NDLI: Caspase-10 is an initiator caspase in death receptor signaling.

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Caspase-10 is an initiator caspase in death receptor signaling.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wong, W. Spencer, D. M. Wang, J. Chun, H. J. Lenardo, M. J.
Description	Author Affiliation: Wang J ( Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11N311, 10 Center Drive, MSC 1892, Bethesda, MD 20892, USA.);
Abstract	A role for caspase-10, previously implicated in the autoimmune lymphoproliferative syndrome, in death receptor signaling has not been directly shown. Here we show that caspase-10 can function independently of caspase-8 in initiating Fas- and tumor necrosis factor-related apoptosis-inducing ligand-receptor-mediated apoptosis. Moreover, Fas crosslinking in primary human T cells leads to the recruitment and activation of caspase-10. Fluorescent resonance energy transfer analysis indicates that the death-effector domains of caspase-8 and -10 both interact with the death-effector domain of FADD. Nonetheless, we find that caspase-8 and -10 may have different apoptosis substrates and therefore potentially distinct roles in death receptor signaling or other cellular processes.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	24
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adaptor Proteins, Signal Transducing Antigens, CD95 Metabolism Apoptosis Carrier Proteins Caspases Signal Transduction Pharmacology Apoptosis Regulatory Proteins B-Lymphocytes Cytology Caspase 10 Caspase 8 Caspase 9 Genetics Cells, Cultured Dendritic Cells Dimerization Enzyme Activation Fas-Associated Death Domain Protein Gene Expression Profiling Jurkat Cells Membrane Glycoproteins T-Lymphocytes TNF-Related Apoptosis-Inducing Ligand Tumor Necrosis Factor-alpha Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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