What is it about?
Normal and beta-thalassemia red cell precursors both exhibit fetal hemolgobin levels that are enhanced by HBS1L knockdown.
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Why is it important?
Promotion of fetal hemoglobin can lessen the severity of beta-thalassemia and sickle cell disease while having less of an effect on cell growth and differentiation.
Perspectives
Chumchuen et al. observed that all isoforms of HBS1L were knocked down in erythroid progenitors from beta-thalassemia and healthy donors. However, they discovered that HBS1L knockdown did in fact boost gamma-globin expression. It does not appear that fetal hemoglobin is generated by altering the expression of transcription factors that are particular to erythroids, such as GATA1, BCL11A, KLF1, or MYB. This necessitates paying closer attention to how HBS1L affects fetal hemoglobin synthesis. It did not seem to directly affect the amount of gamma-globin mRNA when HBS1L was absent. Activating Transcription Factor 4 (ATF4) expression, on the other hand, was markedly elevated and seems to be HBS1L's primary target.
Chayanon Peerapittayamongkol
Department of Biochemistry, Faculty of Medicine Siriraj Hospital, Mahidol University
Read the Original
This page is a summary of: Induction of fetal hemoglobin: Lentiviral shRNA knockdown of HBS1L in β0-thalassemia/HbE erythroid cells, PLoS ONE, March 2023, PLOS,
DOI: 10.1371/journal.pone.0281059.
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