| Autor: |
Vagapova ER; The Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Vavilova Str. 32, Moscow,119991, Russia., Spirin PV; The Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Vavilova Str. 32, Moscow,119991, Russia., Lebedev TD; The Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Vavilova Str. 32, Moscow,119991, Russia., Prassolov VS; The Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Vavilova Str. 32, Moscow,119991, Russia. |
| Jazyk: |
angličtina |
| Zdroj: |
Acta naturae [Acta Naturae] 2018 Jan-Mar; Vol. 10 (1), pp. 15-23. |
| Abstrakt: |
TAL1 (SCL/TAL1, T-cell acute leukemia protein 1) is a transcription factor that is involved in the process of hematopoiesis and leukemogenesis. It participates in blood cell formation, forms mesoderm in early embryogenesis, and regulates hematopoiesis in adult organisms. TAL1 is essential in maintaining the multipotency of hematopoietic stem cells (HSC) and keeping them in quiescence (stage G0). TAL1 forms complexes with various transcription factors, regulating hematopoiesis (E2A/HEB, GATA1-3, LMO1-2, Ldb1, ETO 2 , RUNX1, ERG, FLI1). In these complexes, TAL1 regulates normal myeloid differentiation, controls the proliferation of erythroid progenitors, and determines the choice of the direction of HSC differentiation. The transcription factors TAL1, E2A, GATA1 (or GATA2), LMO2, and Ldb1 are the major components of the SCL complex. In addition to normal hematopoiesis, this complex may also be involved in the process of blood cell malignant transformation. Upregulation of C-KIT expression is one of the main roles played by the SCL complex. Today, TAL1 and its partners are considered promising therapeutic targets in the treatment of T-cell acute lymphoblastic leukemia. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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