[Molecular mechanism of inactivation of TGF-beta receptors during carcinogenesis].
Kim
S J
SJ
Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute. kims@dce41.nci.nih.gov
D030201:Activin Receptors, Type I; D017353:Gene Deletion; D006801:Humans; D009369:Neoplasms / Q000235:genetics*; D015514:Oncogene Proteins, Fusion / Q000502:physiology; D017346:Protein Serine-Threonine Kinases / Q000235:genetics; D051789:Proto-Oncogene Protein c-fli-1; D034802:RNA-Binding Protein EWS; D000077293:Receptor, Transforming Growth Factor-beta Type I; D000077294:Receptor, Transforming Growth Factor-beta Type II; D018125:Receptors, Transforming Growth Factor beta / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D014157:Transcription Factors / Q000502:physiology; D014158:Transcription, Genetic; D016212:Transforming Growth Factor beta / Q000502:physiology
C106031:EWS-FLI fusion protein; D015514:Oncogene Proteins, Fusion; D051789:Proto-Oncogene Protein c-fli-1; D034802:RNA-Binding Protein EWS; D018125:Receptors, Transforming Growth Factor beta; D014157:Transcription Factors; D016212:Transforming Growth Factor beta; D017346:Protein Serine-Threonine Kinases; D030201:Activin Receptors, Type I; D000077293:Receptor, Transforming Growth Factor-beta Type I; D000077294:Receptor, Transforming Growth Factor-beta Type II