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