GATA-related hematologic disorders - PubMed (original) (raw)
Review
. 2016 Aug;44(8):696-705.
doi: 10.1016/j.exphem.2016.05.010. Epub 2016 May 25.
Affiliations
- PMID: 27235756
- DOI: 10.1016/j.exphem.2016.05.010
Free article
Review
GATA-related hematologic disorders
Ritsuko Shimizu et al. Exp Hematol. 2016 Aug.
Free article
Abstract
The transcription factors GATA1 and GATA2 are fundamental regulators of hematopoiesis and have overlapping expression profiles. GATA2 is expressed in hematopoietic stem cells and early erythroid-megakaryocytic progenitors and activates a certain set of early-phase genes, including the GATA2 gene itself. GATA2 also initiates GATA1 gene expression. In contrast, GATA1 is expressed in relatively mature erythroid progenitors and facilitates the expression of genes associated with differentiation, including the GATA1 gene itself; however, GATA1 represses the expression of GATA2. Switching the GATA factors from GATA2 to GATA1 appears to be one of the key regulatory mechanisms underlying erythroid differentiation. Loss-of-function analyses using mice in vivo have indicated that GATA2 and GATA1 are functionally nonredundant and that neither can compensate for the absence of the other. However, transgenic expression of GATA2 under the transcriptional regulation of the Gata1 gene rescues lethal dyserythropoiesis in GATA1-deficient mice, illustrating that the dynamic expression profiles of these GATA factors are critically important for the maintenance of hematopoietic homeostasis. Analysis of naturally occurring leukemias in GATA1-knockdown mice revealed that leukemic stem cells undergo functional alterations in response to exposure to chemotherapeutic agents. This mechanism may also underlie the aggravating features of relapsing leukemias. Recent hematologic analyses have suggested that disturbances in the balance of the GATA factors are associated with specific types of hematopoietic disorders. Here, we describe GATA1- and GATA2-related hematologic diseases, focusing on the regulation of GATA factor gene expression.
Copyright © 2016 ISEH - International Society for Experimental Hematology. Published by Elsevier Inc. All rights reserved.
Similar articles
- GATA factor switching from GATA2 to GATA1 contributes to erythroid differentiation.
Suzuki M, Kobayashi-Osaki M, Tsutsumi S, Pan X, Ohmori S, Takai J, Moriguchi T, Ohneda O, Ohneda K, Shimizu R, Kanki Y, Kodama T, Aburatani H, Yamamoto M. Suzuki M, et al. Genes Cells. 2013 Nov;18(11):921-33. doi: 10.1111/gtc.12086. Epub 2013 Aug 1. Genes Cells. 2013. PMID: 23911012 - A regulatory network governing Gata1 and Gata2 gene transcription orchestrates erythroid lineage differentiation.
Moriguchi T, Yamamoto M. Moriguchi T, et al. Int J Hematol. 2014 Nov;100(5):417-24. doi: 10.1007/s12185-014-1568-0. Epub 2014 Mar 18. Int J Hematol. 2014. PMID: 24638828 Review. - The role of the GATA2 transcription factor in normal and malignant hematopoiesis.
Vicente C, Conchillo A, García-Sánchez MA, Odero MD. Vicente C, et al. Crit Rev Oncol Hematol. 2012 Apr;82(1):1-17. doi: 10.1016/j.critrevonc.2011.04.007. Epub 2011 May 24. Crit Rev Oncol Hematol. 2012. PMID: 21605981 Review. - GATA factor switching during erythroid differentiation.
Kaneko H, Shimizu R, Yamamoto M. Kaneko H, et al. Curr Opin Hematol. 2010 May;17(3):163-8. doi: 10.1097/MOH.0b013e32833800b8. Curr Opin Hematol. 2010. PMID: 20216212 Review. - An intricate regulatory circuit between FLI1 and GATA1/GATA2/LDB1/ERG dictates erythroid vs. megakaryocytic differentiation.
Wang C, Hu M, Yu K, Liu W, Hu A, Kuang Y, Huang L, Gajendran B, Zacksenhaus E, Xiao X, Ben-David Y. Wang C, et al. Mol Med Rep. 2024 Jun;29(6):107. doi: 10.3892/mmr.2024.13231. Epub 2024 May 2. Mol Med Rep. 2024. PMID: 38695236 Free PMC article.
Cited by
- GATA2 deficiency and hemophagocytic lymphohistiocytosis (HLH): a systematic review of reported cases.
Rukerd MRZ, Mirkamali H, Nakhaie M, Alizadeh SD. Rukerd MRZ, et al. BMC Infect Dis. 2024 Nov 4;24(1):1239. doi: 10.1186/s12879-024-10145-1. BMC Infect Dis. 2024. PMID: 39497062 Free PMC article. - Strain-dependent modifiers exacerbate familial leukemia caused by GATA1-deficiency.
Hirano I, Abe K, Engel JD, Yamamoto M, Shimizu R. Hirano I, et al. Exp Hematol Oncol. 2024 Feb 26;13(1):23. doi: 10.1186/s40164-024-00491-w. Exp Hematol Oncol. 2024. PMID: 38409047 Free PMC article. - Activating transcription factor 4 in erythroid development and β -thalassemia: a powerful regulator with therapeutic potential.
Li J, Lv A, Chen M, Xu L, Huang H. Li J, et al. Ann Hematol. 2024 Aug;103(8):2659-2670. doi: 10.1007/s00277-023-05508-8. Epub 2023 Oct 31. Ann Hematol. 2024. PMID: 37906269 Review. - Transcription factor genetics and biology in predisposition to bone marrow failure and hematological malignancy.
Zerella JR, Homan CC, Arts P, Brown AL, Scott HS, Hahn CN. Zerella JR, et al. Front Oncol. 2023 Jun 12;13:1183318. doi: 10.3389/fonc.2023.1183318. eCollection 2023. Front Oncol. 2023. PMID: 37377909 Free PMC article. Review. - hGATA1 Under the Control of a μLCR/β-Globin Promoter Rescues the Erythroid but Not the Megakaryocytic Phenotype Induced by the Gata1 low Mutation in Mice.
Martelli F, Verachi P, Zingariello M, Mazzarini M, Vannucchi AM, Lonetti A, Bacci B, Sarli G, Migliaccio AR. Martelli F, et al. Front Genet. 2021 Oct 11;12:720552. doi: 10.3389/fgene.2021.720552. eCollection 2021. Front Genet. 2021. PMID: 34707640 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical