Study on ion channels properties on neurons differentiation from stem cells, it was found that ion channels and their related small molecular may control the neuronal system development as well as neuronal stem cells fate.

1.  Kv1.3 ion channels regulated neuronal stem cells differentiation.

A small-molecule selective blocker for Kv1.3, Psora-4, induced a significant increase in the percentage of neurons. Knockdown of Kv1.3 in NPCs also promoted neuronal differentiation. Both morphological and electro-physiological analyses suggested that NPC-derived neurons in the presence of Psora-4 were more mature. Their studies reveal a crucial role for the ion channel Kv1.3 in the regulation of NPC differentiation and maturation, making Psora-4 a promising candidate molecule for neural degeneration disease treatment.

2.   SCN1A loss-of-function mutation may be one of the mechanism for epilepsy

Mutations in SCN1A, the gene encoding the α subunit of Nav1.1 channel, can cause epilepsies with wide ranges of clinical phenotypes, which are associated with the contrasting effects of channel loss-of-function or gain-of-function. In this project, CRISPR/Cas9- and TALEN-mediated genome-editing techniques were applied to induced pluripotent stem cell (iPSC)-based-disease model to explore the mechanism of epilepsy caused by SCN1A loss-of-function mutation. Their study fill the gap of their knowledge regarding the relationship between SCN1A mutation effect recorded on exogenously transfected cells and on Nav1.1-expressing neurons, and reveal the physiological basis underlying epileptogenesis caused by SCN1A loss-of-function mutation.

3.TRPV promote the cytotoxicity of H2O2-mediated oxidative stress in cancer cells

Oxidative stress is important for the initiation and progression of cancers, which confers the cells with a survival advantage by inducing oxidative adaption and drug resistance. Their study found that H2O2-mediated oxidative stress increases TRPV2 expression in human hepatoma cells, and suggest that TRPV2 acts as an important enhancer for H2O2-induced cytotoxicity. This process occurred by the inhibition of Akt and Nrf2 as well as the early activation of p38 and JNK1. These findings have important implications for inhibition of oxidative adaption and drug resistance.