2012年4月16日，科罗拉多大学医学院的研究人员发现，缺乏一种特定基因可中断神经管闭合，神经管闭合中断可导致死亡或瘫痪。
神经管(英文：neuraltube)为脊椎动物及原索动物的神经胚期所见到的一种最明显的变化，神经板闭合作为中枢神经系统最初原基的神经管形成过程的总称。其中也包含着伴随形态形成活动、神经母细胞等出现的神经上皮分化过程。这项研究的主要领导者Lee Niswander博士说：mLin41基因的缺陷阻断管神经管闭合，因为没有足够的神经祖细胞产生，相关论文发表在杂志Genes＆Development上。
Niswander和论文的第一作者Jianfu Chen博士等人研究了小鼠神经干细胞。他们认为这些细胞在胚胎发育的不同阶段使用不同的自我更新程序，以满足组织的生长和修复的需求。但调控这些程序的分子机制仍未知。
研究人员发现，小鼠mLin41基因在神经闭合过程中，而不是在大脑发育后期阶段控制神经干细胞的增殖程度。
据Chen描述：有关神经管形成连接方面，小分子RNAs和RNA的调控因子从来没有被研究过。
Niswander是总部设在华盛顿的霍华德·休斯医学研究所的研究员。（生物谷：Bioon.com）
doi:10.1101/gad.187641.112 Genes & Dev. 2012. 26: 803-815
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The ubiquitin ligase mLin41 temporally promotes neural progenitor cell maintenance through FGF signaling
Jianfu Chen, Fan Lai and Lee Niswander
How self-renewal versus differentiation of neural progenitor cells is temporally controlled during early development remains ill-defined. We show that mouse Lin41 (mLin41) is highly expressed in neural progenitor cells and its expression declines during neural differentiation. Loss of mLin41 function in mice causes reduced proliferation and premature differentiation of embryonic neural progenitor cells. mLin41 was recently implicated as the E3 ubiquitin ligase that mediates degradation of Argonaute 2 (AGO2), a key effector of the microRNA pathway. However, our mechanistic studies of neural progenitor cells indicate mLin41 is not required for AGO2 ubiquitination or stability. Instead, mLin41-deficient neural progenitors exhibit hyposensitivity for fibroblast growth factor (FGF) signaling. We show that mLin41 promotes FGF signaling by directly binding to and enhancing the stability of Shc SH2-binding protein 1 (SHCBP1) and that SHCBP1 is an important component of FGF signaling in neural progenitor cells. Thus, mLin41 acts as a temporal regulator to promote neural progenitor cell maintenance, not via the regulation of AGO2 stability, but through FGF signaling.
