S. Jin

Neurology · PLoS Biology · 2010–2012

A researcher in the Science corpus: 4 papers; trusts 4 researchers and is trusted by 8 researchers here, as inferred from the citation graph.

Subfields

• Neurology — 46 citations into it; #351 of 1,455 by trust here, #187 by citations
• Epidemiology — 41 citations into it; #455 of 2,148 by trust here, #387 by citations
• Molecular Biology — 41 citations into it
• Cellular and Molecular Neuroscience — 23 citations into it

Whom S. Jin trusts overall

Their strongest outbound trust, strongest first, inferred from their citations.

1. Derek P. Narendra
2. A. Schapira
3. D. Suen
4. R. Youle
5. Y. Ye

Who trusts S. Jin overall

1. Nicole Exner
2. R. Youle
3. A. Ordureau
4. Gian-Luca McLelland
5. A. Lutz
6. W. Ding
7. M. Lazarou
8. M. H. Yan
9. Koji Yamano
10. Alicia M. Pickrell

Papers from S. Jin's perspective

Ordered by how strongly the researchers S. Jin trusts endorse each paper. Same corpus, a different order for every researcher.

1. Parkin is recruited selectively to impaired mitochondria and promotes their autophagy (Journal of Cell Biology)
2. PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1 (Nature Cell Biology)
3. PINK1-dependent recruitment of Parkin to mitochondria in mitophagy (Proceedings of the National Academy of Sciences of the United States of America)
4. PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin (PLoS Biology)
5. Mitochondrial pathology and muscle and dopaminergic neuron degeneration caused by inactivation of Drosophila Pink1 is rescued by Parkin. (Proceedings of the National Academy of Sciences of the United States of America)
6. Mitochondria in the aetiology and pathogenesis of Parkinson's disease. (Lancet Neurology)
7. Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin (Nature)
8. Loss of PINK1 Function Promotes Mitophagy through Effects on Oxidative Stress and Mitochondrial Fission* (Journal of Biological Chemistry)
9. Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants (Proceedings of the National Academy of Sciences of the United States of America)
10. 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)

Their papers

• Role of PINK1 binding to the TOM complex and alternate intracellular membranes in recruitment and activation of the E3 ligase Parkin (2012) — 654 citations
• PINK1- and Parkin-mediated mitophagy at a glance (2012) — 620 citations
• PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin (2010) — 2,915 citations
• Mitochondrial membrane potential regulates PINK1 import and proteolytic destabilization by PARL (2010) — 1,343 citations