Unc5B associates with LARG to mediate the action of repulsive guidance molecule.
Unc5B associates with LARG to mediate the action of repulsive guidance molecule.
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DOI：
10.1083/jcb.200807029
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发表时间：
2009-03-09
期刊：
影响因子：
--
通讯作者：
Yamashita T
中科院分区：
文献类型：
--
作者：
Hata K;Kaibuchi K;Inagaki S;Yamashita T
神经元轴突在其局部环境中受到吸引和排斥线索的引导。由于排斥性导向分子A（RGMa）最初被鉴定为视觉系统中的轴突排斥剂，因此在发育和成年中枢神经系统中的多种功能已归因于RGMa。RGMa与其受体再生素结合诱导RhoA活化，导致抑制/排斥行为和神经元生长锥的崩溃。然而，调节RhoA激活的确切机制知之甚少。在这项研究中，我们表明，Unc 5 B，netrin受体家族的成员，与再生蛋白作为RGMa的辅助受体相互作用。此外，白血病相关的鸟嘌呤核苷酸交换因子（LARG）与Unc 5 B联合抑制RhoA信号。粘着斑激酶（FAK）参与RGMa诱导的LARG酪氨酸磷酸化以及RhoA活化。这些发现揭示了RGMa介导的多种功能的分子基础。
Neuronal axons are guided by attractive and repulsive cues in their local environment. Because the repulsive guidance molecule A (RGMa) was originally identified as an axon repellent in the visual system, diverse functions in the developing and adult central nervous system have been ascribed to it. RGMa binding to its receptor neogenin induces RhoA activation, leading to inhibitory/repulsive behavior and collapse of the neuronal growth cone. However, the precise mechanisms that regulate RhoA activation are poorly understood. In this study, we show that Unc5B, a member of the netrin receptor family, interacts with neogenin as a coreceptor for RGMa. Moreover, leukemia-associated guanine nucleotide exchange factor (LARG) associates with Unc5B to transduce the RhoA signal. Focal adhesion kinase (FAK) is involved in RGMa-induced tyrosine phosphorylation of LARG as well as RhoA activation. These findings uncover the molecular basis for diverse functions mediated by RGMa.
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影响因子：
4.2
作者：
Manitt, C;Thompson, KM;Kennedy, TE
通讯作者：
Kennedy, TE
RGMA抑制可促进脊髓损伤后的轴突生长和恢复。
DOI：
10.1083/jcb.200508143
发表时间：
2006-04-10
期刊：
The Journal of cell biology
影响因子：
--
作者：
Hata K;Fujitani M;Yasuda Y;Doya H;Saito T;Yamagishi S;Mueller BK;Yamashita T
通讯作者：
Yamashita T
影响因子：
3.5
作者：
Fukuhara, S;Chikumi, H;Gutkind, JS
通讯作者：
Gutkind, JS
影响因子：
3.5
作者：
Driessens, MHE;Olivo, C;Collard, JG
通讯作者：
Collard, JG
影响因子：
4.8
作者：
Chikumi, H;Vázquez-Prado, J;Gutkind, JS
通讯作者：
Gutkind, JS