K. Winklhofer
Neurology · 2012
A researcher in the Science corpus: 1 paper; trusts 7 researchers and is trusted by 0 researchers here, as inferred from the citation graph.
Subfields
- Neurology — 73 citations into it
- Molecular Biology — 49 citations into it
- Epidemiology — 24 citations into it
- Physiology — 23 citations into it
Whom K. Winklhofer trusts overall
Their strongest outbound trust, strongest first, inferred from their citations.
Papers from K. Winklhofer's perspective
Ordered by how strongly the researchers K. Winklhofer trusts endorse each paper. Same corpus, a different order for every researcher.
- PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin (PLoS Biology)
- Parkin is recruited selectively to impaired mitochondria and promotes their autophagy (Journal of Cell Biology)
- Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin (Nature)
- Familial Parkinson disease gene product, parkin, is a ubiquitin-protein ligase (Nature Genetics)
- PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1 (Nature Cell Biology)
- Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin (Nature)
- Loss of PINK1 Function Promotes Mitophagy through Effects on Oxidative Stress and Mitochondrial Fission* (Journal of Biological Chemistry)
- Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress (Proceedings of the National Academy of Sciences of the United States of America)
- Fission and selective fusion govern mitochondrial segregation and elimination by autophagy (EMBO Journal)
- Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin (Proceedings of the National Academy of Sciences of the United States of America)