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Supplementary material 1 350 300 265 250 200 158 139 150 100 50 4 0 Biased Forward- Reverse- any orientation reverse (FR) forward (RF) orientation (FR+RF) Supplemental Figure S1. Biased-orientation of DNA motif sequences of transcription factors in T cells. Total 265 of biased orientation of DNA binding motif sequences of transcription factors were found to affect the expression level of putative transcriptional target genes in T cells of four people in common, whereas only four any orientation (i.e. without considering orientation) of DNA binding motif sequences were found to affect the expression level. １ Forward-reverse orientation in monocytes ZNF93_2 ZNF93_1 ZNF92 ZNF90 ZNF836 ZNF716 ZNF709 ZNF695 ZNF676_2 ZNF676_1 ZNF675 ZNF670 ZNF660 ZNF648 ZNF646 ZNF623 ZNF573 ZNF521 ZNF460 ZNF366 ZNF33B ZNF317 ZNF316 ZNF28 ZNF274 ZNF263_2 ZNF263_1 ZNF219 ZNF214 ZNF148 ZNF143_2 ZNF143_1 ZIC3 ZIC1 ZFP30 ZBTB6 ZBTB33 ZBTB24 YY1 YBX1 XRCC4_2 XRCC4_1 XBP1 WT1 USF TP63 TP53 TFE3 TFAP2A TCF3_2 TCF3_1 TCF12 TBX5 TBP SULT1A2 STAT5B STAT5A_3 STAT5A_2 STAT5A_1 STAT4 STAT3_2 STAT3_1 STAT1_6 STAT1_5 STAT1_4 STAT1_3 STAT1_2 STAT1_1 SRF_2 SRF_1 SPI1_2 SPI1_1 SPEF1 SP1_2 SP1_1 SNTB1 SMC3_2 SMC3_1 SMARCC2_2 SMARCC2_1 SMAD2_SMAD3_SMAD4 SMAD2_2 SMAD2_1 SLC25A20 SIX5 SIRT6 SIN3A SETDB1 RXRA_VDR RUNX2 RREB1_3 RREB1_2 RREB1_1 RFTN1 REST_2 Gene REST_1 RELA RAD21_3 RAD21_2 RAD21_1 PTF1A PROX1 PRDM9 PRDM15 2000 PPARGC1A POU6F1 POU3F2 PLAGL1_2 PLAGL1_1 PITX3 Reverse PITX1 PHOX2B 1000 PAX8 PAX5 PARG_2 PARG_1 NR3C1 NR2F6 NR2F2 NR2C2 0 NR1I2 NKX2−5 NFYB NFKB2 NFKB1 NFIB NFE2 MYB_2 MYB_1 MLXIPL MINI20 MEF2A MAZ_3 MAZ_2 MAZ_1 MAX MAFA LBX2 KLF6 KLF5 KLF3 KLF14_2 KLF14_1 IRF7 IKZF1 HSF2 HOXC9 HOXC11 HOXB1 HOXA7 HOMEZ HNF4A_2 HNF4A_1 HMBOX1_2 HMBOX1_1 HIC1_2 HIC1_1 HES1 HENMT1 GTF3C2 GLIS2 GLI2 GLI1 GCM1_3 GCM1_2 GCM1_1 GATA6 GATA2 FUBP1 FOXO4 FOXN2_2 FOXN2_1 FOXA1 FOSB_2 FOSB_1 FOS_2 FOS_1 ETV4 ETS ESX1 ESR2 EN1 EIF5A2 EHF EGR2_4 EGR2_3 EGR2_2 EGR2_1 EBF E2F8 E2F5 E2F3 E2F_2 E2F_1 DNAAF2 DEC DBP CTCF_8 CTCF_7 CTCF_6 CTCF_5 CTCF_4 CTCF_3 CTCF_2 CTCF_1 CEBPZ_2 CEBPZ_1 CEBPG_2 CEBPG_1 