CAJ | 학술논문

Itch是新近发现的泛素连接酶E3之一,其参与细胞内多种信号蛋白如PLC-γ、PKC-θ、JunB、notch等的泛素化修饰过程,调控细胞表型及功能.Itch缺陷可引起小鼠严重的免疫紊乱和炎症反应,其负向免疫调节作用已在基因敲除动物模型上得以证实.近年来的研究对Itch结构、调控和被调控途径、参与的信号通路等有了更进一步的认识,逐步揭示出Itch在T细胞增殖、分化和诱导免疫耐受中的作用机制.
Itch시신근발현적범소련접매E3지일,기삼여세포내다충신호단백여PLC-γ、PKC-θ、JunB、notch등적범소화수식과정,조공세포표형급공능.Itch결함가인기소서엄중적면역문란화염증반응,기부향면역조절작용이재기인고제동물모형상득이증실.근년래적연구대Itch결구、조공화피조공도경、삼여적신호통로등유료경진일보적인식,축보게시출Itch재T세포증식、분화화유도면역내수중적작용궤제.
Itch, one of the main E3 ligases, plays an important role in immune responses as a negative regulator in the ubiquitination of PLC-γ, PKC-θ, JunB,and notch. Itch deficiency leads to sever inflammatory disorders and immunological abnormality. Many efforts have been made in disclosing the Itch-promoted protein ubiquitination, modulation of its ligase, transdution of downstream signals in T cell anergy and differentiation in the past years.