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Requirement of activating transcription factor 5 for murine fetal liver erythropoiesis
Author(s) -
Zhang Shuping,
Chen JaneJane
Publication year - 2020
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/bjh.16202
Subject(s) - erythropoiesis , transcription factor , fetus , ineffective erythropoiesis , medicine , cancer research , biology , andrology , pregnancy , genetics , anemia , gene
Activating transcription factor 5 (ATF5) is necessary for the development of various tissues, particularly under stress. Dysfunctions of ATF5 have been shown to be involved in many diseases. The exact function of ATF5 is tissue‐specific, and its role in erythropoiesis is still unknown. We here employed the loss of function strategy to investigate the role of ATF5 in murine erythropoiesis. We found that knockdown of Atf5 impaired the proliferation of fetal liver erythroid progenitors. Furthermore, erythroid differentiation was inhibited by ATF5 deficiency. Our study suggests that ATF5 may be a potential therapeutic target for treating blood diseases with ineffective erythropoiesis.