BRF1_2 BRF1_1 BBX 5 − YY1 EBF EN1 ETS TBP BBX EHF USF DBP DEC WT1 GLI1 GLI2 IRF7 MAX SIX5 ZIC1 ZIC3 NFIB E2F3 E2F5 E2F8 KLF3 KLF5 KLF6 TP53 TP63 PAX5 PAX8 LBX2 TFE3 ETV4 TBX5 ESX1 HSF2 NFE2 XBP1 YBX1 ESR2 HES1 RELA NFYB MAFA IKZF1 PITX1 PITX3 SIRT6 NR1I2 GLIS2 STAT4 SIN3A E2F_1 E2F_2 ZFP30 SP1_1 SP1_2 GATA2 GATA6 TCF12 ZNF28 ZNF90 ZNF92 PTF1A SRF_1 SRF_2 ZBTB6 FOS_1 FOS_2 NR2F2 NR2F6 SPEF1 FOXA1 FUBP1 MAZ_1 MAZ_2 MAZ_3 MINI20 NFKB1 NFKB2 RFTN1 SNTB1 NR2C2 NR3C1 MYB_1 MYB_2 SPI1_1 SPI1_2 PROX1 FOXO4 HOXA7 HOXB1 MEF2A EIF5A2 RUNX2 HOXC9 HIC1_1 HIC1_2 PRDM9 STAT5B MLXIPL HOMEZ TCF3_1 TCF3_2 ZNF148 ZNF214 ZNF219 ZNF274 ZNF316 ZNF317 ZNF366 ZNF460 ZNF521 ZNF573 ZNF623 ZNF646 ZNF648 ZNF660 ZNF670 ZNF675 ZNF695 ZNF709 ZNF716 ZNF836 BRF1_1 BRF1_2 ZBTB24 ZBTB33 TFAP2A ZNF33B NKX2 CTCF_1 CTCF_2 CTCF_3 CTCF_4 CTCF_5 CTCF_6 CTCF_7 CTCF_8 REST_1 REST_2 PARG_1 PARG_2 GTF3C2 EGR2_1 EGR2_2 EGR2_3 EGR2_4 FOSB_1 FOSB_2 POU3F2 POU6F1 SETDB1 SMC3_1 SMC3_2 HOXC11 DNAAF2 STAT1_1 STAT1_2 STAT1_3 STAT1_4 STAT1_5 STAT1_6 STAT3_1 STAT3_2 PHOX2B GCM1_1 GCM1_2 GCM1_3 KLF14_1 KLF14_2 PRDM15 HENMT1 ZNF93_1 ZNF93_2 SULT1A2 RAD21_1 RAD21_2 RAD21_3 FOXN2_1 FOXN2_2 HNF4A_1 HNF4A_2 CEBPZ_1 CEBPZ_2 RREB1_1 RREB1_2 RREB1_3 XRCC4_1 XRCC4_2 SMAD2_1 SMAD2_2 CEBPG_1 CEBPG_2 STAT5A_1 STAT5A_2 STAT5A_3 ZNF143_1 ZNF143_2 ZNF263_1 ZNF263_2 ZNF676_1 ZNF676_2 SLC25A20 PLAGL1_1 PLAGL1_2 HMBOX1_1 HMBOX1_2 PPARGC1A RXRA_VDR SMARCC2_1 SMARCC2_2 SMAD2_SMAD3_SMAD4 Forward Supplemental Figure S2. Pairs of biased orientation of DNA binding motif sequences of transcription factors enriched in upstream and downstream of genes. The number of genes with a pair of forward-reverse orientation of DNA motif sequences was counted using all pairs of the DNA motif sequences found in open chromatin regions, and statistical tests (chi-square test) were conducted in monocytes and T cells. ２ Reverse-forward orientation in monocytes ZSCAN5B ZSCAN2_2 ZSCAN2_1 ZNF770 ZNF721 ZNF711 ZNF687 ZNF682 ZNF672 ZNF671 ZNF670 ZNF652 ZNF641 ZNF584 ZNF579 ZNF547 ZNF449 ZNF350 ZNF343 ZNF337 ZNF331 ZNF316 ZNF30_2 ZNF30_1 ZNF286B ZNF28 ZNF233 ZNF225 ZNF202 ZNF195 ZNF181 ZNF148 ZNF121 ZNF112 