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. 2019 Nov 13;39(11):BSR20190604. doi: 10.1042/BSR20190604

Figure 2. Known expressions and functions of BCL11A.

Figure 2

BCL11A is highly expressed in brain and most hematopoietic system cells. Overexpression of BCL11A was found in hematological malignancies and some malignant solid tumors, such as TNBC and NSCLC. 2p15-p16.1 microdeletions lead to haploinsufficiency of BCL11A and may lead to 2p15-p16.1 microdeletion syndrome. BCL11A gene SNPs or DNA methylation may contribute to the development of T2D. In erythroid biology, BCL11A directly inhibits γ-globin and plays a crucial role in fetal-to-adult hemoglobin switching, suggesting that BCL11A is a promising therapeutic gene for β-hemoglobinopathies; CLP, common lymphoid progenitor; DC cell, dendritic cell; ETP, early T-cell progenitor; HbA, adult hemoglobin; HbF, fetal hemoglobin; HSC, hematopoietic stem cell; NSCLC, non-small cell lung cancer; SNP, single-nucleotide polymorphism; T2D, Type II diabetes; TNBC, triple-negative breast cancer.