What is he best known for?
The fields of study he is best known for:
- Gene
- Enzyme
- Cell membrane
His primary scientific interests are in Cell biology, Biochemistry, Autophagosome membrane, Autophagosome and Autophagy database.
His research on Cell biology often connects related topics like Autophagy-Related Protein 8 Family.
Takeshi Noda has included themes like ATG8 and ATG16L1 in his Biochemistry study.
His Autophagosome membrane study combines topics from a wide range of disciplines, such as Endoplasmic reticulum, Omegasome and Autophagy-Related Protein 7.
In his study, which falls under the umbrella issue of Autophagosome, ATG5 is strongly linked to MAP1LC3B.
The various areas that he examines in his Autolysosome study include Chaperone-mediated autophagy and Autophagosome maturation.
His most cited work include:
- LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing (5044 citations)
- LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing (5044 citations)
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (4170 citations)
What are the main themes of his work throughout his whole career to date?
Takeshi Noda mainly focuses on Cell biology, Biochemistry, Autophagosome, Vacuole and Mutant.
Takeshi Noda has researched Cell biology in several fields, including Lysosome, Autophagosome membrane and Autophagy-Related Protein 8 Family.
His studies deal with areas such as ATG8, MAP1LC3B and Autophagy-Related Protein 7 as well as Autophagosome membrane.
His Biochemistry research is multidisciplinary, relying on both Lipid-anchored protein and BAG3.
Particularly relevant to Autolysosome is his body of work in Autophagosome.
His studies in Autolysosome integrate themes in fields like Chaperone-mediated autophagy and Autophagosome maturation.
He most often published in these fields:
- Cell biology (86.18%)
- Biochemistry (40.65%)
- Autophagosome (34.15%)
What were the highlights of his more recent work (between 2013-2021)?
- Cell biology (86.18%)
- Vacuole (32.52%)
- Biochemistry (40.65%)
In recent papers he was focusing on the following fields of study:
His primary areas of study are Cell biology, Vacuole, Biochemistry, Autophagosome and Lysosome.
While the research belongs to areas of Cell biology, Takeshi Noda spends his time largely on the problem of Protein subunit, intersecting his research to questions surrounding Endosome.
The concepts of his Vacuole study are interwoven with issues in GTPase, Yeast, TORC1 signaling, Cytosol and Regulation of gene expression.
His Biochemistry study incorporates themes from ATG16L1 and BAG3.
Takeshi Noda combines subjects such as MAP1LC3B and BECN1 with his study of Autophagosome.
The study incorporates disciplines such as NAD+ kinase, Viability assay, Intracellular and Mineralization in addition to Lysosome.
Between 2013 and 2021, his most popular works were:
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (4170 citations)
- Porphyromonas gingivalis promotes invasion of oral squamous cell carcinoma through induction of proMMP9 and its activation (108 citations)
- Atg9A trafficking through the recycling endosomes is required for autophagosome formation (68 citations)
In his most recent research, the most cited papers focused on:
- Gene
- Enzyme
- Cell membrane
The scientist’s investigation covers issues in Cell biology, Autolysosome, Computational biology, Chaperone-mediated autophagy and Autophagosome.
The Cell biology study combines topics in areas such as Protein subunit, ATG16L1 and BAG3.
His biological study spans a wide range of topics, including ATG8, Atg1 and TFEB.
His work carried out in the field of Autolysosome brings together such families of science as BECN1 and Multicellular organism.
His work deals with themes such as MAP1LC3B, Sequestosome 1 and Physiology, which intersect with Computational biology.
His Autophagosome research includes elements of Cytoplasm and Signal transducing adaptor protein.
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