TET2 in Normal and Malignant Hematopoiesis. Review uri icon

Overview

abstract

  • The ten-eleven translocation (TET) family of enzymes were originally cloned from the translocation breakpoint of t(10;11) in infant acute myeloid leukemia (AML) with subsequent genomic analyses revealing somatic mutations and suppressed expression of TET family members across a range of malignancies, particularly enriched in hematological neoplasms. The TET family of enzymes is responsible for the hydroxylation of 5-methylcytosines (5-mC) to 5-hydroxymethylcytosine (5-hmC), followed by active and passive mechanisms leading to DNA demethylation. Given the complexity and importance of DNA methylation events in cellular proliferation and differentiation, it comes as no surprise that the TET family of enzymes is intricately regulated by both small molecules and regulatory cooperating proteins. Here, we review the structure and function of TET2, its interactions with cooperating mutations and small molecules, and its role in aberrant hematopoiesis.

publication date

  • August 1, 2017

Research

keywords

  • DNA Methylation
  • DNA-Binding Proteins
  • Epigenesis, Genetic
  • Hematologic Neoplasms
  • Hematopoiesis
  • Proto-Oncogene Proteins

Identity

PubMed Central ID

  • PMC5538403

Scopus Document Identifier

  • 85045865243

Digital Object Identifier (DOI)

  • 10.1101/cshperspect.a026518

PubMed ID

  • 28242787

Additional Document Info

volume

  • 7

issue

  • 8