ZIC2 ZIC1 ZBTB7B ZBTB7A ZBTB2 ZBTB18_2 ZBTB18_1 WT1 USF1 TRIM28 TP53 THRB TFAP2E TFAP2B TFAP2A TEAD1 TCF7 TBP_3 TBP_2 TBP_1 STAT5B STAT5A STAT1 SRF_5 SRF_4 SRF_3 SRF_2 SRF_1 SPIC SPI1 SP8 SP4_2 SP4_1 SP3 SP2 SP1 SOX9_3 SOX9_2 SOX9_1 SOX2 SOX11 Gene SMAD9 SMAD4_2 SMAD4_1 SMAD3_2 2500 SMAD3_1 RXRB RXRA_2 RXRA_1 RFX5 2000 RFX3 REST RBAK RAD21 PSMD9 PPARG 1500 POU5F1 POU3F2 POU2F2 POLR3A PLAG1 Forward PBX3 1000 PBX1 PAX6 PAX5_2 PAX5_1 PAX3 500 PAX1 PARP1 OBOX2 NR5A2 NR2F1 NKX3−1 0 NFY NFKB2 NFE2L3 NFE2L2 NFATC1 NANOG MZF1 MYOG MYF6 MYEF2 MYC_MAX MSX2 MAFK LHX4 KLF16 ISL1 IRX2 IRF9 IRF8 IRF4_3 IRF4_2 IRF4_1 IRF3_2 IRF3_1 HSF2 HSF1_2 HSF1_1 HOXD1 HNF1B HAND1_TCF3 GTF2I GABPB1_GABPB2 GABPA FOXR1 FOXP2 FOX FLI1 ETV7 ETV6 ETV5 ETV3 ETV2 ETS2_2 ETS2_1 EP300 ELF5 ELF2 EBF1 E2F3 E2F2 DOBOX5 DNAAF2 CTCF_3 CTCF_2 CTCF_1 CREM CEBPZ CEBPB CDX2 CD59 BDP1 BCL6 BCL3 BCL11A_2 BCL11A_1 ATF3_2 ATF3_1 ATF2_ATF4 ASCL2 ALX1 AHR 1 − SP1 SP2 SP3 SP8 FOX FLI1 NFY ISL1 AHR WT1 IRF8 IRF9 ZIC1 ZIC2 SPI1 IRX2 SPIC E2F2 E2F3 ELF2 ELF5 TP53 PAX1 PAX3 PAX6 ALX1 BCL3 BCL6 EBF1 ETV2 ETV3 ETV5 ETV6 ETV7 LHX4 TCF7 CD59 HSF2 PBX1 PBX3 RFX3 RFX5 USF1 MZF1 SOX2 BDP1 CDX2 MYF6 REST MSX2 RBAK THRB MAFK RXRB GTF2I STAT1 CREM KLF16 MYOG EP300 SP4_1 SP4_2 TBP_1 TBP_2 TBP_3 ZNF28 SRF_1 SRF_2 SRF_3 SRF_4 SRF_5 ZBTB2 PARP1 SOX11 NR2F1 ASCL2 PLAG1 FOXP2 NFKB2 NR5A2 RAD21 TEAD1 FOXR1 HNF1B IRF3_1 IRF3_2 IRF4_1 IRF4_2 IRF4_3 GABPA CEBPZ MYEF2 PPARG HOXD1 OBOX2 CEBPB ATF3_1 ATF3_2 PSMD9 SMAD9 STAT5A STAT5B PAX5_1 PAX5_2 TRIM28 ETS2_1 ETS2_2 ZNF112 ZNF121 ZNF148 ZNF181 ZNF195 ZNF202 ZNF225 ZNF233 ZNF316 ZNF331 ZNF337 ZNF343 ZNF350 ZNF449 ZNF547 ZNF579 ZNF584 ZNF641 ZNF652 ZNF670 ZNF671 ZNF672 ZNF682 ZNF687 ZNF711 ZNF721 ZNF770 NANOG HSF1_1 HSF1_2 NFE2L2 NFE2L3 NFATC1 TFAP2A TFAP2B TFAP2E SOX9_1 SOX9_2 SOX9_3 NKX3 CTCF_1 CTCF_2 CTCF_3 ZBTB7A ZBTB7B POU2F2 POU3F2 POU5F1 RXRA_1 RXRA_2 DNAAF2 POLR3A DOBOX5 ZNF30_1 ZNF30_2 ZNF286B SMAD3_1 SMAD3_2 SMAD4_1 SMAD4_2 ZSCAN5B ZBTB18_1 ZBTB18_2 BCL11A_1 BCL11A_2 MYC_MAX ZSCAN2_1 ZSCAN2_2 ATF2_ATF4 HAND1_TCF3 GABPB1_GABPB2 Reverse ３ Forward-reverse orientation in T cells ZNF880 ZNF846 ZNF84 ZNF790 ZNF786 ZNF770_2 