mol Cell Biol 8:405-13. 2007
  2. ncbi Caspase mechanisms
    Guy S Salvesen
    Program on Apoptosis and Cell Death, Burnham Institute for Medical Research, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    Adv Exp Med Biol 615:13-23. 2008
  3. ncbi Mechanism of XIAP-mediated inhibition of caspase-9
    Eric N Shiozaki
    Department of Molecular Biology, Lewis Thomas Laboratory, Princeton University, Princeton, NJ 08544, USA
    Mol Cell 11:519-27. 2003
  4. ncbi Molecular mechanisms of caspase regulation during apoptosis
    Stefan J Riedl
    Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Washington Road, Princeton, New Jersey 08544, USA
    Nat Rev Mol Cell Biol 5:897-907. 2004
  5. ncbi XIAP inhibits caspase-3 and -7 using two binding sites: evolutionarily conserved mechanism of IAPs
    Fiona L Scott
    Program in Apoptosis and Cell Death Research, The Burnham Institute, La Jolla, CA 92037, USA
    EMBO J 24:645-55. 2005
  6. ncbi Structure of the apoptotic protease-activating factor 1 bound to ADP
    Stefan J Riedl
    Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Washington Road, Princeton, New Jersey 08544, USA
    Nature 434:926-33. 2005
  7. ncbi Structure of Apaf-1 in the auto-inhibited form: a critical role for ADP
    Qing Bao
    Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Princeton, New Jersey 08544, USA
    Cell Cycle 4:1001-3. 2005
  8. ncbi A structure of the human apoptosome at 12.8 A resolution provides insights into this cell death platform
    Xinchao Yu
    Department of Physiology and Biophysics, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Structure 13:1725-35. 2005

Research Grants

  1. The Mechanism of DISC Formation
    Stefan J Riedl; Fiscal Year: 2010

Collaborators

  • Guy Salvesen
  • Jean-Bernard Denault
  • Yigong Shi
  • Xinchao Yu
  • Fiona L Scott
  • Qing Bao
  • Eric N Shiozaki
  • Christopher R Booth
  • Steven J Ludtke
  • Martin Renatus
  • Christopher W Akey
  • Hwain Shin
  • Devrim Acehan
  • Xiaodong Wang
  • Emad S Alnemri
  • Pingwei Li
  • Daniel J Rigotti
  • Srinivasa M Srinivasula
  • Jijie Chai
  • Robert Fairman

Detail Information

Publications8

  1. ncbi The apoptosome: signalling platform of cell death
    Stefan J Riedl
    Program in Apoptosis and Cell Death Research, The Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Nat Rev Mol Cell Biol 8:405-13. 2007
    ..The formation of the apoptosome and the activation of its effector, caspase-9, reveals a sophisticated mechanism that might be more common than was initially thought...
  2. ncbi Caspase mechanisms
    Guy S Salvesen
    Program on Apoptosis and Cell Death, Burnham Institute for Medical Research, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    Adv Exp Med Biol 615:13-23. 2008
    ....
  3. ncbi Mechanism of XIAP-mediated inhibition of caspase-9
    Eric N Shiozaki
    Department of Molecular Biology, Lewis Thomas Laboratory, Princeton University, Princeton, NJ 08544, USA
    Mol Cell 11:519-27. 2003
    ..Thus, XIAP sequesters caspase-9 in a monomeric state, which serves to prevent catalytic activity. These studies, in conjunction with other observations, define a unified mechanism for the activation of all caspases...
  4. ncbi Molecular mechanisms of caspase regulation during apoptosis
    Stefan J Riedl
    Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Washington Road, Princeton, New Jersey 08544, USA
    Nat Rev Mol Cell Biol 5:897-907. 2004
    ..This article reviews these latest advances and describes our present understanding of caspase regulation during apoptosis...
  5. ncbi XIAP inhibits caspase-3 and -7 using two binding sites: evolutionarily conserved mechanism of IAPs
    Fiona L Scott
    Program in Apoptosis and Cell Death Research, The Burnham Institute, La Jolla, CA 92037, USA
    EMBO J 24:645-55. 2005
    ..Since apical caspases utilize this cleavage site differently, we predict that the origin of the death stimulus should dictate the efficiency of inhibition by XIAP...
  6. ncbi Structure of the apoptotic protease-activating factor 1 bound to ADP
    Stefan J Riedl
    Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Washington Road, Princeton, New Jersey 08544, USA
    Nature 434:926-33. 2005
    ..Apaf-1 binds to and hydrolyses ATP/dATP and their analogues. The binding and hydrolysis of nucleotides seem to drive conformational changes that are essential for the formation of the apoptosome and the activation of caspase-9...
  7. ncbi Structure of Apaf-1 in the auto-inhibited form: a critical role for ADP
    Qing Bao
    Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Princeton, New Jersey 08544, USA
    Cell Cycle 4:1001-3. 2005
    ..elegans, it is unclear whether they employ similar mechanisms for their own activation and for activating caspases. Much of the underlying mechanisms remain to be investigated by structural biology and biochemistry...
  8. ncbi A structure of the human apoptosome at 12.8 A resolution provides insights into this cell death platform
    Xinchao Yu
    Department of Physiology and Biophysics, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Structure 13:1725-35. 2005
    ..This model provides insights into the roles of dATP and cytochrome c in assembly. Our structure also reveals how a CARD ring and the central hub combine to create a platform for procaspase-9 activation...

Research Grants3

  1. The Mechanism of DISC Formation
    Stefan J Riedl; Fiscal Year: 2010
    ..Since the DISC represents a prime target for homeostasis and proliferation in liver cells, it is an ideal candidate for drug development against hepatocellular carcinoma and the damaging effect of alcohol abuse. ..