Transmembrane domain of the AEV erb B oncogene protein is not required for partial manifestation of the transformed phenotype.
The transmembrane domain was deleted from within the v-erb B protein coding region of avian erythroblastosis virus. The mutant oncogene encoded a shortened, apparently soluble form of the normally membrane bound v-erb B protein. Despite this alteration in subcellular distribution, the mutant polypeptide retained the ability to induce fibroblast transformation by several parameters, including the ability to display anchorage-independent growth. It appears that the transmembrane domain, although important for full manifestation of the transformed phenotype, is not essential for v-erb B-mediated oncogenic transformation.
D001355:Alpharetrovirus / Q000235:genetics; D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000235:genetics* / Q000473:pathology; D002478:Cells, Cultured; D002642:Chick Embryo; D003593:Cytoplasm / Q000502:physiology; D066246:ErbB Receptors / Q000235:genetics; D004912:Erythrocytes; D005347:Fibroblasts; D006031:Glycosylation; D008565:Membrane Proteins / Q000502:physiology; D009856:Oncogene Proteins, Viral / Q000235:genetics*; D009857:Oncogenes; D010641:Phenotype; D011505:Protein-Tyrosine Kinases / Q000235:genetics*; D012995:Solubility; D013329:Structure-Activity Relationship
D008565:Membrane Proteins; D009856:Oncogene Proteins, Viral; D066246:ErbB Receptors; D011505:Protein-Tyrosine Kinases