Abstract
In normal cells, the strength and duration of proliferative signaling pathways are tightly regulated. In oncogenic settings, negative regulation is often bypassed to allow constitutive activation of these pathways. In our recent manuscript, we identify a mechanism that allows the v-Abl oncogene to bypass negative regulation by SOCS-1 to constitutively activate Jak-Stat signaling. The mechanism involves post-translational modifications of SOCS-1 that disrupt its interaction with the proteasome, thereby preventing it from targeting activated Jak kinases for degradation. In this review, we discuss the implications of these findings for our understanding of v-Abl oncogenesis and the regulation of SOCS protein function.
Original language | English (US) |
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Pages (from-to) | 1486-1488 |
Number of pages | 3 |
Journal | Cell Cycle |
Volume | 3 |
Issue number | 12 |
DOIs | |
State | Published - Dec 2004 |
Externally published | Yes |
Keywords
- BCR-Abl
- Cytokine
- Elongin BC
- Jak
- SOCS-1
- Stat
- v-Abl
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology
- Cell Biology