Calnexin suppresses GD3 synthase-induced apoptosis BARBARA TOMASSINI * , FLORENCE MALISAN * , LUIGI FRANCHI * , CHIARA NICOLÒ * , GLORIA BREA CALVO * , TAKASHI SAITO † and ROBERTO TESTI * ,1 * Laboratory of Immunology and Signal Transduction, Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, Rome, Italy; and † Department of Molecular Genetics, Chiba University Graduate School of Medicine, Chiba, and Laboratory of Cell Signaling, RIKEN Center for Allergy and Immunology, Yokohama, Japan 1 Correspondence: Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, via Montpellier 1, 00133 Rome, Italy. E-mail: roberto.testi@flashnet.it <h3>SPECIFIC AIMS</h3> Stress-induced intracellular GD3 accumulation can be followed by adaptation and differentiation or mitochondrial damage and apoptosis. We asked whether this could be dictated by subcellular localization of the GD3 synthase, which is in turn controlled by calnexin. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Calnexin retains the GD3 synthase (ST8) in the endoplasmic reticulum (ER)</h3> Chicken ST8 was shown to be normally expressed in the Golgi. Accordingly, the enforced expression of the human ST8 in Chinese hamster ovary (CHO) cells results in its accumulation at the Golgi level (<h3>Fig. 1</h3> A). Since the ST8, via its multiple
End of preview. The entire article is 3 pages. To view the full-text, please rent this article to continue.
/lp/fed-of-american-socs-for-experimental-biology/calnexin-suppresses-gd3-synthase-induced-apoptosis-VTnUNDcjP8
Welcome to DeepDyve! Rent Premier Research Articles and Save Up to 90%
Calnexin suppresses GD3 synthase-induced apoptosis
TOMASSINI, BARBARA; MALISAN, FLORENCE; FRANCHI, LUIGI; NICOLÒ, CHIARA; CALVO, GLORIA BREA; SAITO, TAKASHI; TESTI, ROBERTO
Follow The FASEB Journal
, Volume 18 (13): 1553
Fed of American Socs for Experimental Biology – Oct 1, 2004
More Info
More Like This Article
View All dataSource[]=actageo&dataSource[]=aspet&dataSource[]=aaos&dataSource[]=aacc&dataSource[]=aacr&dataSource[]=aea&dataSource[]=aip&dataSource[]=ajnr&dataSource[]=ams&dataSource[]=aps_physical&dataSource[]=appi_book&dataSource[]=appi_journal&dataSource[]=apha&dataSource[]=asip&dataSource[]=asm&dataSource[]=asn&dataSource[]=aspb&dataSource[]=avs&dataSource[]=annual_reviews&dataSource[]=arxiv&dataSource[]=acm&dataSource[]=berghahn&dataSource[]=cabi&dataSource[]=clinical_trials&dataSource[]=dailymed&dataSource[]=degruyter&dataSource[]=du_press&dataSource[]=esa&dataSource[]=eu_press&dataSource[]=elsevier&dataSource[]=emerald&dataSource[]=ejtr&dataSource[]=emea&dataSource[]=epo&dataSource[]=faseb&dataSource[]=gsa&dataSource[]=health_affairs&dataSource[]=hindawi&dataSource[]=imanager&dataSource[]=imedpub&dataSource[]=informa_healthcare&dataSource[]=informs&dataSource[]=iop&dataSource[]=iucr&dataSource[]=iospress&dataSource[]=jbjs&dataSource[]=leftcoast&dataSource[]=lu_press&dataSource[]=mesharpe&dataSource[]=mary_ann_liebert&dataSource[]=medline&dataSource[]=mit_press&dataSource[]=nature&dataSource[]=oxford&dataSource[]=pier_professional&dataSource[]=pnas&dataSource[]=portlandpress&dataSource[]=psyc_articles&dataSource[]=psyc_books&dataSource[]=psyc_critiques&dataSource[]=plos_journal&dataSource[]=pubmed_central&dataSource[]=rsna&dataSource[]=rockefeller&dataSource[]=rcn&dataSource[]=ria&dataSource[]=rsc&dataSource[]=sage&dataSource[]=spie&dataSource[]=springer_journal&dataSource[]=springer&dataSource[]=taylor_francis&dataSource[]=aps&dataSource[]=the_scientist&dataSource[]=uc_press&dataSource[]=uspto_abstract&dataSource[]=wiley&dataSource[]=pct
© 2012 DeepDyve, Inc. All rights reserved.
Terms of Service | Privacy Policy
