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PBX3 PBX3 PBX3 PBX3 PBX3 PBX3 PBX3 PBX3 PBX3 SP1 FOS FOS SP1 FOS SP1 SP1FOS FOS SP1 SP1FOS SP1FOS FOSSP1 FOSSP1 NRF1 NRF1 NRF1 NRF1 NRF1 NRF1 NRF1 NRF1 NRF1 NRF1PBX3 PBX3 NRF1 NRF1PBX3 NRF1 PBX3 NRF1 PBX3 PBX3 NRF1 NRF1 PBX3 PBX3NRF1 PBX3 NRF1 EGR1 SP1 SP1 EGR1 EGR1 SP1 EGR1SP1 EGR1 SP1 SP1EGR1 EGR1SP1 SP1EGR1 EGR1SP1 EBF1inputRFX5 RFX5EBF1input inputRFX5EBF1 inputRFX5 EBF1 EBF1inputRFX5 EBF1 inputRFX5 RFX5inputEBF1 EBF1RFX5input RFX5EBF1input EGR1input IRF3 FOSFOS IRF3 inputEGR1 inputFOSEGR1 IRF3 inputIRF3FOSEGR1 inputEGR1FOSIRF3 FOSinputIRF3EGR1 inputEGR1IRF3FOS IRF3inputFOSEGR1 EGR1IRF3FOS input EBF1PAX5PAX5SRFSTAT1 FOS FOS PAX5STAT1EBF1SRF SRFFOSPAX5STAT1PAX5EBF1 STAT1SRFFOSPAX5PAX5 EBF1 PAX5STAT1EBF1SRFFOS EBF1 FOSSTAT1PAX5PAX5SRF PAX5PAX5STAT1SRFFOSEBF1 EBF1SRFFOSPAX5STAT1 FOSSTAT1PAX5PAX5SRFEBF1 TCF3 BHLHE40SRFMAXinputRFX5 RFX5inputBHLHE40MAXTCF3SRF BHLHE40TCF3MAXSRF RFX5input RFX5SRFinputMAXTCF3BHLHE40 BHLHE40MAXinputTCF3RFX5SRF TCF3 RFX5inputSRFMAXBHLHE40 RFX5BHLHE40inputTCF3MAXSRF SRFBHLHE40RFX5MAXTCF3input BHLHE40RFX5TCF3MAXSRFinput TCF12BCL3PAX5PAX5ZEB1MXI1MAX USF1IRF3 IRF3 MXI1TCF12BCL3MXI1PAX5MAXPAX5ZEB1USF1 USF1 MAXTCF12MXI1MXI1BCL3ZEB1PAX5PAX5IRF3 MXI1IRF3ZEB1TCF12MAXPAX5PAX5BCL3 USF1 USF1 MAXMXI1MXI1TCF12BCL3PAX5ZEB1PAX5 IRF3 TCF12IRF3BCL3PAX5PAX5ZEB1MAXMXI1MXI1USF1 BCL3PAX5MXI1TCF12MAXZEB1IRF3USF1 IRF3USF1MXI1TCF12MAXMXI1PAX5BCL3PAX5ZEB1 USF1TCF12BCL3IRF3MAXZEB1MXI1MXI1PAX5PAX5 LV1 BCL11APOU2F2TCF12MEF2CEGR1STAT1inputUSF2 POU2F2BCL11AinputSTAT1MEF2CUSF2TCF12EGR1 USF2EGR1POU2F2TCF12MEF2CinputSTAT1BCL11A POU2F2inputSTAT1EGR1MEF2CBCL11ATCF12USF2 USF2 BCL11APOU2F2TCF12STAT1MEF2CinputEGR1 POU2F2TCF12BCL11ASTAT1inputMEF2CEGR1USF2 inputPOU2F2MEF2CSTAT1BCL11ATCF12EGR1USF2 EGR1POU2F2USF2BCL11ASTAT1TCF12MEF2Cinput USF2POU2F2MEF2CBCL11ATCF12STAT1EGR1input BCL11APOU2F2EBF1SRFELF1 ZNF143 POU2F2EBF1BCL11ASRFELF1ZNF143 ELF1POU2F2BCL11ASRF EBF1ZNF143 ZNF143ELF1 POU2F2SRFBCL11A EBF1 ZNF143BCL11APOU2F2EBF1 ELF1SRF ZNF143EBF1 POU2F2BCL11ASRFELF1 ZNF143POU2F2BCL11ASRFELF1EBF1 ELF1EBF1SRFPOU2F2BCL11AZNF143 ZNF143POU2F2SRFBCL11AELF1EBF1 32% of variance TCF3NFATC1STAT5ARUNX3MEF2ASPI1RUNX3ATF2BHLHE40EBF1ELF1 ATF3ZNF143 EBF1NFATC1BHLHE40STAT5AATF2SPI1RUNX3RUNX3TCF3MEF2AELF1ATF3 