E
Emad S. Alnemri
Researcher at Thomas Jefferson University
Publications - 228
Citations - 75133
Emad S. Alnemri is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: Apoptosis & Caspase. The author has an hindex of 106, co-authored 223 publications receiving 67441 citations. Previous affiliations of Emad S. Alnemri include QIMR Berghofer Medical Research Institute & Laval University.
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Journal ArticleDOI
Activation of a CrmA-insensitive, p35-sensitive Pathway in Ionizing Radiation-induced Apoptosis
Rakesh Datta,Hiromi Kojima,David Banach,Nancy J. Bump,Robert V. Talanian,Emad S. Alnemri,Ralph R. Weichselbaum,Ralph R. Weichselbaum,Winnie W. Wong,Donald Kufe +9 more
TL;DR: The results demonstrate that the IR-induced proteolytic activity is directly inhibited by the addition of purified recombinant p35, but not by CrmA and that the CPP32 protease is sensitive to p35 and not CrmA.
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Cleavage and Activation of p21-activated Protein Kinase γ-PAK by CPP32 (Caspase 3) EFFECTS OF AUTOPHOSPHORYLATION ON ACTIVITY
Barbara N. Walter,Zhongdong Huang,Rolf Jakobi,Polygena T. Tuazon,Emad S. Alnemri,Gerald Litwack,Jolinda A. Traugh +6 more
TL;DR: In this paper, an autophosphorylation of recombinant γ-PAK (Pak2, PAK I) via cleavage by CPP32 (caspase 3) during apoptosis and plays a key role in regulation of cell death.
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Activation of internucleosomal DNA cleavage in human CEM lymphocytes by glucocorticoid and novobiocin. Evidence for a non-Ca2(+)-requiring mechanism(s).
Emad S. Alnemri,Gerald Litwack +1 more
TL;DR: It is proposed that the majority of nuclear chromatin is maintained in a highly compact and charge-neutralized state and that disruption of this highly ordered structure may lead to the exposure and unmasking of internucleosomal linker DNA regions which are substrates for a constitutive non Ca2(+)-dependent endonuclease.
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Characterization of a novel and specific inhibitor for the pro-apoptotic protease Omi/HtrA2.
Lucia Cilenti,Younghee Lee,Sibylle Hess,Srinivasa M. Srinivasula,Kwon Moo Park,Daniela Junqueira,Hedvika Davis,Joseph V. Bonventre,Emad S. Alnemri,Antonis S. Zervos +9 more
TL;DR: Ucf-101, when tested in caspase-9 (−/−) null fibroblasts, was found to inhibit Omi/HtrA2-induced cell death.
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SUMO-mediated regulation of NLRP3 modulates inflammasome activity.
Rachael Barry,Rachael Barry,Sidonie Wicky John,Gianmaria Liccardi,Tencho Tenev,Isabel Jaco,Chih-Hong Chen,Justin Choi,Paulina Kasperkiewicz,Teresa Fernandes-Alnemri,Emad S. Alnemri,Marcin Drag,Yuan Chen,Pascal Meier +13 more
TL;DR: It is shown that post-translational modification of NLRP3 by sumoylation suppresses inflammasome activity, and that desumoylation of NL RP3 by the SENP6 and SENP7 proteases promotesNLRP3 activation.