Characterization of gangliosides in human leucocytes

Tsuboyama, A; Takaku, F; Sakamoto, Shigemi; Kano, Yoshiaki; Ariga, Toshio; Miyatake, Tadashi

doi:10.1038/bjc.1980.339

Cited by 13 publications

(7 citation statements)

References 10 publications

(9 reference statements)

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“…The finding that GM3 is the predominant ganglioside of normal human lymphocytes is in agreement with the results of Tsuboyama et al (1980( ), Macher et al (1981, and Westrick er a!. (1983), who were the first to use purified MN cell preparations for their analyses.…”

Section: Discussionsupporting

confidence: 91%

“…Hildebrand et al (1972) found only one ganglioside, GM3, in all of the 6 CLL samples studied. With the newly developed high-performance thin-layer chromatography, 4 gangliosides, GM3, GM2, GM1 and an unidentified compound with a lower TLC mobility than GMI (54.9%, 16.2%, 20.5% and 8.4%, respectively) were demonstrated in one case of CLL (Tsuboyama et al, 1980). Another one-case study (Goff ef al., 1983) found 2 major (GM3 and GD3) and 3 minor, unidentified gangliosides of higher polarity.…”

Section: Discussionmentioning

confidence: 94%

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Gangliosides in human chronic lymphocytic leukaemia

Anh-Tuan

Pick

Vajda³

et al. 1985

Intl Journal of Cancer

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Gangliosides were analysed by elaborated overpressured thin-layer chromatography (OPTLC) in 6 cell samples from 5 patients with chronic lymphocytic leukaemia (CLL) of B-cell origin, and 4 individual lymphocyte preparations from normal blood donors. The principal difference in the ganglioside profile between these two counterparts appears to be the presence of GD3 and the predominance of the less polar compounds (GM3, GM2, GM1) in CLL cells. Qualitatively, GD3 accounted for about 5.5% of the total CLL gangliosides, whereas it was not detectable in normal lymphocytes. Quantitatively, GM3 constituted more than 81% of the total CLL gangliosides, a proportion more than twice as high as that found in normal lymphocytes. Three other minor gangliosides were isolated from CLL cells; these were shown to be GM2 (trace amounts), GM1 (7.7%), and GD1 (4%). The expression of individual gangliosides varied greatly among the various CLL samples obtained from different patients, and even from the same patient, if examined at different times. No gangliosides were found in the supernatant collected from CLL cells subjected to a temperature shift (0 degrees C to 37 degrees C) or in the cell-free medium harvested from the CLL cells kept in overnight culture.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 94%

Gangliosides in human chronic lymphocytic leukaemia

Anh-Tuan

Pick

Vajda³

et al. 1985

Intl Journal of Cancer

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“…The initial BKV infection of a child likely occurs in the tonsils, where GD1b and GT1b have both been observed (48). BKV infection then progresses to peripheral blood mononuclear cells, from which these two gangliosides have also been extracted (50). Finally, BKV remains subclinical for the lifetime of the host in the kidney, where it has been shown that GD1b and GT1b are present in both cortical tubular and medullary tissue (28).…”

Section: Discussionmentioning

confidence: 99%

Identification of Gangliosides GD1b and GT1b as Receptors for BK Virus

Low¹,

Magnuson

Tsai

et al. 2006

J Virol

169

155

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Gangliosides have been shown to be plasma membrane receptors for both murine polyomavirus and SV40, while JC virus uses serotonin receptors. In contrast, little is known of the membrane receptor and entry pathway for BK virus (BKV), which can cause severe disease in immunosuppressed bone marrow and renal transplant patients. Using sucrose flotation assays, we investigated BKV binding to and interaction with human erythrocyte membranes and determined that this interaction was dependent on a neuraminidase-sensitive, proteinase K-resistant molecule. BKV was found to interact with the gangliosides GT1b and GD1b. The terminal ␣2-8-linked disialic acid motif, present in both of these gangliosides, is likely to be important for this interaction. We also determined that the addition of GD1b and GT1b to LNCaP cells, which are normally resistant to BKV infection, made them susceptible to the virus. In addition, BKV interacted with membranes extracted from the endoplasmic reticulum (ER) and infection was blocked by the addition of brefeldin A, which interferes with transport from the ER to the Golgi apparatus. These data demonstrate that BKV uses the gangliosides GT1b and GD1b as receptors and passes through the ER on the way to the nucleus.

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“…These sialogangliosides have been found as receptors on the surface of mononuclear cells (27) and also on cortical tubular and medullary tissue (28) and have been implicated in erythrocyte hemaglutination seen as a result of BKV infection. This activity is sensitive to neuraminidase treatment, which removes the terminal sialic acid of many gangliosides and glycoproteins (29).…”

Section: Discussionmentioning

confidence: 99%

Reining in Polyoma Virus Associated Nephropathy: Design and Characterization of a Template Mimicking BK Viral Coat Protein Cellular Binding

et al. 2012

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The BK polyoma virus is a leading cause of chronic post kidney transplantation rejection. One target for therapeutic intervention is the initial association of the BK virus with the host cell. We hypothesize that the rate of BKV infection can be curbed by competitively preventing viral binding to cells. The x-ray structures of homologous viruses complexed with N-terminal glycoproteins suggest that the BC and HI loops of the viral coat are determinant for binding and thereby, infection of the host cell. The large size of the viral coat precludes it from common biophysical and small molecule screening studies. Hence, we sought to develop a smaller protein template incorporating the identified binding loops of the BK viral coat in a manner that adequately mimics the binding activity of the BK virus coat protein to cells. Such a mimic may serve as a tool for the identification of inhibitors of BK viral progression. Herein, we report the design and characterization of a reduced-size and soluble template derived from a four helix protein—TM1526 of Thermatoga maritima archaea bacteria—which maintains the topological display of the BC and HI loops as found in the viral coat protein, VP1, of BKV. We demonstrate that the GT1b and GD1b sialogangliosides, which bind to the VP1 of BKV, also associate with our BKV-template. Employing a GFP-tagged template, we show host cell association that is dose dependent and that can be reduced by neuraminidase treatment. These data demonstrate that the BKV-template mimics the host-cell binding observed for the wild-type virus coat protein, VP1.

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Characterization of gangliosides in human leucocytes

Cited by 13 publications

References 10 publications

Gangliosides in human chronic lymphocytic leukaemia

Gangliosides in human chronic lymphocytic leukaemia

Identification of Gangliosides GD1b and GT1b as Receptors for BK Virus

Reining in Polyoma Virus Associated Nephropathy: Design and Characterization of a Template Mimicking BK Viral Coat Protein Cellular Binding

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