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) |
|---|---|
| Pages (from-to) | 1486-1488 |
| Number of pages | 3 |
| Journal | Cell cycle (Georgetown, Tex.) |
| Volume | 3 |
| Issue number | 12 |
| State | Published - Dec 2004 |
| Externally published | Yes |
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Keywords
- BCR-Abl
- Cytokine
- Elongin BC
- Jak
- SOCS-1
- Stat
- v-Abl
ASJC Scopus subject areas
- Cell Biology
- Biochemistry
- Molecular Biology
Cite this
Abl oncogene bypasses normal regulation of JAK/STAT activation. / Limnander, André; Rothman, Paul B.
In: Cell cycle (Georgetown, Tex.), Vol. 3, No. 12, 12.2004, p. 1486-1488.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Abl oncogene bypasses normal regulation of JAK/STAT activation
AU - Limnander, André
AU - Rothman, Paul B
PY - 2004/12
Y1 - 2004/12
N2 - 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.
AB - 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.
KW - BCR-Abl
KW - Cytokine
KW - Elongin BC
KW - Jak
KW - SOCS-1
KW - Stat
KW - v-Abl
UR - http://www.scopus.com/inward/record.url?scp=17144424612&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=17144424612&partnerID=8YFLogxK
M3 - Article
C2 - 15611644
AN - SCOPUS:17144424612
VL - 3
SP - 1486
EP - 1488
JO - Cell Cycle
JF - Cell Cycle
SN - 1538-4101
IS - 12
ER -