ZNF143 ATF3BHLHE40TCF3ELF1NFATC1STAT5AMEF2AATF2RUNX3RUNX3SPI1EBF1ZNF143 ZNF143ELF1 STAT5ASPI1NFATC1MEF2AATF2RUNX3TCF3ATF3RUNX3BHLHE40EBF1 ATF3 BHLHE40ZNF143NFATC1STAT5ARUNX3EBF1TCF3ATF2SPI1MEF2AELF1 ZNF143EBF1TCF3NFATC1STAT5ARUNX3RUNX3MEF2AATF2BHLHE40ELF1ATF3SPI1 ZNF143MEF2AATF3NFATC1BHLHE40SPI1ATF2ELF1TCF3STAT5ARUNX3RUNX3EBF1 SPI1ELF1EBF1BHLHE40NFATC1STAT5ARUNX3RUNX3TCF3ATF2ATF3MEF2AZNF143 ZNF143BHLHE40TCF3MEF2ASTAT5ANFATC1ATF3RUNX3ATF2ELF1EBF1SPI1 BCL3PMLZBTB33NFATC1MTA3MEF2CYY1ZEB1 USF1 ZBTB33NFATC1MTA3PMLPMLBCL3MEF2CYY1USF1ZEB1 USF1 ZEB1MEF2CPMLBCL3ZBTB33PMLNFATC1YY1YY1MTA3 YY1 ZBTB33PMLNFATC1MTA3MEF2CZEB1BCL3 USF1 USF1 NFATC1MTA3ZBTB33YY1PMLBCL3MEF2CZEB1 ZBTB33PMLNFATC1MTA3BCL3MEF2CYY1YY1ZEB1 USF1 ZBTB33NFATC1MEF2CPMLPMLBCL3MTA3ZEB1USF1 YY1YY1 USF1NFATC1PMLPMLMTA3BCL3MEF2CZBTB33ZEB1 YY1 YY1 MEF2CUSF1PMLPMLNFATC1BCL3MTA3ZEB1ZBTB33 POU2F2MTA3BATFMEF2AATF2SRF NFE2USF2ATF3 POU2F2ATF2USF2NFE2MTA3BATFMEF2ASRFATF3 ATF3USF2NFE2POU2F2MEF2ASRFMTA3BATFATF2 POU2F2SRFMTA3ATF2MEF2AATF3BATFNFE2USF2 USF2ATF3NFE2 POU2F2MTA3BATFATF2MEF2ASRF POU2F2MTA3MEF2AATF2BATFSRFUSF2NFE2ATF3 ATF3POU2F2MEF2AATF2BATFMTA3SRFNFE2USF2 USF2POU2F2SRFMTA3ATF2BATFATF3NFE2MEF2A POU2F2NFE2USF2MEF2ASRFATF2ATF3MTA3BATF STAT5ABCLAF1ZBTB33SPI1IRF4RXRAETS1STAT3ETS1 ZBTB33STAT3SPI1STAT5AIRF4RXRABCLAF1ETS1 RXRASTAT5ABCLAF1ZBTB33ETS1IRF4STAT3SPI1ETS1 ETS1ETS1ZBTB33BCLAF1SPI1STAT5ASTAT3RXRAIRF4 ZBTB33STAT3STAT5AETS1BCLAF1IRF4ETS1SPI1RXRA ZBTB33STAT5ABCLAF1ETS1ETS1STAT3RXRAIRF4 SPI1 ZBTB33RXRASPI1STAT3BCLAF1IRF4STAT5AETS1ETS1 SPI1 ETS1STAT5ABCLAF1ETS1STAT3IRF4ZBTB33RXRA STAT5ABCLAF1RXRAETS1ETS1STAT3IRF4SPI1ZBTB33 IRF4RXRA IRF4RXRA RXRAIRF4 RXRAIRF4 IRF4RXRA RXRAIRF4 RXRAIRF4 IRF4RXRA RXRA IRF4 SPI1BCLAF1JUNDGABPAinputinputinput JUNDinputinputinputSPI1BCLAF1GABPA GABPAinputBCLAF1inputSPI1input JUNDGABPA inputBCLAF1inputinputSPI1JUND inputJUNDinputinputBCLAF1SPI1 GABPA BCLAF1inputinput inputGABPASPI1JUND JUND input SPI1BCLAF1inputinput GABPA GABPA SPI1 JUNDBCLAF1inputinputinput JUNDBCLAF1SPI1inputGABPAinputinput GABPAinput NFE2SIX5 NFE2input GABPASIX5 NFE2GABPA input SIX5 GABPASIX5 input NFE2 NFE2 inputSIX5 GABPA SIX5input NFE2GABPA inputSIX5NFE2GABPA GABPA NFE2inputSIX5 NFE2SIX5 GABPAinput BATFSTAT3JUND SIX5 JUNDBATFSTAT3 SIX5 