Erythroid Differentiation

Our Group organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Erythroid Differentiation

PU.1 is a member of the Ezb transformation-specific sequence family of transcription factors and is expressed mainly in granulocytic, monocytic and B-lymphoid cells [1]. The downregulation of PU.1 was reported to play a role in the pathogenesis of various hematological malignancies, including Acute Myeloid Leukemia (AML) [2], multiple myeloma [3] and Myelodysplastic Syndrome (MDS) [4]. PU.1 is also normally present in immature erythroid cells [5], and several reports have indicated that their downregulation is required for erythroid terminal differentiation [6-9]. Constitutive upregulation of PU.1 is believed to be the main cause for a blockade in the differentiation process of Murine Erythroleukemia (MEL) cells [6-9]. However, several findings [10-12] indicate a requirement for PU.1 expression for erythroid differentiation. Back et al. [10] have reported an important study. They produced a line of PU.1 deficient mice carrying a green fluorescent protein reporter at this locus. They revealed that, PU.1 deficient fetal erythroid progenitors lose their self-renewal capacity and undergo proliferation arrest, premature differentiation and apoptosis [10]. A recent study by Wantakal et al. [11] demonstrated that PU.1 regulates an extensive network of genes that constitute major pathways for controlling the growth and survival of immature erythroid cells. They further revealed that fetal liver erythroid progenitors, the earliest erythroid-committed cells, are dramatically reduced in vivo in mice with low PU.1 expression [11] more


  • Share this page
  • Facebook
  • Twitter
  • LinkedIn
  • Google+
  • Pinterest
  • Blogger