The TET2 interactors and their links to hematological malignancies

IUBMB Life. 2015 Jun;67(6):438-45. doi: 10.1002/iub.1389. Epub 2015 Jun 22.

Abstract

Ten-eleven translocation (TET) family proteins are dioxygenases that oxidize 5-methylcytosine to 5-hydroxymethylcytosine, 5-formylcytosine, and 5-carboxylcytosine in DNA, early steps of active DNA demethylation. TET2, the second member of TET protein family, is frequently mutated in patients with hematological malignancies, leading to aberrant DNA methylation profiling and decreased 5hmC levels. Located in the nucleus and acting as a DNA-modifying enzyme, TET2 is thought to exert its function via TET2-containing protein complexes. Identifying the interactome network of TET2 likely holds the key to uncover the mechanisms by which TET2 exerts its function in cells. Here, we review recent literature on TET2 interactors and discuss their possible roles in TET2 loss-mediated dysregulation of hematopoiesis and pathogenesis of hematological malignancies.

Keywords: human molecular disease; molecular genetics; protein function; proteonomics.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • 5-Methylcytosine / analogs & derivatives
  • Animals
  • Cytosine / analogs & derivatives
  • Cytosine / metabolism
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism*
  • Dioxygenases
  • Epigenesis, Genetic
  • Genes, Tumor Suppressor
  • Hematologic Neoplasms / genetics
  • Hematologic Neoplasms / metabolism*
  • Hematologic Neoplasms / physiopathology
  • Hematopoiesis / physiology*
  • Humans
  • Mice
  • Mutation
  • Protein Interaction Maps
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins / metabolism*

Substances

  • DNA-Binding Proteins
  • Proto-Oncogene Proteins
  • 5-hydroxymethylcytosine
  • 5-Methylcytosine
  • Cytosine
  • Dioxygenases
  • TET2 protein, human