Mutant Cbl proteins as oncogenic drivers in myeloproliferative disorders

Mayumi Naramura, Scott Nadeau, Bhopal Mohapatra, Gulzar Ahmad, Chandrani Mukhopadhyay, Martin Sattler, Srikumar M. Raja, Amarnath Natarajan, Vimla Band, Hamid Band

Research output: Contribution to journalArticlepeer-review

39 Scopus citations


Casitas B-lineage lymphoma (Cbl) family proteins are evolutionarily-conserved attenuators of protein tyrosine kinase (PTK) signaling. Biochemical analyses over the past two decades have firmly established that the negative regulatory functions of Cbl proteins are mediated through their ability to facilitate ubiquitination and thus promote degradation of PTKs. As aberrant activation of PTKs is frequently associated with oncogenesis, it has long been postulated that loss of normal Cbl functions may lead to unregulated activation of PTKs and cellular transformation. In the last few years, mutations in the CBL gene have been identified in a subset of human patients with myeloid malignancies. Here we discuss insights gained from the analyses of Cbl mutants both in human patients and in animal models and propose potential mechanisms of oncogenesis through this pathway.

Original languageEnglish (US)
Pages (from-to)245-250
Number of pages6
Issue number3
StatePublished - 2011


  • Cbl
  • E3 ubiquitin ligase
  • Leukemia
  • Protein tyrosine kinase
  • Signal transduction

ASJC Scopus subject areas

  • Oncology


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