Regulation of the human HBA genes by KLF4 in erythroid cell lines. (Articolo in rivista)

Type
Label
  • Regulation of the human HBA genes by KLF4 in erythroid cell lines. (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1111/j.1365-2141.2004.05153.x (literal)
Alternative label
  • Marini MG; Porcu L; Asunis I; Loi MG; Ristaldi MS; Porcu S; Ikuta T; Cao A; Moi P. (2010)
    Regulation of the human HBA genes by KLF4 in erythroid cell lines.
    in British journal of haematology (Print)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Marini MG; Porcu L; Asunis I; Loi MG; Ristaldi MS; Porcu S; Ikuta T; Cao A; Moi P. (literal)
Pagina inizio
  • 748 (literal)
Pagina fine
  • 758 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 149 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
  • 10 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 5 (literal)
Note
  • PubMe (literal)
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • INN, CNR (National Research Council) - Cagliar Dipartimento di Scienze Biomediche e Biotecnologie Università di Cagliari (literal)
Titolo
  • Regulation of the human HBA genes by KLF4 in erythroid cell lines. (literal)
Abstract
  • KLF1/EKLF and related Krueppel-like factors (KLFs) are variably implicated in the regulation of the HBB-like globin genes. Prompted by the observation that four KLF sites are distributed in the human alpha-globin gene (HBA) promoter, we investigated if KLFs could also act to modulate the expression of the HBA genes. Among the KLFs tested, only KLF4/GKLF bound specifically to three out of four alpha-globin KLF sites. The occupancy of the same sites by KLF4 in vivo was confirmed by chromatin immunoprecipitation assays with KLF4-specific antibodies. In luciferase reporter assays in MEL cells, high levels of the wild type HBA promoter, but not mutated promoters bearing point mutations that disrupted KLF4-DNA binding, were transactivated by over-expression of KLF4. In K562 cells, induced KLF4 expression with a Tet-off regulated cassette stimulated the expression of the endogenous HBA genes. In a complementary assay in the same cell line, knocking down KLF4 with lentiviral delivered sh-RNAs caused a parallel decrease in the transcription of the HBA genes. All experiments combined support a regulatory role of KLF4 in the control of HBA gene expression. (literal)
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