Young Chul Kim

Molecular Biology · 2013–2015

A researcher in the Science corpus: 4 papers; trusts 29 researchers and is trusted by 0 researchers here, as inferred from the citation graph.

Subfields

Whom Young Chul Kim trusts overall

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

  1. K. Inoki
  2. Joungmok Kim
  3. Philippe P Roux
  4. K. Guan
  5. Y. Sancak
  6. Dos D. Sarbassov
  7. B. Manning
  8. David M. Sabatini
  9. L. Bar-Peled
  10. J. Blenis

Who trusts Young Chul Kim overall

  1. Fiona M Menzies
  2. Asier González González
  3. Alec C. Kimmelman
  4. C. Yun
  5. K. Guan

Papers from Young Chul Kim's perspective

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

  1. TSC2 mediates cellular energy response to control cell growth and survival. (Cell)
  2. TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling (Nature Cell Biology)
  3. TOR signaling in growth and metabolism. (Cell)
  4. Tuberous sclerosis complex gene products, Tuberin and Hamartin, control mTOR signaling by acting as a GTPase-activating protein complex toward Rheb. (Current Biology)
  5. Phosphorylation and functional inactivation of TSC2 by Erk implications for tuberous sclerosis and cancer pathogenesis. (Cell)
  6. Tumor-promoting phorbol esters and activated Ras inactivate the tuberous sclerosis tumor suppressor complex via p90 ribosomal S6 kinase. (Proceedings of the National Academy of Sciences of the United States of America)
  7. Amino acids mediate mTOR/raptor signaling through activation of class 3 phosphatidylinositol 3OH-kinase. (Proceedings of the National Academy of Sciences of the United States of America)
  8. The TSC1-2 tumor suppressor controls insulin–PI3K signaling via regulation of IRS proteins (Journal of Cell Biology)
  9. Identification of the tuberous sclerosis complex-2 tumor suppressor gene product tuberin as a target of the phosphoinositide 3-kinase/akt pathway. (Molecules and Cells)
  10. Raptor, a binding partner of target of rapamycin (TOR), mediates TOR action. (Cell)

Their papers