Ras/ERK1/2-mediated STAT3 Ser727 Phosphorylation by Familial Medullary Thyroid Carcinoma-associated RET Mutants Induces Full Activation of STAT3 and Is Required for c-fos Promoter Activation, Cell Mitogenicity, and Transformation

This publication has 24 references indexed in Scilit:

• Current concepts in RET-related genetics, signaling and therapeutics
  Trends in Genetics, 2006
• Cellular effects of imatinib on medullary thyroid cancer cells harboring multiple endocrine neoplasia Type 2A and 2B associated RET mutations
  Surgery, 2006
• Evaluation of potential mechanisms underlying genotype–phenotype correlations in multiple endocrine neoplasia type 2
  Oncogene, 2006
• RET-Familial Medullary Thyroid Carcinoma Mutants Y791F and S891A Activate a Src/JAK/STAT3 Pathway, Independent of Glial Cell Line–Derived Neurotrophic Factor
  Cancer Research, 2005
• Central Role of the Threonine Residue within the p+1 Loop of Receptor Tyrosine Kinase in STAT3 Constitutive Phosphorylation in Metastatic Cancer Cells
  Molecular and Cellular Biology, 2004
• MEN2A-RET-induced cellular transformation by activation of STAT3
  Oncogene, 2001
• Characterization of intracellular signals via tyrosine 1062 in RET activated by glial cell line-derived neurotrophic factor
  Oncogene, 2000
• STAT signaling in the pathogenesis and treatment of leukemias
  Oncogene, 2000
• Biological and biochemical properties of Ret with kinase domain mutations identified in multiple endocrine neoplasia type 2B and familial medullary thyroid carcinoma
  Oncogene, 1999
• TRANSCRIPTIONAL RESPONSES TO POLYPEPTIDE LIGANDS: The JAK-STAT Pathway
  Annual Review of Biochemistry, 1995