Abl oncogene bypasses normal regulation of JAK/STAT activation

André Limnander, Paul B Rothman

Research output: Contribution to journalArticle

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 languageEnglish (US)
Pages (from-to)1486-1488
Number of pages3
JournalCell cycle (Georgetown, Tex.)
Volume3
Issue number12
StatePublished - Dec 2004
Externally publishedYes

Fingerprint

Suppressor of Cytokine Signaling Proteins
abl Genes
Manuscripts
Proteasome Endopeptidase Complex
Post Translational Protein Processing
Carcinogenesis
Phosphotransferases
Chemical activation
Degradation

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 journalArticle

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