Identification of a novel, alternatively spliced isoform and single nucleotide polymorphisms in the murine Pea-15 gene

Identification of a novel, alternatively spliced isoform and single nucleotide polymorphisms in... Mammalian Genome 12, 172–174 (2001). DOI: 10.1007/s003350010243 Incorporating Mouse Genome © Springer-Verlag New York Inc. 2001 Identification of a novel, alternatively spliced isoform and single nucleotide polymorphisms in the murine Pea-15 gene 1, 1, 2 1 D. Alan Underhill, * Kyle J. Vogan, ** T. Michael Underhill, Philippe Gros Department of Biochemistry, McGill University, Montreal, Quebec, H3G 1Y6, Canada Division of Oral Biology, University of Western Ontario, London, Ontario, N6A 5C1, Canada Received: 17 August 2000 / Accepted: 19 September 2000 Pea-15 (a 15-kDa phosphoprotein enriched in astrocytes; Estelle ´s apoptosis and integrin function have important roles during em- et al. 1996) belongs to a family of death-effector-domain (DED) bryonic development, prompting us to examine the integrity of the proteins originally defined by the pro-apoptotic protein FADD Pea-15 transcript in Lp embryos. (Muzio et al. 1996). The death-effector-domain functions as a To obtain more detailed expression data in the neural tube, the protein-protein interface that couples polypeptides in the apoptotic pathway. In CD95 (Fas/APO-1)-mediated apoptosis, the FADD DED recruits FLICE, a member of the ICE/CED-3 family of cys- teine proteases, and physically links the Fas/APO-1 receptor to this proapoptotic cysteine protease (Muzio et al. 1996). Pea-15 has an antagonistic http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Mammalian Genome Springer Journals

Identification of a novel, alternatively spliced isoform and single nucleotide polymorphisms in the murine Pea-15 gene

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Publisher
Springer-Verlag
Copyright
Copyright © 2001 by Springer-Verlag New York Inc.
Subject
Life Sciences; Cell Biology; Animal Genetics and Genomics; Human Genetics
ISSN
0938-8990
eISSN
1432-1777
D.O.I.
10.1007/s003350010243
Publisher site
See Article on Publisher Site

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