STAT3BATFSIX5JUNDSIX5 STAT3JUNDBATF BATFSTAT3JUNDSIX5 SIX5STAT3BATF JUND JUND BATFSTAT3SIX5 JUNDBATFSTAT3SIX5 JUND STAT3SIX5BATF input input input input input input input input input FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS FOS ZNF143ZNF143 ZNF143ZNF143 ZNF143 ZNF143ZNF143 ZNF143ZNF143 ZNF143ZNF143 ZNF143ZNF143 ZNF143ZNF143 ZNF143 SIX5 ATF3 IRF3IRF3 IRF3IRF3 ATF3SIX5 ATF3 IRF3IRF3 SIX5 SIX5 IRF3IRF3ATF3 ATF3 SIX5 IRF3IRF3 IRF3IRF3SIX5 ATF3 ATF3 IRF3IRF3SIX5 IRF3IRF3ATF3SIX5 IRF3ATF3IRF3SIX5 SIX5USF2USF1 USF2 USF1SIX5 USF1 USF2 SIX5 SIX5 USF2USF1 USF2USF1 SIX5 SIX5 USF2USF1 USF2USF1SIX5 USF2USF1SIX5 USF2USF1SIX5 NFE2 SP1PBX3 PBX3SP1NFE2 NFE2 PBX3SP1 SP1NFE2PBX3 NFE2 SP1PBX3 PBX3 SP1 NFE2 SP1NFE2PBX3 PBX3NFE2SP1 NFE2SP1PBX3 NFE2 USF1ATF3USF2 SP1 LV2 SP1NFE2 USF2USF1ATF3 USF1USF2ATF3NFE2 SP1 ATF3SP1NFE2USF2USF1 NFE2USF1USF2ATF3 SP1 SP1 USF2USF1NFE2ATF3 ATF3SP1USF2NFE2USF1 NFE2USF1USF2SP1ATF3 USF2USF1ATF3SP1NFE2 PBX3 7% of variance PBX3 PBX3 PBX3 PBX3 PBX3 PBX3 PBX3 PBX3 RFX5NRF1 RFX5 NRF1 NRF1 RFX5 NRF1RFX5 NRF1RFX5 NRF1RFX5 NRF1 RFX5 RFX5 NRF1 RFX5 NRF1 input input RFX5NRF1 inputRFX5inputNRF1 NRF1 RFX5input input NRF1inputinputRFX5 NRF1input inputRFX5 NRF1inputinputRFX5 NRF1 RFX5input input inputRFX5input NRF1 RFX5inputinput NRF1 inputinput inputinput input input inputinput inputinput inputinput inputinput inputinput inputinput ETS1 BHLHE40inputinputinput inputBHLHE40inputinputETS1 BHLHE40inputinput ETS1input ETS1 inputinputinput BHLHE40 BHLHE40inputETS1inputinput inputinputETS1inputBHLHE40 BHLHE40inputinputinputETS1 BHLHE40ETS1inputinputinput BHLHE40ETS1 inputinputinput input inputSTAT3BHLHE40STAT1MAXSTAT1MAXEBF1 inputSTAT3BHLHE40EBF1inputSTAT1STAT1MAX MAXBHLHE40STAT1STAT1STAT3inputEBF1input inputinputSTAT1STAT3STAT1MAXMAXBHLHE40EBF1 BHLHE40inputMAXMAXSTAT3inputEBF1STAT1STAT1 EBF1 STAT1STAT1STAT3MAXMAXBHLHE40inputinput input STAT1BHLHE40STAT3STAT1MAXEBF1MAXinput EBF1BHLHE40STAT3MAXSTAT1inputinput BHLHE40STAT1STAT1MAXSTAT3MAXEBF1inputinput JUNDSTAT3GABPAGABPAETS1SRFELF1EBF1ELF1MXI1MXI1SRFSRF JUNDEBF1STAT3MXI1MXI1ELF1SRFSRFELF1ETS1GABPA SRFSRFGABPAGABPAMXI1ELF1MXI1ELF1SRFETS1STAT3EBF1 JUNDGABPA ELF1ELF1ETS1STAT3MXI1SRFJUNDSRFSRF EBF1 STAT3JUNDMXI1MXI1EBF1ETS1ELF1ELF1SRFSRFGABPAGABPA EBF1 