Caenorhabditis elegans CED-9 protein is a bifunctional cell-death inhibitor
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[1] John Calvin Reed. Double identity for proteins of the Bcl-2 family , 1997, Nature.
[2] A. Chinnaiyan,et al. Interaction of CED-4 with CED-3 and CED-9: A Molecular Framework for Cell Death , 1997, Science.
[3] G. Núñez,et al. Interaction and Regulation of Subcellular Localization of CED-4 by CED-9 , 1997, Science.
[4] Daniel J. Hoeppner,et al. Interaction between the C. elegans cell-death regulators CED-9 and CED-4 , 1997, Nature.
[5] Junying Yuan,et al. Human ICE/CED-3 Protease Nomenclature , 1996, Cell.
[6] H. Horvitz,et al. The Caenorhabditis elegans cell-death protein CED-3 is a cysteine protease with substrate specificities similar to those of the human CPP32 protease. , 1996, Genes & development.
[7] D. Nicholson. ICE/CED3-like Proteases as Therapeutic Targets for the Control of Inappropriate Apoptosis , 1996, Nature Biotechnology.
[8] H. Horvitz,et al. Developing Caenorhabditis elegans neurons may contain both cell-death protective and killer activities. , 1996, Genes & development.
[9] J. Mankovich,et al. Inhibition of ICE family proteases by baculovirus antiapoptotic protein p35. , 1995, Science.
[10] H. Horvitz,et al. Inhibition of the Caenorhabditis elegans cell-death protease CED-3 by a CED-3 cleavage site in baculovirus p35 protein , 1995, Nature.
[11] G M Rubin,et al. Expression of baculovirus P35 prevents cell death in Drosophila. , 1994, Development.
[12] Z. Oltvai,et al. BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax , 1994, Nature.
[13] H. Horvitz,et al. Activation of C. elegans cell death protein CED-9 by an ammo-acid substitution in a domain conserved in Bcl-2 , 1994, Nature.
[14] J. Rothman,et al. Baculovirus p35 prevents developmentally programmed cell death and rescues a ced‐9 mutant in the nematode Caenorhabditis elegans. , 1994, The EMBO journal.
[15] H. Horvitz,et al. C. elegans cell survival gene ced-9 encodes a functional homolog of the mammalian proto-oncogene bcl-2 , 1994, Cell.
[16] D. Bredesen,et al. Expression of the Baculovirus p35 Gene Inhibits Mammalian Neural Cell Death , 1993, Journal of neurochemistry.
[17] Shai Shaham,et al. The C. elegans cell death gene ced-3 encodes a protein similar to mammalian interleukin-1β-converting enzyme , 1993, Cell.
[18] I. Weissman,et al. Prevention of programmed cell death in Caenorhabditis elegans by human bcl-2. , 1992, Science.
[19] H. Horvitz,et al. The Caenorhabditis elegans cell death gene ced-4 encodes a novel protein and is expressed during the period of extensive programmed cell death. , 1992, Development.
[20] K. O. Elliston,et al. A novel heterodimeric cysteine protease is required for interleukin-1βprocessing in monocytes , 1992, Nature.
[21] M. Hengartner,et al. Caenorhabditis elegans gene ced-9 protects cells from programmed cell death , 1992, Nature.
[22] C. March,et al. Molecular cloning of the interleukin-1 beta converting enzyme. , 1992, Science.
[23] R. J. Clem,et al. Prevention of apoptosis by a baculovirus gene during infection of insect cells. , 1991, Science.
[24] R. Schreiber,et al. Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death , 1990, Nature.
[25] S. Korsmeyer,et al. Deregulated Bcl-2 gene expression selectively prolongs survival of growth factor-deprived hemopoietic cell lines. , 1990, Journal of immunology.
[26] David L. Vaux,et al. Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells , 1988, Nature.
[27] J. Sklar,et al. Cloning and structural analysis of cDNAs for bcl-2 and a hybrid bcl-2/immunoglobulin transcript resulting from the t(14;18) translocation , 1986, Cell.
[28] Y. Tsujimoto,et al. Analysis of the structure, transcripts, and protein products of bcl-2, the gene involved in human follicular lymphoma. , 1986, Proceedings of the National Academy of Sciences of the United States of America.
[29] H. Horvitz,et al. Genetic control of programmed cell death in the nematode C. elegans , 1986, Cell.