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TAK1 is activated by TGF-β signaling and controls axonal growth during brain development Free
Jingwen Yu1,2,†, Feng Zhang2,†, Shuo Wang2, Yongqing Zhang2, Ming Fan1,3,*, and Zhiheng Xu2,4,*
1Department of Neuroscience, Capital Medical University, Beijing 100069, China
2State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China
3Institute of Basic Medical Sciences, Beijing 100850, China
4Parkinson's Disease Center, Beijing Institute for Brain Disorders, Beijing 100053, China *Correspondence to:Ming Fan, E-mail: fanmingchina@126.com; Zhiheng Xu, E-mail: zhxu@genetics.ac.cn
J Mol Cell Biol, Volume 6, Issue 4, August 2014, 349-351,  https://doi.org/10.1093/jmcb/mju030

Dear Editor,

Mammalian central nervous system neurons show asymmetry during early brain development that defines the elaborate function of neural circuitry (Kriegstein and Noctor, 2004). Many intracellular signaling pathways, which are important for the transition to the polarized state and the development of axons and dendrites, have been identified (Barnes and Polleux, 2009). How these pathways are initiated during neuronal development in vivo remained elusive until Yi et al. (2010) found that transforming growth factor-β (TGF-β) is essential for the differentiation and growth of axons. JNK is also crucial for neuronal polarity and axon formation (Oliva et al., 2006). However, whether and how JNK is activated by TGF-β signaling during brain development is not clear.