Abstract
Previous studies have shown that patients with the axonal form of Guillain-Barré syndrome (GBS) develop autoantibodies against GM1 ganglioside (GM1). Nerve growth factor (NGF) is essential for neuronal survival in vivo and its functional receptor is Trk-tyrosine kinase. Here, we examined the biological effects of sera from patients with the axonal form of GBS on the morphology and the phosphorylation state of Trk-tyrosine kinase in PC12 cells. Furthermore, we examined the effect of the sera on the integrity of membrane lipid rafts biochemically. The data show that anti-GM1 antibodies found in patients' sera but not control sera inhibit NGF-induced Trk autophosphorylation. Most intriguingly, the autoantibodies alter the distribution of Trk in lipid rafts without shifting the distribution of a rafts marker protein. These data strongly suggest that anti-GM1 antibodies directly influence the integrity of the signaling platform, lipid rafts, implicating the importance of lipid rafts in the development of this disorder.
| Original language | English |
|---|---|
| Pages (from-to) | 355-362 |
| Number of pages | 8 |
| Journal | Molecular and Cellular Neuroscience |
| Volume | 45 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 01-12-2010 |
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All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cellular and Molecular Neuroscience
- Cell Biology
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Anti-GM1 antibodies affect the integrity of lipid rafts. / Ueda, Akihiro; Shima, Sayuri; Miyashita, Tadayuki; Ito, Shinji; Ueda, Masami; Kusunoki, Susumu; Asakura, Kunihiko; Mutoh, Tatsuro.
In: Molecular and Cellular Neuroscience, Vol. 45, No. 4, 01.12.2010, p. 355-362.Research output: Contribution to journal › Article
TY - JOUR
T1 - Anti-GM1 antibodies affect the integrity of lipid rafts
AU - Ueda, Akihiro
AU - Shima, Sayuri
AU - Miyashita, Tadayuki
AU - Ito, Shinji
AU - Ueda, Masami
AU - Kusunoki, Susumu
AU - Asakura, Kunihiko
AU - Mutoh, Tatsuro
PY - 2010/12/1
Y1 - 2010/12/1
N2 - Previous studies have shown that patients with the axonal form of Guillain-Barré syndrome (GBS) develop autoantibodies against GM1 ganglioside (GM1). Nerve growth factor (NGF) is essential for neuronal survival in vivo and its functional receptor is Trk-tyrosine kinase. Here, we examined the biological effects of sera from patients with the axonal form of GBS on the morphology and the phosphorylation state of Trk-tyrosine kinase in PC12 cells. Furthermore, we examined the effect of the sera on the integrity of membrane lipid rafts biochemically. The data show that anti-GM1 antibodies found in patients' sera but not control sera inhibit NGF-induced Trk autophosphorylation. Most intriguingly, the autoantibodies alter the distribution of Trk in lipid rafts without shifting the distribution of a rafts marker protein. These data strongly suggest that anti-GM1 antibodies directly influence the integrity of the signaling platform, lipid rafts, implicating the importance of lipid rafts in the development of this disorder.
AB - Previous studies have shown that patients with the axonal form of Guillain-Barré syndrome (GBS) develop autoantibodies against GM1 ganglioside (GM1). Nerve growth factor (NGF) is essential for neuronal survival in vivo and its functional receptor is Trk-tyrosine kinase. Here, we examined the biological effects of sera from patients with the axonal form of GBS on the morphology and the phosphorylation state of Trk-tyrosine kinase in PC12 cells. Furthermore, we examined the effect of the sera on the integrity of membrane lipid rafts biochemically. The data show that anti-GM1 antibodies found in patients' sera but not control sera inhibit NGF-induced Trk autophosphorylation. Most intriguingly, the autoantibodies alter the distribution of Trk in lipid rafts without shifting the distribution of a rafts marker protein. These data strongly suggest that anti-GM1 antibodies directly influence the integrity of the signaling platform, lipid rafts, implicating the importance of lipid rafts in the development of this disorder.
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UR - http://www.scopus.com/inward/citedby.url?scp=77957955083&partnerID=8YFLogxK
U2 - 10.1016/j.mcn.2010.07.008
DO - 10.1016/j.mcn.2010.07.008
M3 - Article
C2 - 20659560
AN - SCOPUS:77957955083
VL - 45
SP - 355
EP - 362
JO - Molecular and Cellular Neurosciences
JF - Molecular and Cellular Neurosciences
SN - 1044-7431
IS - 4
ER -