P. Pandolfi

Molecular Biology · 2000–2016

A researcher in the Science corpus: 36 papers; trusts 30 researchers and is trusted by 36 researchers here, as inferred from the citation graph.

Subfields

Whom P. Pandolfi trusts overall

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

  1. Lewis C. Cantley
  2. B. Manning
  3. L. Salmena
  4. D. Guertin
  5. Philippe P Roux
  6. K. Inoki
  7. Takashi Nagano
  8. Christopher Potter
  9. Margaret S. Ebert

Who trusts P. Pandolfi overall

  1. T. Balla
  2. Andrea Y. Weiβe
  3. Arkaitz Carracedo
  4. D. Altomare
  5. J. Testa
  6. R. Bernardi
  7. R. Shaw
  8. Yvonne Tay
  9. Paul Jorgensen

Papers from P. Pandolfi's perspective

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

  1. Phosphorylation and Regulation of Akt/PKB by the Rictor-mTOR Complex (Science)
  2. The phosphoinositide 3-kinase pathway. (Science)
  3. The biology and clinical relevance of the PTEN tumor suppressor pathway. (Journal of Clinical Oncology)
  4. Enhanced sensitivity of PTEN-deficient tumors to inhibition of FRAP/mTOR (Proceedings of the National Academy of Sciences of the United States of America)
  5. 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)
  6. The phosphatidylinositol 3-Kinase–AKT pathway in human cancer (Nature Reviews. Cancer)
  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. Rheb is a direct target of the tuberous sclerosis tumour suppressor proteins (Nature Cell Biology)
  9. Tuberous sclerosis complex gene products, Tuberin and Hamartin, control mTOR signaling by acting as a GTPase-activating protein complex toward Rheb. (Current Biology)
  10. mTOR inhibition induces upstream receptor tyrosine kinase signaling and activates Akt. (Cancer Research)

Their papers