Abstract
There is considerable evidence that links the activation of cellular genes to oncogenesis. We previously reported that structural rearrangements in the cellular oncogene c-erbB correlate with the development of erythroblastosis induced by avian leukosis virus (ALV). c-erbB recently has been shown to be related to the gene encoding growth factor receptor. We now have characterized the detailed mechanisms of c-erbB activation by ALV proviruses. We report here that the ALV proviral integration sites are clustered 5' to the region where homology to v-erbB starts, suggesting that interruption in this region of c-erbB is important for its activation. The proviruses are oriented in the same transcriptional direction as c-erbB and usually are full-size. The latter finding is in contrast to the frequent deletions observed within the c-myc-linked proviruses in B-cell lymphomas. We have also identified a second c-erbB allele, which differs from the previously known allele primarily by a deletion in an intron region. This allele is also oncogenic upon mutation by an ALV provirus.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2287-2291 |
| Number of pages | 5 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Volume | 82 |
| Issue number | 8 |
| State | Published - 1985 |
| Externally published | Yes |
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ASJC Scopus subject areas
- General
- Genetics
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c-erbB activation in avian leukosis virus-induced erythroblastosis : Clustered integration sites and the arrangement of provirus in the c-erbB alleles. / Raines, M. A.; Lewis, W. G.; Crittenden, L. B.; Kung, Hsing-Jien.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 82, No. 8, 1985, p. 2287-2291.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - c-erbB activation in avian leukosis virus-induced erythroblastosis
T2 - Clustered integration sites and the arrangement of provirus in the c-erbB alleles
AU - Raines, M. A.
AU - Lewis, W. G.
AU - Crittenden, L. B.
AU - Kung, Hsing-Jien
PY - 1985
Y1 - 1985
N2 - There is considerable evidence that links the activation of cellular genes to oncogenesis. We previously reported that structural rearrangements in the cellular oncogene c-erbB correlate with the development of erythroblastosis induced by avian leukosis virus (ALV). c-erbB recently has been shown to be related to the gene encoding growth factor receptor. We now have characterized the detailed mechanisms of c-erbB activation by ALV proviruses. We report here that the ALV proviral integration sites are clustered 5' to the region where homology to v-erbB starts, suggesting that interruption in this region of c-erbB is important for its activation. The proviruses are oriented in the same transcriptional direction as c-erbB and usually are full-size. The latter finding is in contrast to the frequent deletions observed within the c-myc-linked proviruses in B-cell lymphomas. We have also identified a second c-erbB allele, which differs from the previously known allele primarily by a deletion in an intron region. This allele is also oncogenic upon mutation by an ALV provirus.
AB - There is considerable evidence that links the activation of cellular genes to oncogenesis. We previously reported that structural rearrangements in the cellular oncogene c-erbB correlate with the development of erythroblastosis induced by avian leukosis virus (ALV). c-erbB recently has been shown to be related to the gene encoding growth factor receptor. We now have characterized the detailed mechanisms of c-erbB activation by ALV proviruses. We report here that the ALV proviral integration sites are clustered 5' to the region where homology to v-erbB starts, suggesting that interruption in this region of c-erbB is important for its activation. The proviruses are oriented in the same transcriptional direction as c-erbB and usually are full-size. The latter finding is in contrast to the frequent deletions observed within the c-myc-linked proviruses in B-cell lymphomas. We have also identified a second c-erbB allele, which differs from the previously known allele primarily by a deletion in an intron region. This allele is also oncogenic upon mutation by an ALV provirus.
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UR - http://www.scopus.com/inward/citedby.url?scp=0021821784&partnerID=8YFLogxK
M3 - Article
C2 - 2986110
AN - SCOPUS:0021821784
VL - 82
SP - 2287
EP - 2291
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 8
ER -