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Associate Researcher Wang Chenji , School of Life Sciences, Fudan University, and Researcher Gao Kun from Shanghai First Maternity and Infant Health Hospital jointly published an online article entitled " SPOP mutations promote p62 / SQSTM1- The latest research results of dependent autophagy and Nrf2 activation in prostate cancer” .
Autophagy is highly conserved in eukaryotic cells, through which cells degrade intracellular components and recycle the degraded nutrients
.
Autophagy and the ubiquitin- proteasome system ( UPS ), two major protein quality control pathways, have long been thought to be independent of each other, however recent studies have shown that these two processes are closely related and run through a common ubiquitin Chemical signals regulate each other
p62/SQSTM1 is an important selective autophagy receptor that drives ubiquitination-dependent autophagic degradation
.
At the same time, the receptor is also a regulator of oxidative stress signaling, helping cells to cope with oxidative stress by activating the Nrf2 pathway .
p62 dysfunction is closely related to a variety of neurodegenerative diseases and carcinogenesis .
Although the pathophysiological importance of p62 is widely recognized, its dynamic regulation under basal and stress conditions is still not fully understood .
In prostate cancer, the SPOP gene encoding the substrate recognition subunit of Cullin 3 E3 ubiquitin ligase complex is frequently mutated, but the molecular mechanism of SPOP mutation leading to prostate cancer is still not fully understood .
Shi Qing, a postdoctoral fellow at the School of Life Sciences of Fudan University, Jin Xiaofeng, an associate professor of Ningbo University, Zhang Pingzhao, an associate researcher of the Department of Pathology, Fudan University School of Medicine, and Li Qian, an undergraduate student of Ningbo University School of Medicine are the co-first authors of the paper
.
Associate researcher Wang Chenji and researcher Gao Kun are the co-corresponding authors of the paper
Original link: https://