ZNF770_1 ZNF75A ZNF721 ZNF717 ZNF714 ZNF701 ZNF681 ZNF676 ZNF668 ZNF639 ZNF616 ZNF585A ZNF582 ZNF568 ZNF546 ZNF534 ZNF355P ZNF287 ZNF263 ZNF253 ZNF219 ZNF124 ZNF117 ZIC1 ZFX ZFP3 ZFP14 ZEB1 ZBTB7B ZBTB7A ZBTB33 YBX1 TP63 TP53_3 TP53_2 TP53_1 TLX1 THRA TFCP2 TFAP4 TCF7L2_2 TCF7L2_1 TCF4 TBXT TBP TAL1 SRP9 SREBF2 SPI1_2 SPI1_1 SPDEF SP1_2 SP1_1 SOX5 SOX18 SOX13 SOAT1 SMC3 RREB1_2 RREB1_1 RREB RFX3 REL_2 REL_1 RARB RAD21 PRDM9 PRDM15 POU4F1 PLAG1 PITX2 PITX1_2 PITX1_1 Gene PDX1 PCBP1 PAX2 P50_P50 OTX2_2 OTX2_1 NRF1 NR2F2 1500 NR2C2_2 NR2C2_1 NR0B1 NFYA NFY NFKB1 NFIX NFE2_3 1000 NFE2_2 NFE2_1 NFATC2 MZF1 Reverse MYC_2 MYC_1 MXI1 MNX1 MINI20 500 MAF LHX8 LHX6 KLF1_2 KLF1_1 JDP2 IRF5 IRF 0 INSM2 INSM1 HPV16GP4 HOXA7_2 HOXA7_1 HOXA2 HOXA13 HNF1B HNF1A HMGA2_2 HMGA2_1 HIC1 HEY1 HBP1 GLIS2 GLI1 GFI1B_2 GFI1B_1 GFI1 GATA5 GATA4 GATA GABPA FOXO6 FOXO3 FOXN4 FOXJ3 FOXF2 FOXA3 ETV4_2 ETV4_1 ETV3 EP300_2 EP300_1 EMBP1 ELK1 ELF5 ELF4 ELF3 ELF1 EHF_2 EHF_1 EGR4 EGR3_2 EGR3_1 EGR2_2 EGR2_1 EGR1_2 EGR1_1 EBF1 E2F6 E2F4 DUX1 DLX3_2 DLX3_1 DDIT3_CEBPA DBX1 CUX1 CTCF_3 CTCF_2 CTCF_1 CEBPZ CEBPE CDC5L_2 CDC5L_1 BRCA1 BDP1 BCL6 BATF BARX2 BACH1 ARID3A AR APEX1 AR IRF ZFX TBP NFY MAF GLI1 IRF5 ZIC1 GFI1 TAL1 HIC1 NFIX MXI1 E2F4 E2F6 ELF1 ELF3 ELF4 ELF5 TLX1 TP63 BATF PAX2 ELK1 JDP2 ZFP3 GATA BCL6 EBF1 ETV3 LHX6 LHX8 TCF4 ZEB1 RFX3 TBXT NFYA YBX1 SOX5 BDP1 DBX1 HBP1 HEY1 MZF1 NRF1 PDX1 SRP9 CUX1 DUX1 THRA EGR4 MNX1 PITX2 RARB RREB SMC3 GLIS2 SP1_1 SP1_2 ZFP14 TFAP4 GATA4 GATA5 FOXJ3 INSM1 INSM2 ZNF84 REL_1 REL_2 EHF_1 EHF_2 SOAT1 FOXF2 SOX13 SOX18 NR2F2 TFCP2 PLAG1 FOXA3 APEX1 MINI20 NFKB1 NR0B1 RAD21 FOXN4 BARX2 HNF1A HNF1B PCBP1 SPI1_1 SPI1_2 BACH1 GABPA FOXO3 FOXO6 HOXA2 BRCA1 CEBPZ MYC_1 MYC_2 SPDEF CEBPE EMBP1 KLF1_1 KLF1_2 PRDM9 TP53_1 TP53_2 TP53_3 ARID3A ZNF117 ZNF124 ZNF219 ZNF253 ZNF263 ZNF287 ZNF534 ZNF546 ZNF568 ZNF582 ZNF616 ZNF639 ZNF668 ZNF676 ZNF681 ZNF701 ZNF714 ZNF717 ZNF721 ZNF786 ZNF790 ZNF846 ZNF880 DLX3_1 DLX3_2 ETV4_1 ETV4_2 NFE2_1 NFE2_2 NFE2_3 ZBTB33 OTX2_1 OTX2_2 NFATC2 ZNF75A CTCF_1 CTCF_2 CTCF_3 ZBTB7A ZBTB7B EGR1_1 EGR1_2 EGR2_1 EGR2_2 EGR3_1 EGR3_2 HOXA13 PITX1_1 PITX1_2 POU4F1 SREBF2 GFI1B_1 