FAT1 钙黏蛋白在 NTera2 细胞分化过程中控制着神经突生成。

FAT1 cadherin controls neuritogenesis during NTera2 cell differentiation.

机构信息

Department of Pharmacology, Faculty of Pharmacy, Elmergib University, Alkhoms, Libya; School of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW, 2308, Australia.

Children's Cancer Institute, Lowy Cancer Research Centre, UNSW Australia, Randwick, NSW 2031, Australia.

出版信息

Biochem Biophys Res Commun. 2019 Jun 30;514(3):625-631. doi: 10.1016/j.bbrc.2019.04.197. Epub 2019 May 7.

DOI:10.1016/j.bbrc.2019.04.197

PMID:31076104

Abstract

Fat1 cadherin is broadly expressed throughout the nervous system and has been implicated in neuronal differentiation. Here we examined the functional contribution of FAT1 during neuronal differentiation of the Ntera2 cell line model. FAT1 expression was increased during the retinoic acid (RA)-induced differentiation of NTera2 cells. Depletion of FAT1 with siRNA decreased the number of neurites produced after RA treatment. Moreover, FAT1 silencing also led to decreased Ser127-phosphorylation of YAP along with transcriptional increases in the Hippo target genes CTGF and ANKRD1, suggesting FAT1 alters Hippo signalling during differentiation. In the context of the Ntera2 model, FAT1 is required for efficient neuritogenesis, acting as a regulator of neurite formation during the early stages of differentiation.

摘要

Fat1 钙黏蛋白广泛表达于整个神经系统，并已被牵连到神经元分化中。在这里，我们研究了 Fat1 在 Ntera2 细胞系模型的神经元分化过程中的功能贡献。Fat1 的表达在视黄酸（RA）诱导的 Ntera2 细胞分化过程中增加。用 siRNA 耗尽 Fat1 会减少 RA 处理后产生的神经突数量。此外，Fat1 沉默还导致 YAP 的 Ser127 磷酸化减少，以及 Hippo 靶基因 CTGF 和 ANKRD1 的转录增加，表明 Fat1 在分化过程中改变 Hippo 信号。在 Ntera2 模型的背景下，Fat1 是有效神经突生成所必需的，它作为分化早期神经突形成的调节剂。