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Jing Quan

Researcher at Chinese Ministry of Education

Publications -  8
Citations -  209

Jing Quan is an academic researcher from Chinese Ministry of Education. The author has contributed to research in topics: Lipid metabolism & Metabolite. The author has an hindex of 5, co-authored 8 publications receiving 71 citations. Previous affiliations of Jing Quan include Central South University.

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ACSL family: The regulatory mechanisms and therapeutic implications in cancer.

TL;DR: In this article, the differential regulatory mechanisms of the ACSL family members as well as their functions in carcinogenesis were addressed. And the clinical therapeutic implications of ACSLs, which might serve as valuable biomarkers and therapeutic targets for precision cancer treatment.
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Natural alkaloid and polyphenol compounds targeting lipid metabolism: Treatment implications in metabolic diseases.

TL;DR: Alkaloid and polyphenol are promising candidates for metabolic diseases to ameliorate lipid metabolism abnormalities to improve or even curing lipid metabolism-related diseases.
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Treatment implications of natural compounds targeting lipid metabolism in nonalcoholic fatty liver disease, obesity and cancer

TL;DR: This review describes the regulatory machinery of lipid metabolism and its deregulation in metabolic diseases and enumerates and integrates the mechanism of action of some natural compounds, including terpenoids and flavonoids, to ameliorate the development of metabolic diseases by targeting lipid metabolism.
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DHRS2 mediates cell growth inhibition induced by Trichothecin in nasopharyngeal carcinoma.

TL;DR: It is demonstrated that TCN is able to induce growth inhibition of NPC in vitro and in vivo by up-regulating DHRS2, and may be a target for the development of targeted therapies against NPC.
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Posttranslational regulation of PGC-1α and its implication in cancer metabolism

TL;DR: A better understanding of the elegant function of P GC‐1α in cancer progression could provide novel insights into therapeutic interventions through the targeting of PGC‐1 α signaling.