GFI1B_2 PRDM15 EP300_1 EP300_2 P50_P50 ZNF355P ZNF585A CDC5L_1 CDC5L_2 NR2C2_1 NR2C2_2 HOXA7_1 HOXA7_2 RREB1_1 RREB1_2 HMGA2_1 HMGA2_2 TCF7L2_1 TCF7L2_2 ZNF770_1 ZNF770_2 HPV16GP4 DDIT3_CEBPA Forward ４ Reverse-forward orientation in T cells ZNF880 ZNF777 ZNF773 ZNF770 ZNF721 ZNF718 ZNF714 ZNF658 ZNF625 ZNF592 ZNF580 ZNF549 ZNF526 ZNF484 ZNF468 ZNF44 ZNF410 ZNF41 ZNF341 ZNF300 ZNF282 ZNF28 ZNF267 ZNF257 ZNF256 ZNF239 ZNF219 ZNF214 ZNF189 ZNF180 ZNF174 ZNF17 ZNF143 ZNF134 ZIC1 ZFP69B ZFP2 ZBTB7A ZBTB41 ZBTB4 ZBTB33 ZBTB18 YY2 YY1 THRB TEAD1 TCF12_2 TCF12_1 TAL1 SRF_2 SRF_1 SPIC SPI1 SP2_2 SP2_1 SOX2 SMARC SIX6 RUNX2_2 RUNX2_1 RREB1 RORA RFX1_2 RFX1_1 REST RELB RELA REL Gene RARA RAD21 PSMD9 PPARGC1A PPARD POU2F2 PITX3 1500 PBX3_2 PBX3_1 PARP1 NRG2 NR4A1 NR3C1 NKX2−5_2 NKX2−5_1 1000 NKX2−4 NKX2−1 NFYA Forward NFY NFKB1_3 NFKB1_2 NFKB1_1 500 NFE2L2 MYOG MYCN MXI1 MTF1_2 MTF1_1 MLX 0 MEIS1 LHX6 LHX4 LBX1 KLF8 KLF6 KLF16 KLF13 IRF8 IRF5 IRF HSF1 HOXB6 HOXA10 HLTF_2 HLTF_1 HAND1 GTF2I GFI1 GATA4 GATA1_2 GATA1_1 GABPA FOXP3 FOXO3 FOXN4 FOXJ3_2 FOXJ3_1 FOXG1 FOXA2 FOXA1 FOXA FOS_2 FOS_1 ETV6 ETV3 ETV1 ETS2
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    The Capacity of Long-Term in Vitro Proliferation of Acute Myeloid Leukemia Cells Supported Only by Exogenous Cytokines Is Associated with a Patient Subset with Adverse Outcome Annette K. Brenner, Elise Aasebø, Maria Hernandez-Valladares, Frode Selheim, Frode Berven, Ida-Sofie Grønningsæter, Sushma Bartaula-Brevik and Øystein Bruserud Supplementary Material S2 of S31 Table S1. Detailed information about the 68 AML patients included in the study. # of blasts Viability Proliferation Cytokine Viable cells Change in ID Gender Age Etiology FAB Cytogenetics Mutations CD34 Colonies (109/L) (%) 48 h (cpm) secretion (106) 5 weeks phenotype 1 M 42 de novo 241 M2 normal Flt3 pos 31.0 3848 low 0.24 7 yes 2 M 82 MF 12.4 M2 t(9;22) wt pos 81.6 74,686 low 1.43 969 yes 3 F 49 CML/relapse 149 M2 complex n.d. pos 26.2 3472 low 0.08 n.d. no 4 M 33 de novo 62.0 M2 normal wt pos 67.5 6206 low 0.08 6.5 no 5 M 71 relapse 91.0 M4 normal NPM1 pos 63.5 21,331 low 0.17 n.d. yes 6 M 83 de novo 109 M1 n.d. wt pos 19.1 8764 low 1.65 693 no 7 F 77 MDS 26.4 M1 normal wt pos 89.4 53,799 high 3.43 2746 no 8 M 46 de novo 26.9 M1 normal NPM1 n.d. n.d. 3472 low 1.56 n.d. no 9 M 68 MF 50.8 M4 normal D835 pos 69.4 1640 low 0.08 n.d.
