scispace - formally typeset
J

Jieqiong Tan

Researcher at Central South University

Publications -  99
Citations -  2370

Jieqiong Tan is an academic researcher from Central South University. The author has contributed to research in topics: Medicine & Autophagy. The author has an hindex of 18, co-authored 67 publications receiving 1353 citations.

Papers
More filters
Journal ArticleDOI

PINK1-PRKN/PARK2 pathway of mitophagy is activated to protect against renal ischemia-reperfusion injury

TL;DR: It is shown thatmitophagy is induced in renal proximal tubular cells in both in vitro and in vivo models of ischemic AKI, indicating that PINK1-PARK2-mediated mitophagy plays an important role in mitochondrial quality control, tubular cell survival, and renal function during AKI.
Journal ArticleDOI

BNIP3 Protein Suppresses PINK1 Kinase Proteolytic Cleavage to Promote Mitophagy.

TL;DR: It is demonstrated that BCL2/adenovirus E1B 19-kDa interacting protein 3 (BNIP3), a mitochondrial BH3-only protein, interacts with PINK1 to promote the accumulation of full-length Pink1 on the outer membrane of mitochondria, which facilitates parkin recruitment and PINK 1/parkin-mediated mitophagy.
Journal ArticleDOI

Isorhynchophylline, a natural alkaloid, promotes the degradation of alpha-synuclein in neuronal cells via inducing autophagy.

TL;DR: Data from this study raise the possibility that oxindole alkaloid derivatives may serve as a means to stimulate autophagy in neuronal cells, thereby exerting preventive and therapeutic values against neurodegenerative diseases such as Parkinson disease by reducing pathogenic protein aggregates in neurons.
Journal ArticleDOI

Regulation of Intracellular Manganese Homeostasis by Kufor-Rakeb Syndrome-associated ATP13A2 Protein

TL;DR: The results suggest that ATP13A2 plays important roles in protecting cells against manganese cytotoxicity via regulating intracellularManganese homeostasis and provides a potential mechanism of KRS and parkinsonism pathogenesis.
Journal ArticleDOI

Functional cooperation of miR-125a, miR-125b, and miR-205 in entinostat-induced downregulation of erbB2/erbB3 and apoptosis in breast cancer cells

TL;DR: The data suggest that epigenetic regulation via miRNA-dependent or -independent mechanisms may represent a novel approach to treat breast cancer patients with erbB2-overexpressing tumors.