Blood: Transcription Factor ATF4 Activates BCL11A Transcription to Silent Fetal Hemoglobin Expression
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Last Update: 2020-06-24
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Source: Internet
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Author: User
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Fetal hemoglobin reactivation remains a critical goal for the treatment of patients with sickle cell disease and beta-thalassemiaPrevious researchers have found that fetal gamma-globin gene silencing requires the involvement of red blood cell-specific eIF2 alpha kinase HRI, suggesting that HRI may provide a pharmacological target for raising fetal hemoglobin levelsIn this study, through CRISPR-CAS9-oriented human red blood cell loss screening, the transcription factor ATF4, a known HRI-regulated protein, is a new gamma-bead protein regulatory factorATF4 directly stimulates the transcription of BCL11A by binding with the enhancers of the gamma-pearl transcription inhibitor BCL11A and promoting the enhanced child-starter contact of BCL11ANotably, HRI defective mice showed normal Bcl11a levels, indicating species selective regulation, as explained by the researchers by proving that there is a similar ATF4 sequence on the Bcl11a enhancer in mice that is largely optionalIn summary, this study reveals the linear signaling pathways from HRI to ATF4 to BCL11A to gamma-beadprotein, and illustrates the potential limitations of mouse globin gene regulation models
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