A crucial role of heme-regulated eIF2α kinase in maintaining cytoskeletal meshwork under an oxygen deficient condition

• 来源期刊: 科学通报（英文版）
• 年，卷（期）: 2017,（15）
• 页码范围: 1045-1047
• 页数: 3页
• 语种: 英文

摘要

During erythroid differentiation,heme-regulated eIF2α kinase (Hri) is necessary to coordinate translation of globin mRNAs with the availability of heme for the production of large amounts of hemoglobin in red blood ceils (RBCs) [1].Our previous study indicated that there were 73 differentially expressed genes in Hri-/-(knockout,KO) erythroid precursors (i.e.E14.5 fetal liver cells),compared to WT cells [2].After further analysis of these genes,we found that a few genes were implicated in the construction of membrane and cytoskeleton,including Gsn,ADD1,erythrocyte protein band 7.2 (Epb7.2,also named as stomatin),vesicle-associated membrane protein 3 (VAMP3),glycophorin A (GYPA),aquaporin 1 (Aqp1),β2 microglobulin (β2m) and integrin subunit beta 1 (Itgb1).All these genes were significantly downregulated in Hri-/-erythroid precursors in our microarray analysis [2].Here,qRT-PCR analysis displayed an overall 30-80％ decline at the mRNA expression level in Hri-/-E14.5 fetal liver cells,compared to Hri+/+ (WT) cells (Fig.S1),consistent with the microarray data.We then looked for the inborn impairments in Hri deficient cells.