ETS1SRFSRFSTAT3MXI1MXI1ELF1SRFGABPAGABPA JUND JUND MXI1ELF1SRFSTAT3SRFETS1ELF1SRFEBF1 GABPAGABPA GABPAGABPA ELF1ELF1EBF1SRFJUNDSRFETS1MXI1STAT3MXI1 JUND ETS1SRFELF1STAT3ELF1MXI1MXI1SRFEBF1SRFGABPAGABPA JUNDRXRARXRAZEB1SRFEGR1ZEB1PAX5 JUND RXRAPAX5ZEB1ZEB1SRFEGR1 EGR1ZEB1ZEB1PAX5RXRASRF JUND EGR1SRFRXRAJUNDZEB1ZEB1PAX5 JUNDEGR1RXRAZEB1PAX5ZEB1SRF PAX5ZEB1RXRAEGR1ZEB1RXRASRF JUND JUND RXRARXRAPAX5SRFEGR1ZEB1ZEB1 JUNDEGR1SRFPAX5ZEB1RXRAZEB1RXRA JUNDRXRARXRASRFZEB1EGR1ZEB1PAX5 IRF4SPI1IRF4RUNX3EBF1MEF2CPAX5PAX5EGR1 EBF1SPI1RUNX3IRF4IRF4PAX5MEF2CPAX5EGR1 EGR1PAX5PAX5MEF2CRUNX3IRF4IRF4SPI1EBF1 SPI1MEF2CIRF4RUNX3PAX5EGR1PAX5 EBF1 RUNX3EBF1IRF4IRF4SPI1MEF2CPAX5PAX5EGR1 EBF1 RUNX3PAX5MEF2CEGR1IRF4 SPI1 MEF2CPAX5SPI1PAX5EGR1RUNX3IRF4IRF4EBF1 SPI1EBF1IRF4PAX5RUNX3IRF4PAX5MEF2CEGR1 EGR1MEF2CRUNX3IRF4PAX5IRF4EBF1SPI1 BATFBCLAF1ZBTB33MEF2AATF2MEF2CRUNX3MEF2AATF2 EBF1PAX5EGR1 ZBTB33BATFATF2ATF2RUNX3MEF2APAX5EBF1MEF2CBCLAF1EGR1 EGR1MEF2CPAX5MEF2AMEF2ABCLAF1ZBTB33ATF2RUNX3EBF1ATF2BATF ZBTB33BCLAF1ATF2MEF2CMEF2AATF2RUNX3BATFPAX5EGR1 EBF1 BATFZBTB33RUNX3ATF2BCLAF1ATF2MEF2APAX5MEF2AEBF1MEF2CEGR1 EBF1 ZBTB33BCLAF1RUNX3PAX5EGR1MEF2AMEF2CMEF2AATF2ATF2BATF MEF2AZBTB33MEF2CMEF2AEGR1PAX5ATF2BCLAF1ATF2BATFRUNX3EBF1 EBF1BATFRUNX3BCLAF1PAX5ATF2MEF2AMEF2AEGR1MEF2CZBTB33 EGR1MEF2CMEF2ABCLAF1RUNX3ATF2ATF2BATFPAX5EBF1ZBTB33 BCLAF1STAT5AZBTB33NFATC1BATFNFATC1MTA3STAT5AYY1POU2F2SPI1BCL11APOU2F2TCF12BCL3 ZBTB33POU2F2POU2F2NFATC1NFATC1MTA3BCL11ASTAT5ASPI1STAT5ABATFBCL3YY1TCF12BCLAF1 POU2F2POU2F2BCL3TCF12NFATC1ZBTB33NFATC1YY1STAT5AYY1STAT5ABCL11ABCLAF1MTA3BATFSPI1 YY1 ZBTB33POU2F2BCLAF1POU2F2STAT5ASTAT5ASPI1NFATC1NFATC1MTA3BATFBCL3BCL11ATCF12 NFATC1MTA3NFATC1ZBTB33BCL11AYY1POU2F2STAT5APOU2F2BATFTCF12BCLAF1BCL3SPI1 POU2F2ZBTB33NFATC1STAT5ANFATC1TCF12BCL3BCL11ABCLAF1MTA3YY1YY1BATF SPI1 POU2F2POU2F2ZBTB33NFATC1BCL3SPI1BCL11ABATFSTAT5ABCLAF1TCF12STAT5AMTA3 YY1YY1 SPI1 POU2F2NFATC1NFATC1STAT5ABCLAF1MTA3BCL11ASTAT5ABATFBCL3TCF12ZBTB33 YY1 YY1 POU2F2STAT5ASTAT5ABCLAF1NFATC1BCL11ABCL3NFATC1TCF12BATFMTA3ZBTB33SPI1 SPI1MTA3BCL11ABCL3PMLTCF12 MTA3BCL11APMLPMLSPI1TCF12BCL3 TCF12PMLBCL3PMLBCL11AMTA3SPI1 PMLSPI1MTA3TCF12BCL11ABCL3 BCL11AMTA3PMLTCF12BCL3SPI1 TCF12PMLBCL11AMTA3BCL3 SPI1 BCL11ATCF12PMLPMLSPI1BCL3MTA3 SPI1 PMLMTA3BCL11APMLTCF12BCL3 