What is he best known for?
The fields of study he is best known for:
Cell biology, Autophagy, Biochemistry, Programmed cell death and Mitochondrion are his primary areas of study.
His biological study spans a wide range of topics, including Ubiquitin, Cytoskeleton, Microfilament and Mitophagy.
His research in Autophagy is mostly focused on Autolysosome.
His work in Biochemistry tackles topics such as Pharmacology which are related to areas like Liver cell and Necrosis.
His Programmed cell death research is multidisciplinary, incorporating elements of Sequestosome 1, Computational biology, Autophagosome and Physiology.
His Mitochondrion study integrates concerns from other disciplines, such as Liver disease, Function and Mitochondrial permeability transition pore.
His most cited work include:
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (4170 citations)
- Guidelines for the use and interpretation of assays for monitoring autophagy (3242 citations)
- Linking of Autophagy to Ubiquitin-Proteasome System Is Important for the Regulation of Endoplasmic Reticulum Stress and Cell Viability (582 citations)
What are the main themes of his work throughout his whole career to date?
Wen-Xing Ding mostly deals with Autophagy, Cell biology, Liver injury, Mitochondrion and Programmed cell death.
His research on Autophagy concerns the broader Biochemistry.
His work deals with themes such as TFEB and Cellular homeostasis, which intersect with Cell biology.
The Liver injury study combines topics in areas such as Alcoholic liver disease and Fatty liver.
His research integrates issues of Cancer cell and Proteasome inhibitor in his study of Programmed cell death.
His work carried out in the field of Pharmacology brings together such families of science as Necrosis and CYP2E1.
He most often published in these fields:
- Autophagy (57.45%)
- Cell biology (46.28%)
- Liver injury (34.57%)
What were the highlights of his more recent work (between 2018-2021)?
- Autophagy (57.45%)
- Liver injury (34.57%)
- Cell biology (46.28%)
In recent papers he was focusing on the following fields of study:
His primary scientific interests are in Autophagy, Liver injury, Cell biology, TFEB and Cancer research.
His Autophagy research is multidisciplinary, incorporating perspectives in Fatty liver, PI3K/AKT/mTOR pathway, Programmed cell death and Pancreatitis.
His Programmed cell death study combines topics from a wide range of disciplines, such as Chaperone-mediated autophagy, Ubiquitin and Computational biology.
The study incorporates disciplines such as Acetaminophen, Mitochondrion and Mitophagy in addition to Liver injury.
Wen-Xing Ding combines subjects such as Catabolism and Cell with his study of Cell biology.
His Cancer research study combines topics in areas such as Oxidative phosphorylation, Immune system, KEAP1, Knockout mouse and Ubiquitin ligase.
Between 2018 and 2021, his most popular works were:
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) (38 citations)
- Double deletion of PINK1 and Parkin impairs hepatic mitophagy and exacerbates acetaminophen-induced liver injury in mice. (29 citations)
- Emerging and established modes of cell death during acetaminophen-induced liver injury (23 citations)
In his most recent research, the most cited papers focused on:
His scientific interests lie mostly in Programmed cell death, Liver injury, Autophagy, Cell biology and Apoptosis.
His studies in Programmed cell death integrate themes in fields like Chaperone-mediated autophagy, PI3K/AKT/mTOR pathway and Computational biology.
His Liver injury study combines topics in areas such as Protein kinase A, PINK1, Mitophagy, Fatty liver and Mitochondrion.
His Autophagy research is multidisciplinary, incorporating perspectives in Protein kinase B, Cancer research, Pathogenesis, Inflammation and Fibrosis.
His Cell biology research includes elements of TFEB, Lysosome and Cell.
His study in Apoptosis is interdisciplinary in nature, drawing from both Oxidative stress, Superoxide dismutase, Acetaminophen, Pharmacology and Necrosis.
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