Impaired Shc, Ras, and MAPK Activation but Normal Akt Activation in FL5.12 Cells Expressing an Insulin-like Growth Factor I Receptor Mutated at Tyrosines 1250 and 1251

This publication has 54 references indexed in Scilit:

• Activation of JNK by Epac Is Independent of Its Activity as a Rap Guanine Nucleotide Exchanger
  Journal of Biological Chemistry, 2003
• Type 1 insulin-like growth factor regulates MT1-MMP synthesis and tumor invasion via PI 3-kinase/Akt signaling
  Oncogene, 2003
• Insulin‐like growth factor‐1 activates Akt and Jun N‐terminal kinases (JNKs) in promoting the survival of T lymphocytes
  Immunology, 2002
• Cooperative Regulation of the Invasive and Metastatic Phenotypes by Different Domains of the Type I Insulin-like Growth Factor Receptor β Subunit
  Published by Elsevier ,2001
• Transient Activation of Jun N-terminal Kinases and Protection from Apoptosis by the Insulin-like Growth Factor I Receptor Can Be Suppressed by Dicumarol
  Published by Elsevier ,2001
• Crk Activation of JNK via C3G and R-Ras
  Journal of Biological Chemistry, 2000
• Relative Involvement of Shc Tyrosine 239/240 and Tyrosine 317 on Insulin Induced Mitogenic Signaling in Rat1 Fibroblasts Expressing Insulin Receptors
  Biochemical and Biophysical Research Communications, 1998
• At the onset of transformation polyomavirus middle-T recruits shc and src to a perinuclear compartment coincident with condensation of endosomes
  Oncogene, 1998
• The Tyrosine Residue at 1250 of the Insulin-like Growth Factor I Receptor Is Required for Ligand-Mediated Internalization
  Biochemical and Biophysical Research Communications, 1997
• Src Phosphorylates the Insulin-like Growth Factor Type I Receptor on the Autophosphorylation Sites
  Journal of Biological Chemistry, 1996