PMLPMLTCF12BCL11AMTA3BCL3SPI1 POU2F2TCF3TCF3 POU2F2TCF3TCF3 TCF3POU2F2TCF3 POU2F2TCF3TCF3 POU2F2TCF3TCF3 POU2F2TCF3TCF3 POU2F2TCF3TCF3 POU2F2TCF3TCF3 POU2F2TCF3TCF3 ZNF143ZNF143 ZNF143 ZNF143 ZNF143ZNF143 ZNF143ZNF143 ZNF143ZNF143 ZNF143ZNF143 ZNF143ZNF143 ZNF143 SIX5 SIX5 SIX5 SIX5 SIX5 SIX5 SIX5 SIX5 SIX5 SIX5GABPAGABPA GABPA SIX5 GABPAGABPA SIX5 GABPASIX5 SIX5 GABPAGABPA SIX5 GABPAGABPA SIX5GABPAGABPA GABPAGABPA SIX5 SIX5 GABPAGABPA ETS1 ETS1ETS1 ETS1ETS1 ETS1ETS1 ETS1ETS1 ETS1ETS1 ETS1ETS1 ETS1ETS1 ETS1ETS1 ATF3ELF1EGR1TCF3SRFEGR1 TCF3EGR1EGR1ELF1SRF ATF3 ATF3TCF3EGR1SRFEGR1ELF1 ELF1 EGR1SRFATF3EGR1TCF3 ATF3 TCF3EGR1EGR1ELF1SRF TCF3 EGR1EGR1SRFELF1ATF3
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  • Supplementary Data

    Supplementary Data

    SUPPLEMENTARY DATA A cyclin D1-dependent transcriptional program predicts clinical outcome in mantle cell lymphoma Santiago Demajo et al. 1 SUPPLEMENTARY DATA INDEX Supplementary Methods p. 3 Supplementary References p. 8 Supplementary Tables (S1 to S5) p. 9 Supplementary Figures (S1 to S15) p. 17 2 SUPPLEMENTARY METHODS Western blot, immunoprecipitation, and qRT-PCR Western blot (WB) analysis was performed as previously described (1), using cyclin D1 (Santa Cruz Biotechnology, sc-753, RRID:AB_2070433) and tubulin (Sigma-Aldrich, T5168, RRID:AB_477579) antibodies. Co-immunoprecipitation assays were performed as described before (2), using cyclin D1 antibody (Santa Cruz Biotechnology, sc-8396, RRID:AB_627344) or control IgG (Santa Cruz Biotechnology, sc-2025, RRID:AB_737182) followed by protein G- magnetic beads (Invitrogen) incubation and elution with Glycine 100mM pH=2.5. Co-IP experiments were performed within five weeks after cell thawing. Cyclin D1 (Santa Cruz Biotechnology, sc-753), E2F4 (Bethyl, A302-134A, RRID:AB_1720353), FOXM1 (Santa Cruz Biotechnology, sc-502, RRID:AB_631523), and CBP (Santa Cruz Biotechnology, sc-7300, RRID:AB_626817) antibodies were used for WB detection. In figure 1A and supplementary figure S2A, the same blot was probed with cyclin D1 and tubulin antibodies by cutting the membrane. In figure 2H, cyclin D1 and CBP blots correspond to the same membrane while E2F4 and FOXM1 blots correspond to an independent membrane. Image acquisition was performed with ImageQuant LAS 4000 mini (GE Healthcare). Image processing and quantification were performed with Multi Gauge software (Fujifilm). For qRT-PCR analysis, cDNA was generated from 1 µg RNA with qScript cDNA Synthesis kit (Quantabio). qRT–PCR reaction was performed using SYBR green (Roche).
