The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia.
Journal
Experimental hematology
ISSN: 1873-2399
Titre abrégé: Exp Hematol
Pays: Netherlands
ID NLM: 0402313
Informations de publication
Date de publication:
07 2023
07 2023
Historique:
received:
16
02
2023
revised:
03
05
2023
accepted:
07
05
2023
pmc-release:
01
07
2024
medline:
30
6
2023
pubmed:
13
5
2023
entrez:
12
5
2023
Statut:
ppublish
Résumé
Hematopoiesis is an exquisitely regulated process of cellular differentiation to create diverse cell types of the blood. Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia (AML), in which generation of the myeloid lineage of differentiated cells is interrupted. In this literature review, we discuss how the chromatin remodeling DEK protein can control hematopoietic stem cell quiescence, hematopoietic progenitor cell proliferation, and myelopoiesis. We further discuss the oncogenic consequences of the t(6;9) chromosomal translocation, which creates the DEK-NUP214 (aka: DEK-CAN) fusion gene, during the pathogenesis of AML. Combined, the literature indicates that DEK is crucial for maintaining homeostasis of hematopoietic stem and progenitor cells, including myeloid progenitors.
Identifiants
pubmed: 37172756
pii: S0301-472X(23)00225-4
doi: 10.1016/j.exphem.2023.05.002
pmc: PMC10330528
mid: NIHMS1904693
pii:
doi:
Substances chimiques
Oncogene Proteins
0
Chromosomal Proteins, Non-Histone
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
18-27Subventions
Organisme : NCI NIH HHS
ID : R37 CA218072
Pays : United States
Informations de copyright
Copyright © 2023 ISEH -- Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Conflict of Interest Disclosure The authors do not have any conflicts of interest to declare in relation to this work.
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