Development regulation of ganglioside metabolism

Research output: Contribution to journalArticle

143 Citations (Scopus)

Abstract

Various reports have appeared indicating that the expression of gangliosides may be largely regulated at the genetic level. Evidence from analysis of the gene for this enzyme revealed binding sequences for a number of liver restricted transcription factors such as hepatocyte nuclear factor l a, liver specific factors D-binding protein (DBP), and liver enriched transcription activator protein (LAP), as well as the more general transcription factors AP-1 and AP-2. Presumably, the expression of the various glycosyltransferases for ganglioside synthesis may be regulated in an analogous manner. Factors involved in the regulation of ganglioside expression include the proper translocation and sorting of the glycolipid products in multi-glycosyltransferase systems. Disruption of the flow of gangliosides along their biosynthetic pathways also can cause alterations in ganglioside expression. It is demonstrated that polysialogangliosides exerted inhibitory effects feedback control. Another intriguing mechanism for the regulation of ganglioside synthesis states that in cultured cerebellar cells a shift in the biosynthesis from a- to b-series gangliosides occurred when the pH of the medium was lowered from 7.4 to 6.2, with the effect being reversible. Whether changes in pH occur in vivo to effect the shift in biosynthesis of gangliosides during development remains to be substantiated.

Original languageEnglish (US)
Pages (from-to)31-44
Number of pages14
JournalProgress in Brain Research
Volume101
Issue numberC
DOIs
StatePublished - Jan 1 1994
Externally publishedYes

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Gangliosides
Glycosyltransferases
Hepatocyte Nuclear Factors
General Transcription Factors
Glycolipids
Biosynthetic Pathways
Transcription Factor AP-1
Cultured Cells
Carrier Proteins
Transcription Factors
Liver
Enzymes

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Development regulation of ganglioside metabolism. / Yu, Robert K.

In: Progress in Brain Research, Vol. 101, No. C, 01.01.1994, p. 31-44.

Research output: Contribution to journalArticle

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