Activation of c-erbB in avian leukosis virus-induced erythroblastosis leads to the expression of a truncated EGF receptor kinase.
Chicken erythroblastosis caused by avian leukosis virus (ALV) is thought to be mediated by activation of the c-erbB/EGF receptor oncogene by a promoter-insertion mechanism. Here we study the proteins expressed by two ALV-induced leukemias and compare them with the avian EGF receptor and with the oncogene product of avian erythroblastosis virus (v-erbB) which was shown to be a truncated EGF receptor. It appears that the two leukemias express truncated EGF receptors of slightly different sizes with intrinsic tyrosine kinase activity. Hence, acute and chronic retroviruses utilize a common pathway for transformation. Moreover, the proteins expressed in the leukemias are similar to the avian EGF receptor with respect to their phosphopeptide maps, suggesting that they do not carry the C-terminal deletion characteristic of v-erbB.
D001355:Alpharetrovirus / Q000235:genetics*; D000596:Amino Acids / Q000032:analysis; D000818:Animals; D001353:Avian Leukosis / Q000382:microbiology; D001354:Avian Leukosis Virus / Q000235:genetics*; D002460:Cell Line; D002471:Cell Transformation, Neoplastic; D002645:Chickens; D066246:ErbB Receptors; D005796:Genes; D005814:Genes, Viral; D009857:Oncogenes; D010766:Phosphorylation; D011505:Protein-Tyrosine Kinases / Q000235:genetics* / Q000378:metabolism
D000596:Amino Acids; D066246:ErbB Receptors; D011505:Protein-Tyrosine Kinases