Table 1 Transcriptional complexes of TAFs, Mediators, and chromatin remodeling-related cofactors in normal and malignant hematopoietic cells and their functions

From: Interplay between cofactors and transcription factors in hematopoiesis and hematological malignancies

Co-factors Complex components Cell type Functions of TCs
TAFs TAF9–EKLF MEL cells Enhancing transcriptional activation of EKLF to the β-globin gene
TAF9–HDAC1 MEL, K562 and human CD34+ cells Deacetylation of TAF9 by HDAC1 is required for PU.1 transcription
TAF (4/4b, 9, 10, 12) –SAGA or TFIID–GATA1 Mouse and human erythroid cells Regulation of GATA1 target genes and the autologous control of GATA1 expression
TAFII130–NF–E2 K562 and CB3 cells Promotion of Enhancer-dependent transcription of β-globin and α-globin genes
TAF (1, 3, 4, 5, 6, 7, 9 and 10)–CBFβ–MYH11–RUNX1 ME-1 inv (16) cells Guiding the localization of CBFβ or the fused CBFβ–MYH11 to promoter sites
TFIID or SAGA complex–TAF12–TAF4–MYB Murine AML cells (RN2 cells) TAF12 facilitates transcriptional activation of MYB and protects it from degradation
Mediators Med (1, 14, 17)–GATA1 Mouse erythroid leukemia cells As a cofactor for GATA1 to enhance GATA1-mediated transactivation
Med1–vitamin D receptor HL-60 cells Involvement in the differentiation of hematopoietic progenitor cells into monocytes
Med1–retinoic acid receptor HL-60 cells Involvement in the differentiation of hematopoietic progenitor cells into granulocytes
Med (12,13)–p300–CDK8–CCNC HPC-7 cells The maintenance of the active state of hematopoietic enhancers
Med23–MEF2 T-cells and MEF cells MED23 is required for full activity of the MAPK-responsive transcription factor MEF2
BRD4–Mediators (MED12, 13, 23 and 24) Mouse MLL-AF9; NrasG12D AML cells Sustaining expression of BRD4, MYC, and MYB target gene signatures
SWI/SNF BRG1-containing E-RC1 complex-EKLF MEL cells The complex is critical for chromatin remodeling and transcription with EKLF
BRG1–EKLF–TBP–NF–E2–CBP Human CD34+ cells Facilitating chromatin remodeling of the human β-globin promoter and β-globin activation
BRG1–GATA1–Scl/TAL1–mSin3A–HDAC2 MEL cells Repression of protein 4.2 promoter activity in an HDAC-dependent manner
BRG1–BAFs (250A,170, 155, 53A and 47) hESCs Regulation of the pluripotency of hESCs by modulating the acetylation levels of H3K27 at the enhancers of lineage-specific genes
BRG1–BAFs (47, 57, 60a and 170)–PYR complex-NuRD/Mi-2-Ikaros MEL cells Facilitating fetal-to-adult globin gene switching, most likely through an effect on higher-order chromatin structure
BRG1–INI1–RUNX1 Jurkat cells RUNX1 interacts with BRG1 and INI1 and supports binding of SWI/SNF complex to RUNX1 target genes related to hematopoietic lineage progression
BRG1–ATF3–β-actin HL-60 cells ATF-3 cooperates with BRG1 and β-actin to initiate left-handed Z-DNA formation and subsequently transactivate the SLC11A1 gene
C/EBPβ–hBRM–BAF155–Myb HD3 erythroblasts Fusion of N terminus of C/EBPβ with Myb conferred hBrm responsiveness to the chimeric transcription factor and enabled it to activate the mim-1 gene
BRG1–STAT6–NFAT1 Primary mouse Th cells BRG1 recruitment to the Th2 LCR depends both on cytokine signals through STAT6, as well as signaling through the TCR via NFAT1
BAF60B–CEBPε Human promyelocytic cell line NB4 BAF60B interacts with CEBPε and controls expression of neutrophil proteins stored in specific granules
SNF2H-ISWI SNF2H–ACF1–GATA1 MEL and G1E cells NA
SNF2H–ACF1 Murine EL4T cells, Primary CD4T cells Involvement of both repression (e.g., IL-2) and activation (e.g., IL-3) of cytokine genes
SNF2H–CTCF–Cohesin complex MEL and OCI-M2 cells The complex is recruited to the enhancer of SPI1 gene and block its expression
NuRF-ISWI Bptf–Snf2L–pRb–Srf Mice thymocytes Srf recruits NuRF to the Bptf-dependent genes, which is important for CD4/CD8 TCRβ+ thymocytes
Mi-2/NuRD MTA2–MBD3–Mi-2–HDAC1/2–PRC2–DNMT3a–PML–RARα NB4 leukemic cells Establishment and maintenance of aberrant epigenetic silencing imposed by PML-RARα
SALL4–MTA2–Mi-2–HDAC1/2 Human ESCs, NB4 cells Repression of PTEN and SALL1 expression, contributing to self-renewal in ESC and leukemic stem cell
Mi-2/NuRD–P-TEFb complex–PP1–IKAROS Lin- HPCs and Jurkat cells Facilitating transcription elongation of IKAROS-target genes and normal differentiation of hematopoietic progenitor cells
Mi-2β–p300–HEB DP thymocytes Stablizing recruitment of basal transcription factors and causing histone H3-hyperacetylation at the CD4 enhancer
Mi-2β–MOZ–Ikaros–SWI–SNF DP thymocytes Concomitant binding of Mi-2β with Ikaros to the CD4 silencer caused silencer inactivation, thereby allowing for CD4 expression
Mi-2β–KDM6A–CBP–H3K27Ac Human primary AML cells Crosstalk among Mi-2β, KDM6A, H3K27Ac, and CBP toward induction of DOCK5/8 expression and maintenance of Rac GTPase program in AML cells
MTA2/NuRD–AIOLOS/IKAROS or MTA2/NuRD–OCA-B Human pre-B leukemia 697 cells MTA2 cooperates with AIOLOS/IKAROS and OCA-B to suppress Pre-BCR (B cell receptor) genes during the Pre-B to immature B transition
MTA/NuRD MTA1/3–RbAp46-containing NuRD complex–BCL11B Primary human CD4+ T cells, Jurkat cells Regulation of IL-2 gene during activation of human CD4+ T
BCL-6–MTA3-contaning NuRD/Mi-2 corepressor complex Lymphocyte and plasma cells Leading to reprogramming of the plasma cell transcriptional program to a B lymphocyte pattern
  1. NA not applicable.