  • Single-Cell RNA Sequencing Analysis of Human Neural Grafts Revealed Unexpected Cell Type Underlying the Genetic Risk of Parkinson’S Disease

    Single-Cell RNA Sequencing Analysis of Human Neural Grafts Revealed Unexpected Cell Type Underlying the Genetic Risk of Parkinson’S Disease

    Single-cell RNA Sequencing Analysis of Human Neural Grafts Revealed Unexpected Cell Type Underlying the Genetic Risk of Parkinson’s Disease Yingshan Wang1, Gang Wu2 1 Episcopal High School, 1200 N Quaker Ln, Alexandria, VA, USA, 22302 2 Fujian Sanbo Funeng Brain Hospital; Sanbo Brain Hospital Capital Medical University Abstract Parkinson’s disease (PD) is the second most common neurodegenerative disorder, affecting more than 6 million patients globally. Though previous studies have proposed several disease-related molecular pathways, how cell-type specific mechanisms contribute to the pathogenesis of PD is still mostly unknown. In this study, we analyzed single-cell RNA sequencing data of human neural grafts transplanted to the midbrains of rat PD models. Specifically, we performed cell-type identification, risk gene screening, and co-expression analysis. Our results revealed the unexpected genetic risk of oligodendrocytes as well as important pathways and transcription factors in PD pathology. The study may provide an overarching framework for understanding the cell non- autonomous effects in PD, inspiring new research hypotheses and therapeutic strategies. Keywords Parkinson’s Disease; Single-cell RNA Sequencing; Oligodendrocytes; Cell Non-autonomous; Co- expression Analysis; Transcription Factors 1 Table of Contents 1. Introduction ................................................................................................................................. 3 2. Methods......................................................................................................................................
