GATA1 insufficiencies in primary myelofibrosis and other hematopoietic disorders: consequences for therapy.
GATA1 insufficiencies in primary myelofibrosis and other hematopoietic disorders: consequences for therapy.
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DOI：
10.1080/17474086.2018.1436965
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发表时间：
2018-03
影响因子：
2.8
通讯作者：
Migliaccio AR
中科院分区：
文献类型：
--
作者：
Ling T;Crispino JD;Zingariello M;Martelli F;Migliaccio AR
GATA1, the founding member of a family of transcription factors, plays important roles in the development of hematopoietic cells of several lineages. Although loss of GATA1 has been known to impair hematopoiesis in animal models for nearly 25 years, the link between GATA1 defects and human blood diseases has only recently been realized. Here the current understanding of the functions of GATA1 in normal hematopoiesis and how it is altered in disease is reviewed. GATA1 is indispensable mainly for erythroid and megakaryocyte differentiation. In erythroid cells, GATA1 regulates early stages of differentiation, and its deficiency results in apoptosis. In megakaryocytes, GATA1 controls terminal maturation and its deficiency induces proliferation. GATA1 alterations are often found in diseases involving these two lineages, such as congenital erythroid and/or megakaryocyte deficiencies, including Diamond Blackfan Anemia (DBA), and acquired neoplasms, such as acute megakaryocytic leukemia (AMKL) and the myeloproliferative neoplasms (MPNs). Since the first discovery of GATA1 mutations in AMKL, the number of diseases that are associated with impaired GATA1 function has increased to include DBA and MPNs. With respect to the latter, we are only just now appreciating the link between enhanced JAK/STAT signaling, GATA1 deficiency and disease pathogenesis.
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影响因子：
4.8
作者：
Eliades, Alexia;Papadantonakis, Nikolaos;Ravid, Katya
通讯作者：
Ravid, Katya
影响因子：
20.3
作者：
Chagraoui, H;Komura, E;Wendling, F
通讯作者：
Wendling, F
影响因子：
3.5
作者：
Alvarez-Larran, Alberto;Arellano-Rodrigo, Eduardo;Cervantes, Francisco
通讯作者：
Cervantes, Francisco
影响因子：
20.3
作者：
Centurione, L;Di Baldassarre, A;Migliaccio, AR
通讯作者：
Migliaccio, AR
影响因子：
20.3
作者：
Akada, Hajime;Yan, Dongqing;Mohi, M. Golam
通讯作者：
Mohi, M. Golam