Publications by authors named "Helena Lucente"
Article Synopsis
- GFI1B is a key regulator in hematopoiesis, coordinating the assembly of repressor complexes that control gene expression for cell lineage decisions.
- Enforcing GFI1B expression in K562 erythroleukemia cells promotes their differentiation into erythroid cells rather than megakaryocytes, allowing researchers to explore the molecular basis of these differentiation choices.
- The study reveals that GFI1B, through its interaction with LSD1, recruits specific proteins from the BRAF-histone deacetylase complex, which are crucial for enabling erythroid characteristics, indicating the importance of the GFI1B-LSD1 relationship in driving cellular fate decisions.
Proper hematopoietic cell fate decisions require co-ordinated functions of transcription factors, their associated co-regulators, and histone-modifying enzymes. Growth factor independence 1 (GFI1) is a zinc finger transcriptional repressor and master regulator of normal and malignant hematopoiesis. While several GFI1-interacting proteins have been described, how GFI1 leverages these relationships to carry out transcriptional repression remains unclear.
View Article and Find Full Text PDFCell fate specification requires precise coordination of transcription factors and their regulators to achieve fidelity and flexibility in lineage allocation. The transcriptional repressor growth factor independence 1 (GFI1) is comprised of conserved Snail/Slug/Gfi1 (SNAG) and zinc finger motifs separated by a linker region poorly conserved with GFI1B, its closest homolog. Moreover, GFI1 and GFI1B coordinate distinct developmental fates in hematopoiesis, suggesting that their functional differences may derive from structures within their linkers.
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