ArticleBritish journal of haematology2020
Requirement of activating transcription factor 5 for murine fetal liver erythropoiesis.
Article in British journal of haematology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- The lncRNA DUBR is regulated by CTCF and coordinates chromatin landscape and gene expression in hematopoietic cells.Nucleic acids research · 2025Article
- TMEM11 regulates cardiomyocyte proliferation and cardiac repair via METTL1-mediated mCell death and differentiation · 2023Article
- Advancements in Activating Transcription Factor 5 Function in Regulating Cell Stress and Survival.International journal of molecular sciences · 2022Review
- Loss of the mitochondrial phosphate carrier SLC25A3 induces remodeling of the cardiac mitochondrial protein acylome.American journal of physiology. Cell physiology · 2021Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
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.
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