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Oncogenic activation of c-ABL by mutation within its last exon.
| Content Provider | Europe PMC |
|---|---|
| Author | Goga, A McLaughlin, J Pendergast, A M Parmar, K Muller, A Rosenberg, N Witte, O N |
| Abstract | The c-ABL proto-oncogene is a predominantly nuclear localized tyrosine kinase. A random mutagenesis scheme was used to isolate c-ABL mutants whose expression produced a transformed phenotype in rodent fibroblast cells. An in-frame deletion within the central region of the last exon was identified in one ABL mutant. The mechanism of c-ABL oncogenic activation by mutation within the last exon differs both functionally and structurally from those of v-ABL and BCR/ABL. This class of ABL mutants shows increased tyrosine phosphorylation of cellular proteins in vivo but low levels of autophosphorylation. Last-exon ABL mutants are distinguished from v-ABL or BCR/ABL by their inability to transform primary bone marrow cells or support the growth of transformed pre-B cells. These findings define a new mechanism of oncogenic activation for the ABL kinase through mutations in the last exon which do not require amino-terminal deletions or mutations within the src homology regions. Images |
| Related Links | https://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC360140&blobtype=pdf |
| ISSN | 02707306 |
| Volume Number | 13 |
| PubMed Central reference number | PMC360140 |
| Issue Number | 8 |
| PubMed reference number | 8336729 |
| Journal | Mol Cell Biol |
| e-ISSN | 10985549 |
| DOI | 10.1128/mcb.13.8.4967-4975.1993 |
| Language | English |
| Publisher Date | 1993-08-01 |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Molecular Biology |