Hsieh, Chang-HengChang-HengHsiehChou, Chia-ChengChia-ChengChouFang, Ya-ChingYa-ChingFangHsu, Po-HaoPo-HaoHsuChiu, Yi-HungYi-HungChiuYang, Chi-ShengChi-ShengYangJow, Guey-MeiGuey-MeiJowCHIH-YUNG TANGJeng, Chung-JiuanChung-JiuanJeng2023-07-032023-07-032023-01-302045-3701https://scholars.lib.ntu.edu.tw/handle/123456789/633294Mutations in the human gene encoding the neuron-specific Eag1 (KV10.1; KCNH1) potassium channel are linked to congenital neurodevelopmental diseases. Disease-causing mutant Eag1 channels manifest aberrant gating function and defective protein homeostasis. Both the E3 ubiquitin ligase cullin 7 (Cul7) and the small acid protein 14-3-3 serve as binding partners of Eag1. Cul7 mediates proteasomal and lysosomal degradation of Eag1 protein, whereas over-expression of 14-3-3 notably reduces Eag1 channel activity. It remains unclear whether 14-3-3 may also contribute to Eag1 protein homeostasis.enLysosomal degradation; Potassium channel; Proteasomal degradation; Protein interaction; Protein stability; Ubiquitin ligasejournal article10.1186/s13578-023-00969-w367179382-s2.0-85146926824https://api.elsevier.com/content/abstract/scopus_id/85146926824