Increased expression of AML1 during retinoic-acid-induced differentiation of U937 cells

Biochem Biophys Res Commun. 1995 Jun 26;211(3):1023-30. doi: 10.1006/bbrc.1995.1913.

Abstract

The AML1 gene on chromosome 21 is disrupted in the (8;21)(q22;q22) and (3;21)(q26;q22) translocations associated with myelogenous leukemias and encodes a DNA binding protein. From the AML1 gene, three proteins, AML1a, AML1b and AML1c, are produced by alternative splicings. We previously showed that AML1 is potentially involved in myeloid cell differentiation. Here we analyzed the expression of AML1 in myeloid cell lines. It was revealed that AML1b and AML1c are the major AML1 proteins in these cell lines and that prior to morphological and functional differentiation, their expressions increase in U937 cells when treated with all-trans retinoic acid. These data suggest that the expression of AML1 is associated with myeloid cell differentiation.

Publication types

  • Comparative Study

MeSH terms

  • Alternative Splicing
  • Binding Sites
  • Bone Marrow Cells
  • Cell Differentiation / drug effects
  • Core Binding Factor Alpha 2 Subunit
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Hematopoietic Stem Cells / drug effects*
  • Humans
  • Leukemia, Myeloid / etiology*
  • Monocytes / drug effects*
  • Neoplasm Proteins / biosynthesis*
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism
  • Protein Binding
  • Proto-Oncogene Proteins*
  • RNA, Messenger / analysis
  • Transcription Factor AP-2
  • Transcription Factors / biosynthesis*
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Tretinoin / pharmacology*
  • Tumor Cells, Cultured

Substances

  • Core Binding Factor Alpha 2 Subunit
  • DNA-Binding Proteins
  • Neoplasm Proteins
  • Proto-Oncogene Proteins
  • RNA, Messenger
  • RUNX1 protein, human
  • Transcription Factor AP-2
  • Transcription Factors
  • Tretinoin