GD3 nuclear localization after apoptosis induction in HUT-78 cells
Creators
- 1. Department of Biochemical Sciences, University 'La Sapienza', p.le A. Moro, 5, 00185 Rome (Italy)
- 2. Department of Experimental Medicine, University 'La Sapienza', Rome (Italy)
- 3. Department of Infectious Diseases, University 'La Sapienza', Rome (Italy)
- 4. IRCCS San Raffaele-Pisana, Rome (Italy)
Description
Glycosphingolipids are essential components of plasma membrane and act as antigens, mediators of cell adhesion, and modulators of signal transduction. Following activation of the Fas receptor, gangliosides are recuited in various intracellular compartments. We have evaluated whether the pro-apoptotic anti-CD95 antibody induces a nuclear localization of GD3 in HUT-78 cells. Our data shows that GD3 translocation from cytosol to nuclei is strongly correlated to concomitant rapid phosphorylation of histone H1 shortly after induction of apoptosis. This work advances the hypothesis that GD3 induces a post-translational modification of histone H1 thus influencing the apoptosis process through transcriptional activation/repression of specific genes
Availability note (English)
Available from http://dx.doi.org/10.1016/j.bbrc.2007.12.196Additional details
Identifiers
- DOI
- 10.1016/j.bbrc.2007.12.196;
- PII
- S0006-291X(08)00155-1;
Publishing Information
- Journal Title
- Biochemical and Biophysical Research Communications
- Journal Volume
- 368
- Journal Issue
- 3
- Journal Page Range
- p. 495-500
- ISSN
- 0006-291X
- CODEN
- BBRCA9
INIS
- Country of Publication
- United States
- Country of Input or Organization
- International Atomic Energy Agency (IAEA)
- INIS RN
- 39062999
- Subject category
- S60: APPLIED LIFE SCIENCES;
- Descriptors DEI
- ANTIBODIES; ANTIGENS; APOPTOSIS; CELL MEMBRANES; GANGLIOSIDES; GENES; PHOSPHORYLATION; RECEPTORS; TRANSLOCATION
- Descriptors DEC
- CARBOHYDRATES; CELL CONSTITUENTS; CHEMICAL REACTIONS; GLYCOLIPIDS; LIPIDS; MEMBRANE PROTEINS; MEMBRANES; ORGANIC COMPOUNDS; ORGANIC NITROGEN COMPOUNDS; PROTEINS; SACCHARIDES
Optional Information
- Copyright
- Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.