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Baker, R. Roy

doi:10.1023/a:1007567205078

Cited by 6 publications

(1 citation statement)

References 65 publications

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“…Acetylation is a covalent modification of biological molecules, which may profoundly affect their stability, specificity, and function ( 32 , 33 ). Specific acetyltransferases and deacetylases are therefore involved in multiple biological processes, including apoptosis.…”

Section: Resultsmentioning

confidence: 99%

Acetylation Suppresses the Proapoptotic Activity of GD3 Ganglioside

Malisan

Franchi

Tomassini

et al. 2002

The Journal of Experimental Medicine

105

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GD3 synthase is rapidly activated in different cell types after specific apoptotic stimuli. De novo synthesized GD3 accumulates and contributes to the apoptotic program by relocating to mitochondrial membranes and inducing the release of apoptogenic factors. We found that sialic acid acetylation suppresses the proapoptotic activity of GD3. In fact, unlike GD3, 9-O-acetyl-GD3 is completely ineffective in inducing cytochrome c release and caspase-9 activation on isolated mitochondria and fails to induce the collapse of mitochondrial transmembrane potential and cellular apoptosis. Moreover, cells which are resistant to the overexpression of the GD3 synthase, actively convert de novo synthesized GD3 to 9-O-acetyl-GD3. The coexpression of GD3 synthase with a viral 9-O-acetyl esterase, which prevents 9-O-acetyl-GD3 accumulation, reconstitutes GD3 responsiveness and apoptosis. Finally, the expression of the 9-O-acetyl esterase is sufficient to induce apoptosis of glioblastomas which express high levels of 9-O-acetyl-GD3. Thus, sialic acid acetylation critically controls the proapoptotic activity of GD3.

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Section: Resultsmentioning

confidence: 99%