What is he best known for?
The fields of study he is best known for:
The scientist’s investigation covers issues in Cell biology, Ubiquitin, Endosome, Biochemistry and Deubiquitinating enzyme.
His work deals with themes such as Endocytic cycle, Downregulation and upregulation and Lysosome, which intersect with Cell biology.
His research in Ubiquitin intersects with topics in Posttranslational modification, Protein degradation and DNA repair.
His Endosome study incorporates themes from Epidermal growth factor, Epidermal growth factor receptor and Clathrin coat, Endocytosis, Clathrin.
His biological study spans a wide range of topics, including Effector, Sequestosome 1, Computational biology, Programmed cell death and Physiology.
His Neuroscience research is multidisciplinary, incorporating perspectives in Ubiquitin thiolesterase, Cancer, BECN1, Autolysosome and MAP1LC3B.
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)
- Breaking the chains: structure and function of the deubiquitinases. (1307 citations)
What are the main themes of his work throughout his whole career to date?
Cell biology, Ubiquitin, Biochemistry, Endosome and Receptor are his primary areas of study.
His Cell biology research incorporates elements of Endocytic cycle, Endocytosis and Mitophagy.
His studies examine the connections between Ubiquitin and genetics, as well as such issues in Proteasome, with regards to Protein degradation.
Michael J. Clague works mostly in the field of Biochemistry, limiting it down to concerns involving Biophysics and, occasionally, Membrane.
His study looks at the relationship between Endosome and fields such as Wortmannin, as well as how they intersect with chemical problems.
His Phosphorylation research includes elements of Cancer research and Kinase.
He most often published in these fields:
- Cell biology (62.50%)
- Ubiquitin (26.39%)
- Biochemistry (25.69%)
What were the highlights of his more recent work (between 2013-2021)?
- Cell biology (62.50%)
- Ubiquitin (26.39%)
- Mitophagy (6.94%)
In recent papers he was focusing on the following fields of study:
Michael J. Clague mostly deals with Cell biology, Ubiquitin, Mitophagy, Parkin and Cancer research.
Michael J. Clague has researched Cell biology in several fields, including Ribosomal RNA, Proteomics, Centrosome, PINK1 and USP9X.
His Ubiquitin study combines topics from a wide range of disciplines, such as Autophagy, Tyrosine kinase, Protein degradation and DNA repair.
His work in Autophagy addresses issues such as Programmed cell death, which are connected to fields such as Mitochondrial Degradation.
His study in Autolysosome is interdisciplinary in nature, drawing from both Computational biology and Multicellular organism.
The concepts of his Chaperone-mediated autophagy study are interwoven with issues in MAP1LC3B, BECN1, Autophagosome and Physiology.
Between 2013 and 2021, his most popular works were:
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (4170 citations)
- Molecular basis of USP7 inhibition by selective small-molecule inhibitors (159 citations)
- Breaking the chains: deubiquitylating enzyme specificity begets function. (157 citations)
In his most recent research, the most cited papers focused on:
His scientific interests lie mostly in Cell biology, Ubiquitin, Parkin, Computational biology and Mitophagy.
Michael J. Clague combines subjects such as NEDD8 and DNA damage with his study of Cell biology.
Michael J. Clague interconnects Genetic code, Protein degradation, DNA repair and Bioinformatics in the investigation of issues within Ubiquitin.
His Computational biology research is multidisciplinary, relying on both Chaperone-mediated autophagy, BECN1 and Autolysosome.
His Chaperone-mediated autophagy research integrates issues from Multicellular organism and Programmed cell death.
His Autolysosome study combines topics in areas such as MAP1LC3B, Sequestosome 1 and Physiology.
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