  • The E–Id Protein Axis Modulates the Activities of the PI3K–AKT–Mtorc1

    The E–Id Protein Axis Modulates the Activities of the PI3K–AKT–Mtorc1

    Downloaded from genesdev.cshlp.org on October 6, 2021 - Published by Cold Spring Harbor Laboratory Press The E–Id protein axis modulates the activities of the PI3K–AKT–mTORC1– Hif1a and c-myc/p19Arf pathways to suppress innate variant TFH cell development, thymocyte expansion, and lymphomagenesis Masaki Miyazaki,1,8 Kazuko Miyazaki,1,8 Shuwen Chen,1 Vivek Chandra,1 Keisuke Wagatsuma,2 Yasutoshi Agata,2 Hans-Reimer Rodewald,3 Rintaro Saito,4 Aaron N. Chang,5 Nissi Varki,6 Hiroshi Kawamoto,7 and Cornelis Murre1 1Department of Molecular Biology, University of California at San Diego, La Jolla, California 92093, USA; 2Department of Biochemistry and Molecular Biology, Shiga University of Medical School, Shiga 520-2192, Japan; 3Division of Cellular Immunology, German Cancer Research Center, D-69120 Heidelberg, Germany; 4Department of Medicine, University of California at San Diego, La Jolla, California 92093, USA; 5Center for Computational Biology, Institute for Genomic Medicine, University of California at San Diego, La Jolla, California 92093, USA; 6Department of Pathology, University of California at San Diego, La Jolla, California 92093, USA; 7Department of Immunology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan It is now well established that the E and Id protein axis regulates multiple steps in lymphocyte development. However, it remains unknown how E and Id proteins mechanistically enforce and maintain the naı¨ve T-cell fate. Here we show that Id2 and Id3 suppressed the development and expansion of innate variant follicular helper T (TFH) cells. Innate variant TFH cells required major histocompatibility complex (MHC) class I-like signaling and were associated with germinal center B cells.
