S. Schiaffino

Molecular Biology · 2004–2021

A researcher in the Science corpus: 8 papers; trusts 13 researchers and is trusted by 9 researchers here, as inferred from the citation graph.

Subfields

Whom S. Schiaffino trusts overall

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

  1. M. Sandri
  2. Jiandie D. Lin
  3. C. Mammucari
  4. G. Brooks
  5. S. Lecker
  6. Christoph Handschin
  7. Jinghui Zhao
  8. A. Goldberg
  9. R. Bassel-Duby
  10. J. Brault

Who trusts S. Schiaffino overall

  1. P. Bonaldo
  2. M. Sandri
  3. W. Frontera
  4. B. Egan
  5. J. Chal
  6. I. Slaninová
  7. Julien Ochala

Papers from S. Schiaffino's perspective

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

  1. Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy. (Cell)
  2. Insulin-regulated hepatic gluconeogenesis through FOXO1–PGC-1α interaction (Nature)
  3. The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors. (Molecules and Cells)
  4. IKKbeta/NF-kappaB activation causes severe muscle wasting in mice. (Cell)
  5. Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy (Science)
  6. Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB. (Molecules and Cells)
  7. Trehalose, a Novel mTOR-independent Autophagy Enhancer, Accelerates the Clearance of Mutant Huntingtin and α-Synuclein* (Journal of Biological Chemistry)
  8. PGC-1α protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription (Proceedings of the National Academy of Sciences of the United States of America)
  9. Ablation in mice of the mTORC components raptor, rictor, or mLST8 reveals that mTORC2 is required for signaling to Akt-FOXO and PKCalpha, but not S6K1. (Developmental Cell)
  10. Protein degradation by the ubiquitin-proteasome pathway in normal and disease states. (Journal of the American Society of Nephrology)

Their papers