  • Microrna Profiling of Low-Grade Glial and Glioneuronal Tumors Shows An

    Microrna Profiling of Low-Grade Glial and Glioneuronal Tumors Shows An

    Modern Pathology (2017) 30, 204–216 204 © 2017 USCAP, Inc All rights reserved 0893-3952/17 $32.00 MicroRNA profiling of low-grade glial and glioneuronal tumors shows an independent role for cluster 14q32.31 member miR-487b Heather Marion Ames1,4, Ming Yuan1,4, Maria Adelita Vizcaíno1,3, Wayne Yu2 and Fausto J Rodriguez1,2 1Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; 2Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA and 3Department of Cellular and Tissue Biology, Universidad Nacional Autónoma de México, Mexico City, DF, USA Low-grade (WHO I-II) gliomas and glioneuronal tumors represent the most frequent primary tumors of the central nervous system in children. They often have a good prognosis following total resection, however they can create many neurological complications due to mass effect, and may be difficult to resect depending on anatomic location. MicroRNAs have been identified as molecular regulators of protein expression/translation that can repress multiple mRNAs concurrently through base pairing, and have an important role in cancer, including brain tumors. Using the NanoString digital counting system, we analyzed the expression levels of 800 microRNAs in nine low-grade glial and glioneuronal tumor types (n = 45). A set of 61 of these microRNAs were differentially expressed in tumors compared with the brain, and several showed levels varying by tumor type. The expression differences were more accentuated in subependymal giant cell astrocytoma, compared with other groups, and demonstrated the highest degree of microRNA repression validated by RT-PCR, including miR-129-2-3p, miR-219-5p, miR-338-3p, miR-487b, miR-885-5p, and miR-323a-3p.
  • The Id-Protein Family in Developmental and Cancer-Associated Pathways Cornelia Roschger and Chiara Cabrele*

    The Id-Protein Family in Developmental and Cancer-Associated Pathways Cornelia Roschger and Chiara Cabrele*

    Roschger and Cabrele Cell Communication and Signaling (2017) 15:7 DOI 10.1186/s12964-016-0161-y REVIEW Open Access The Id-protein family in developmental and cancer-associated pathways Cornelia Roschger and Chiara Cabrele* Abstract Inhibitors of DNA binding and cell differentiation (Id) proteins are members of the large family of the helix-loop- helix (HLH) transcription factors, but they lack any DNA-binding motif. During development, the Id proteins play a key role in the regulation of cell-cycle progression and cell differentiation by modulating different cell-cycle regulators both by direct and indirect mechanisms. Several Id-protein interacting partners have been identified thus far, which belong to structurally and functionally unrelated families, including, among others, the class I and II bHLH transcription factors, the retinoblastoma protein and related pocket proteins, the paired-box transcription factors, and the S5a subunit of the 26 S proteasome. Although the HLH domain of the Id proteins is involved in most of their protein-protein interaction events, additional motifs located in their N-terminal and C-terminal regions are required for the recognition of diverse protein partners. The ability of the Id proteins to interact with structurally different proteins is likely to arise from their conformational flexibility: indeed, these proteins contain intrinsically disordered regions that, in the case of the HLH region, undergo folding upon self- or heteroassociation. Besides their crucial role for cell-fate determination and cell-cycle progression during development, other important cellular events have been related to the Id-protein expression in a number of pathologies. Dysregulated Id-protein expression has been associated with tumor growth, vascularization, invasiveness, metastasis, chemoresistance and stemness, as well as with various developmental defects and diseases.