  • Epigenetics Page 1

    Epigenetics Page 1

    Epigenetics esiRNA ID Gene Name Gene Description Ensembl ID HU-13237-1 ACTL6A actin-like 6A ENSG00000136518 HU-13925-1 ACTL6B actin-like 6B ENSG00000077080 HU-14457-1 ACTR1A ARP1 actin-related protein 1 homolog A, centractin alpha (yeast) ENSG00000138107 HU-10579-1 ACTR2 ARP2 actin-related protein 2 homolog (yeast) ENSG00000138071 HU-10837-1 ACTR3 ARP3 actin-related protein 3 homolog (yeast) ENSG00000115091 HU-09776-1 ACTR5 ARP5 actin-related protein 5 homolog (yeast) ENSG00000101442 HU-00773-1 ACTR6 ARP6 actin-related protein 6 homolog (yeast) ENSG00000075089 HU-07176-1 ACTR8 ARP8 actin-related protein 8 homolog (yeast) ENSG00000113812 HU-09411-1 AHCTF1 AT hook containing transcription factor 1 ENSG00000153207 HU-15150-1 AIRE autoimmune regulator ENSG00000160224 HU-12332-1 AKAP1 A kinase (PRKA) anchor protein 1 ENSG00000121057 HU-04065-1 ALG13 asparagine-linked glycosylation 13 homolog (S. cerevisiae) ENSG00000101901 HU-13552-1 ALKBH1 alkB, alkylation repair homolog 1 (E. coli) ENSG00000100601 HU-06662-1 ARID1A AT rich interactive domain 1A (SWI-like) ENSG00000117713 HU-12790-1 ARID1B AT rich interactive domain 1B (SWI1-like) ENSG00000049618 HU-09415-1 ARID2 AT rich interactive domain 2 (ARID, RFX-like) ENSG00000189079 HU-03890-1 ARID3A AT rich interactive domain 3A (BRIGHT-like) ENSG00000116017 HU-14677-1 ARID3B AT rich interactive domain 3B (BRIGHT-like) ENSG00000179361 HU-14203-1 ARID3C AT rich interactive domain 3C (BRIGHT-like) ENSG00000205143 HU-09104-1 ARID4A AT rich interactive domain 4A (RBP1-like) ENSG00000032219 HU-12512-1 ARID4B AT rich interactive domain 4B (RBP1-like) ENSG00000054267 HU-12520-1 ARID5A AT rich interactive domain 5A (MRF1-like) ENSG00000196843 HU-06595-1 ARID5B AT rich interactive domain 5B (MRF1-like) ENSG00000150347 HU-00556-1 ASF1A ASF1 anti-silencing function 1 homolog A (S.
  • A Flexible Microfluidic System for Single-Cell Transcriptome Profiling

    A Flexible Microfluidic System for Single-Cell Transcriptome Profiling

    www.nature.com/scientificreports OPEN A fexible microfuidic system for single‑cell transcriptome profling elucidates phased transcriptional regulators of cell cycle Karen Davey1,7, Daniel Wong2,7, Filip Konopacki2, Eugene Kwa1, Tony Ly3, Heike Fiegler2 & Christopher R. Sibley 1,4,5,6* Single cell transcriptome profling has emerged as a breakthrough technology for the high‑resolution understanding of complex cellular systems. Here we report a fexible, cost‑efective and user‑ friendly droplet‑based microfuidics system, called the Nadia Instrument, that can allow 3′ mRNA capture of ~ 50,000 single cells or individual nuclei in a single run. The precise pressure‑based system demonstrates highly reproducible droplet size, low doublet rates and high mRNA capture efciencies that compare favorably in the feld. Moreover, when combined with the Nadia Innovate, the system can be transformed into an adaptable setup that enables use of diferent bufers and barcoded bead confgurations to facilitate diverse applications. Finally, by 3′ mRNA profling asynchronous human and mouse cells at diferent phases of the cell cycle, we demonstrate the system’s ability to readily distinguish distinct cell populations and infer underlying transcriptional regulatory networks. Notably this provided supportive evidence for multiple transcription factors that had little or no known link to the cell cycle (e.g. DRAP1, ZKSCAN1 and CEBPZ). In summary, the Nadia platform represents a promising and fexible technology for future transcriptomic studies, and other related applications, at cell resolution. Single cell transcriptome profling has recently emerged as a breakthrough technology for understanding how cellular heterogeneity contributes to complex biological systems. Indeed, cultured cells, microorganisms, biopsies, blood and other tissues can be rapidly profled for quantifcation of gene expression at cell resolution.
