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Activation of c‐erbB in avian leukosis virus‐induced erythroblastosis leads to the expression of a truncated EGF receptor kinase.
Author(s) -
Lax I.,
Kris R.,
Sasson I.,
Ullrich A.,
Hayman M.J.,
Beug H.,
Schlessinger J.
Publication year - 1985
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1985.tb04062.x
Subject(s) - biology , virology , erbb , receptor , virus , kinase , microbiology and biotechnology , genetics
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.