  • Integration of 198 Chip-Seq Datasets Reveals Human Cis-Regulatory Regions

    Integration of 198 Chip-Seq Datasets Reveals Human Cis-Regulatory Regions

    Integration of 198 ChIP-seq datasets reveals human cis-regulatory regions Hamid Bolouri & Larry Ruzzo Thanks to Stephen Tapscott, Steven Henikoff & Zizhen Yao Slides will be available from: http://labs.fhcrc.org/bolouri/ Email [email protected] for manuscript (Bolouri & Ruzzo, submitted) Kleinjan & van Heyningen, Am. J. Hum. Genet., 2005, (76)8–32 Epstein, Briefings in Func. Genom. & Protemoics, 2009, 8(4)310-16 Regulation of SPi1 (Sfpi1, PU.1 protein) expression – part 1 miR155*, miR569# ~750nt promoter ~250nt promoter The antisense RNA • causes translational stalling • has its own promoter • requires distal SPI1 enhancer • is transcribed with/without SPI1. # Hikami et al, Arthritis & Rheumatism, 2011, 63(3):755–763 * Vigorito et al, 2007, Immunity 27, 847–859 Ebralidze et al, Genes & Development, 2008, 22: 2085-2092. Regulation of SPi1 expression – part 2 (mouse coordinates) Bidirectional ncRNA transcription proportional to PU.1 expression PU.1/ELF1/FLI1/GLI1 GATA1 GATA1 Sox4/TCF/LEF PU.1 RUNX1 SP1 RUNX1 RUNX1 SP1 ELF1 NF-kB SATB1 IKAROS PU.1 cJun/CEBP OCT1 cJun/CEBP 500b 500b 500b 500b 500b 750b 500b -18Kb -14Kb -12Kb -10Kb -9Kb Chou et al, Blood, 2009, 114: 983-994 Hoogenkamp et al, Molecular & Cellular Biology, 2007, 27(21):7425-7438 Zarnegar & Rothenberg, 2010, Mol. & cell Biol. 4922-4939 An NF-kB binding-site variant in the SPI1 URE reduces PU.1 expression & is GGGCCTCCCC correlated with AML GGGTCTTCCC Bonadies et al, Oncogene, 2009, 29(7):1062-72. SATB1 binding site A distal single nucleotide polymorphism alters long- range regulation of the PU.1 gene in acute myeloid leukemia Steidl et al, J Clin Invest.
  • XPO7 Is a Tumor Suppressor Regulating P21cip1-Dependent Senescence

    XPO7 Is a Tumor Suppressor Regulating P21cip1-Dependent Senescence

    Downloaded from genesdev.cshlp.org on September 25, 2021 - Published by Cold Spring Harbor Laboratory Press XPO7 is a tumor suppressor regulating p21CIP1-dependent senescence Andrew J. Innes,1,2,3 Bin Sun,1,2 Verena Wagner,1,2 Sharon Brookes,1,2 Domhnall McHugh,1,2 Joaquim Pombo,1,2 Rosa María Porreca,1,2 Gopuraja Dharmalingam,1,2 Santiago Vernia,1,2 Johannes Zuber,4 Jean-Baptiste Vannier,1,2 Ramón García-Escudero,5,6,7 and Jesús Gil1,2 1MRC London Institute of Medical Sciences (LMS), London W12 0NN, United Kingdom; 2Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, London W12 0NN, United Kingdom; 3Centre for Haematology, Department of Immunology and Inflammation, Imperial College London, London W12 0NN, United Kingdom; 4Research Institute of Molecular Pathology (IMP), 1030 Vienna, Austria; 5Molecular Oncology Unit, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), 28040 Madrid, Spain; 6Research Institute 12 de Octubre (i+12), 28041 Madrid, Spain; 7Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), 28029 Madrid, Spain Senescence is a key barrier to neoplastic transformation. To identify senescence regulators relevant to cancer, we screened a genome-wide shRNA library. Here, we describe exportin 7 (XPO7) as a novel regulator of senescence and validate its function in telomere-induced, replicative, and oncogene-induced senescence (OIS). XPO7 is a bidirec- tional transporter that regulates the nuclear-cytoplasmic shuttling of a broad range of substrates. Depletion of XPO7 results in reduced levels of TCF3 and an impaired induction of the cyclin-dependent kinase inhibitor p21CIP1 during OIS. Deletion of XPO7 correlates with poorer overall survival in several cancer types.