  • HMGB1 in Health and Disease R

    HMGB1 in Health and Disease R

    Donald and Barbara Zucker School of Medicine Journal Articles Academic Works 2014 HMGB1 in health and disease R. Kang R. C. Chen Q. H. Zhang W. Hou S. Wu See next page for additional authors Follow this and additional works at: https://academicworks.medicine.hofstra.edu/articles Part of the Emergency Medicine Commons Recommended Citation Kang R, Chen R, Zhang Q, Hou W, Wu S, Fan X, Yan Z, Sun X, Wang H, Tang D, . HMGB1 in health and disease. 2014 Jan 01; 40():Article 533 [ p.]. Available from: https://academicworks.medicine.hofstra.edu/articles/533. Free full text article. This Article is brought to you for free and open access by Donald and Barbara Zucker School of Medicine Academic Works. It has been accepted for inclusion in Journal Articles by an authorized administrator of Donald and Barbara Zucker School of Medicine Academic Works. Authors R. Kang, R. C. Chen, Q. H. Zhang, W. Hou, S. Wu, X. G. Fan, Z. W. Yan, X. F. Sun, H. C. Wang, D. L. Tang, and +8 additional authors This article is available at Donald and Barbara Zucker School of Medicine Academic Works: https://academicworks.medicine.hofstra.edu/articles/533 NIH Public Access Author Manuscript Mol Aspects Med. Author manuscript; available in PMC 2015 December 01. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Mol Aspects Med. 2014 December ; 0: 1–116. doi:10.1016/j.mam.2014.05.001. HMGB1 in Health and Disease Rui Kang1,*, Ruochan Chen1, Qiuhong Zhang1, Wen Hou1, Sha Wu1, Lizhi Cao2, Jin Huang3, Yan Yu2, Xue-gong Fan4, Zhengwen Yan1,5, Xiaofang Sun6, Haichao Wang7, Qingde Wang1, Allan Tsung1, Timothy R.
  • Supplemental Table S1 (A): Microarray Datasets Characteristics

    Supplemental Table S1 (A): Microarray Datasets Characteristics

    Supplemental table S1 (A): Microarray datasets characteristics Title Summary Samples Literature ref. GEO ref. Acquisition of granule Gene expression profiling of 27 (1) GSE 11859 neuron precursor identity cerebellar tumors generated and Hedgehog‐induced from various early and late medulloblastoma in mice. stage CNS progenitor cells Medulloblastomas derived Study of mouse 5 (2) GSE 7212 from Cxcr6 mutant mice medulloblastoma in response respond to treatment with to inhibitor of Smoothened a Smoothened inhibitor Expression profiles of Identification of distinct classes 10 (3) GSE 9299 mouse medulloblastoma of up‐regulated or down‐ 339 & 340 regulated genes during Hh dependent tumorigenesis Genetic alterations in Identification of differently 10 (4) GSE 6463 mouse medulloblastomas expressed genes among CGNPs 339 & and generation of tumors and CGNPs transfected with 340 from cerebellar granule retroviruses that express nmyc neuron precursors or cyclin‐d1 Patched heterozygous Analysis of granule cell 14 (5) GSE 2426 model of medulloblastoma precursors, pre‐neoplastic cells, GDS1110 and tumor cells 1. Schuller U, Heine VM, Mao J, Kho AT, Dillon AK, Han YG, et al. Acquisition of granule neuron precursor identity is a critical determinant of progenitor cell competence to form Shh‐induced medulloblastoma. Cancer Cell 2008;14:123‐134. 2. Sasai K, Romer JT, Kimura H, Eberhart DE, Rice DS, Curran T. Medulloblastomas derived from Cxcr6 mutant mice respond to treatment with a smoothened inhibitor. Cancer Res 2007;67:3871‐3877. 3. Mao J, Ligon KL, Rakhlin EY, Thayer SP, Bronson RT, Rowitch D, et al. A novel somatic mouse model to survey tumorigenic potential applied to the Hedgehog pathway. Cancer Res 2006;66:10171‐10178.