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Ying Su

Researcher at Nanjing University of Chinese Medicine

Publications -  10
Citations -  111

Ying Su is an academic researcher from Nanjing University of Chinese Medicine. The author has contributed to research in topics: Chemistry & Medicine. The author has an hindex of 3, co-authored 3 publications receiving 25 citations.

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Endoplasmic reticulum stress and protein degradation in chronic liver disease.

TL;DR: The protein degradation process regulated by UPR has great significance in many chronic liver diseases, including non-alcoholic fatty liver disease, alcoholic liver disease (ALD), viral hepatitis, liver fibrosis, and hepatocellular carcinoma(HCC).
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Methionine metabolism in chronic liver diseases: an update on molecular mechanism and therapeutic implication.

TL;DR: The latest achievements related to methionine metabolism and CLD are reviewed, from molecular mechanisms to clinical research, and some insights into the future direction of basic and clinical research are provided.
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Novel copper complex CTB regulates methionine cycle induced TERT hypomethylation to promote HCC cells senescence via mitochondrial SLC25A26.

TL;DR: It is found that CTB-induced upregulation of SLC25A26 could cause abnormal methylation of TERT and inhibited TERT expression, which is considered to be an essential cause of cell senescence, and the inhibitory effect of CTB on the methionine cycle depends on mitochondrial carrier protein SLC 25A26.
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Curcumol alleviates liver fibrosis by inducing endoplasmic reticulum stress-mediated necroptosis of hepatic stellate cells through Sirt1/NICD pathway

TL;DR: It is proved that ER stress regulated curcumol-induced necroptosis in HSCs via Sirtuin-1(Sirt1)/Notch signaling pathway, which led to degradation of NICD, thereby inhibiting Notch signalling pathway to alleviate liver fibrosis.
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Deacetylation of MTHFD2 by SIRT4 senses stress signal to inhibit cancer cell growth by remodeling folate metabolism

TL;DR: This study reveals that SIRT4 senses folate availability to control MTHFD2 K50 acetylation and its protein stability, bridging nutrient/folate stress and cellular redox to act on cancer cell growth.