Gangliosides as modulators of cell function

Zeller, Cynthia B.; Marchase, Richard B.

doi:10.1152/ajpcell.1992.262.6.c1341

Cited by 202 publications

(72 citation statements)

References 83 publications

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“…Gangliosides are GSLs containing sialic acid that locate to the external leaflet of the plasma membrane and are particularly abundant in the central nervous system. The roles of gangliosides in the developing and adult central nervous system are not fully understood, but they are believed to function in the regulation of receptor-mediated cellsignaling pathways [7][8][9][10] . The biosynthesis and degradation of gangliosides are well characterized 11 .…”

Section: E T T E R Smentioning

confidence: 99%

Infantile-onset symptomatic epilepsy syndrome caused by a homozygous loss-of-function mutation of GM3 synthase

et al. 2004

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Section: E T T E R Smentioning

confidence: 99%

Infantile-onset symptomatic epilepsy syndrome caused by a homozygous loss-of-function mutation of GM3 synthase

et al. 2004

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“…T he sialic acid-containing glycosphingolipids, the gangliosides, may play important roles in both neuronal (Ledeen and Wu 1992) and non-neuronal (Hakomori and Igarashi 1993;Zeller and Marchase 1992) tissues. Most of the proposed functions of gangliosides are related to their localization at the plasma membrane, where they have been shown by biochemical analyses to be enriched (Yu and Saito 1989), although low levels of gangliosides have also been detected in intracellular membranes (Matyas and Morre 1987).…”

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Determination of the Localization of Gangliosides Using Anti-ganglioside Antibodies: Comparison of Fixation Methods

Schwarz

Futerman

1997

J Histochem Cytochem.

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SUMMARYMany studies have examined the localization of gangliosides using anti-ganglioside antibodies, although widely differing conclusions have been reached. We now demonstrate that the apparent localization of gangliosides can be greatly influenced by the fixation method. Using monoclonal antibody (MAb) A2B5 (which reacts with a variety of gangliosides), hippocampal neurons were labeled at the cell surface when incubated with the antibody before fixation, but when incubated after fixation the cells displayed a variety of labeling patterns, depending on the fixation method. Biochemical analysis demonstrated that some of the fixatives (particularly acetone and methanol) significantly reduced or completely depleted cellular gangliosides, implying that the immunoreactivity observed with A2B5, and with other antibodies, was not due to gangliosides. When neurons were incubated with an anti-GD1b antibody prefixation, uniform labeling of the plasma membrane was observed, but after ganglioside depletion using biochemical inhibitors of ganglioside synthesis no cell surface labeling was detected. However, even in cells depleted of gangliosides, labeling of both the cell surface and intracellular compartments was observed when the anti-GD1b antibody was applied after fixation. Moreover, after fixation, antibodies to GM4 and GD2 reacted with hippocampal neurons, although these gangliosides are absent from these neurons. In contrast, the JONES antibody (which reacts with 9-O -acetylated GD3) labeled neurons with a similar pattern, essentially irrespective of the fixation method. These observations demonstrate that great care must be taken in assigning gangliosides to specific cell populations or to intracellular locations solely on the basis of use of anti-ganglioside antibodies, and suggest that optimal fixation conditions must be established for each anti-ganglioside antibody. (J Histochem Cytochem 45:611-618, 1997)

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“…The biological roles of glycosphingolipids have been extensively studied and their involvements in key cellular events as well as their particularly important functions in animal brain tissue are well known [8], [15], [20] and [24]. The idea that there are alterations in glycosphingolipid metabolism in Alzheimer's disease arose from biochemical studies of brain gangliosides pattern [1], [11], and [20].…”

Section: Commentmentioning

confidence: 99%

Ganglioside catabolism is altered in fibroblasts and leukocytes from Alzheimer's disease patients

Kalanj-Bognar

2006

Neurobiology of Aging

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Gangliosides as modulators of cell function

Cited by 202 publications

References 83 publications

Infantile-onset symptomatic epilepsy syndrome caused by a homozygous loss-of-function mutation of GM3 synthase

Infantile-onset symptomatic epilepsy syndrome caused by a homozygous loss-of-function mutation of GM3 synthase

Determination of the Localization of Gangliosides Using Anti-ganglioside Antibodies: Comparison of Fixation Methods

Ganglioside catabolism is altered in fibroblasts and leukocytes from Alzheimer's disease patients

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