Cell surface galactosyltransferase mediates the initiation of neurite outgrowth from PC12 cells on laminin.
Cell surface galactosyltransferase mediates the initiation of neurite outgrowth from PC12 cells on laminin.
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细胞表面半乳糖基转移酶介导层粘连蛋白上PC12细胞的神经突生长的启动。
DOI：
10.1083/jcb.110.2.461
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发表时间：
1990-02
期刊：
影响因子：
--
通讯作者：
Shur BD
中科院分区：
文献类型：
--
作者：
Begovac PC;Shur BD
PC 12嗜铬细胞瘤细胞以及体外外周和中枢神经系统神经元的神经突生长由细胞外基质分子层粘连蛋白介导。我们最近已经表明，间充质细胞在层粘连蛋白上的扩散和迁移部分是由细胞表面酶β 1，4半乳糖基转移酶（GalTase）介导的。GalTase位于迁移细胞的板状伪足上，在那里它通过结合层粘连蛋白中的特异性N-连接寡糖而作为层粘连蛋白受体发挥作用（Runyan等人，1988年; Eckstein和Shur，1989年）。在本研究中，我们研究了是否半乳糖苷酶的功能相似，在中性产物层粘连蛋白使用生化和免疫分析。干扰细胞表面GalTase活性的试剂（包括抗GalTase IgG和Fab片段以及GalTase修饰蛋白α-乳白蛋白）抑制了PC 12神经突生长。对照试剂对神经突生长没有影响。此外，通过早期半乳糖基化或酶促去除GalTase底物来阻断层粘连蛋白基质上的GalTase底物也抑制了神经突生长。相反，通过添加UDP-半乳糖，完成GalTase酶促反应，而不适当的糖核苷酸没有影响，神经突生长得到增强。所有这些治疗的效果都具有剂量和/或时间依赖性。表面GalTase的功能在神经突的起始和伸长，虽然GalTase扰动的影响是最引人注目的神经突形成的起始阶段。与此一致，表面GalTase通过间接免疫荧光定位于生长锥和发育中的神经突。总的来说，这些结果表明，半乳糖苷酶介导层粘连蛋白上的神经突生长的起始，并在较小程度上介导神经突伸长。此外，这项研究表明，从间充质细胞和神经元细胞的过程延伸部分依赖于层粘连蛋白中的特定寡糖残基。
Neurite outgrowth from PC12 pheochromocytoma cells, as well as from peripheral and central nervous system neurons in vitro, is mediated by the extracellular matrix molecule, laminin. We have recently shown that mesenchymal cell spreading and migration on laminin is mediated, in part, by the cell surface enzyme, beta 1,4 galactosyltransferase (GalTase). GalTase is localized on lamellipodia of migrating cells where it functions as a laminin receptor by binding to specific N- linked oligosaccharides in laminin (Runyan et al., 1988; Eckstein and Shur, 1989). In the present study, we examined whether GalTase functions similarly during neutrite outgrowth on laminin using biochemical and immunological analyses. PC12 neurite outgrowth was inhibited by reagents that perturb cell surface GalTase activity, including anti-GalTase IgG and Fab fragments, as well as the GalTase modifier protein alpha-lactalbumin. Control reagents had no effect on neurite outgrowth. Furthermore, blocking GalTase substrates on laminin matrices by earlier galactosyltion or enzymatic removal of GalTase substrates also inhibited neurite outgrowth. Conversely, neurite outgrowth was enhanced by the addition of UDP-galactose, which completes the GalTase enzymatic reaction, while inappropriate sugar nucleotides had no effect. The effects of all these treatments were dose and/or time dependent. Surface GalTase was shown to function during both neurite initiation and elongation, although the effects of GalTase perturbation were most striking during the initiation stages of neurite formation. Consistent with this, surface GalTase was localized by indirect immunofluorescence to the growth cone and developing neurite. Collectively, these results demonstrate that GalTase mediates the initiation of neurite outgrowth on laminin, and to a lesser extent, neurite elongation. Furthermore, this study demonstrates that process extension from both mesenchymal cells and neuronal cells is partly dependent upon specific oligosaccharide residues in laminin.
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DOI：
10.1083/jcb.107.5.1863
发表时间：
1988-11
期刊：
The Journal of cell biology
影响因子：
--
作者：
Runyan RB;Versalovic J;Shur BD
通讯作者：
Shur BD
DOI：
10.1083/jcb.103.6.2457
发表时间：
1986-12
期刊：
The Journal of cell biology
影响因子：
--
作者：
通讯作者：
--
影响因子：
2.7
作者：
ROGERS, SL;LETOURNEAU, PC;FURCHT, LT
通讯作者：
FURCHT, LT
DOI：
10.1101/sqb.1983.048.01.065
发表时间：
1983-01-01
期刊：
COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY
影响因子：
--
作者：
LANDER, AD;TOMASELLI, K;REICHARDT, LF
通讯作者：
REICHARDT, LF
影响因子：
2.9
作者：
REICHARDT, LF;BIXBY, JL;TOMASELLI, KJ
通讯作者：
TOMASELLI, KJ