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Comparison of Genes Expressed in Primed States of Human And

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Comparison of genes expressed in primed states of human and monkey PSCs monkey_primed human_primed human_primed_AND_monkey_primed HAUS3 LINC00266-3 ISG15 SH3BP2 OR4F29 AGRN RGS12 MT-TM B3GALT6 NAT8L MT-TW PUSL1 GRK4 MT-TD GLTPD1 C4orf48 MT-TK VWA1 NELFA LOC100287497 C1orf86 DGKQ MIR200B SKI RNF212 MIR429 RER1 WHSC1 ATAD3C FAM213B - ATAD3A TPRG1L IDUA TP73 AJAP1 PIGG LINC00337 KCNAB2 C1orf159 HES3 RNF207 KLHL17 LOC100130071 PHF13 UBE2J2 HMGN2P17 CAMTA1 ACAP3 RBP7 VAMP3 CPSF3L PEX14 PARK7 SSU72 TARDBP H6PD SLC35E2B LOC100996614 SLC25A33 MIB2 RNU5E-1 NMNAT1 PRKCZ PLOD1 UBE4B ARHGEF16 TNFRSF8 KIF1B MEGF6 VPS13D PGD CEP104 SNORA59A UBIAD1 DFFB PRAMEF7 FBXO44 ICMT CHCHD2P6 DRAXIN ZBTB48 SZRD1 AGTRAP NPHP4 LOC440570 CLCN6 CHD5 RNU1-1 MFN2 PER3 ACTL8 MIIP PLEKHG5 IGSF21 TMEM51 THAP3 KLHDC7A EFHD2 TMEM201 RP1-8B22.1 DNAJC16 C1orf127 RPS14P3 PLEKHM2 APITD1 HTR6 SPEN MASP2 UBXN10 NECAP2 PTCHD2 FAM43B MRTO4 FBXO6 CDA PQLC2 NPPA PPP1R11P1 MINOS1 KIAA2013 HS6ST1P1 OTUD3 PDPN LOC101060684 PINK1 TNFRSF1B NBPF3 ALPL DDI2 LINC00339 CDC42 PRDM2 C1QB ZBTB40 KAZ PNRC2 EPHB2 FAM131C LOC100996626 KDM1A FBLIM1 GRHL3 TCEB3 C1ORF144 NIPAL3 PITHD1 ZBTB17 RCAN3 SRRM1 U1 NCMAP CLIC4 CROCC SDHD TMEM50A ALDH4A1 FAM110D TMEM57 ARHGEF10L CNKSR1 LDLRAP1 ECE1 LIN28A MAN1C1 TCEA3 HMGN2 SEPN1 RPL11 NUDC PDIK1L E2F2 TRNP1 ZNF593 RAP1GAP RP11-40H20.5 CEP85 ZNF436 SCARNA1 SH3BGRL3 GALE SMPDL3B CD52 LYPLA2 RCC1 DHDDS PAQR7 SNHG3 ARID1A CATSPER4 TRNAU1AP PIGV MTFR1L RNU11 ZDHHC18 UBXN11 TINAGL1 TMEM222 SLC9A1 FAM167B GPR3 RPS6KA1 RP1-27O5.3 TMA7 6-16 RP4-803A2.1 FAM76A SYTL1 RNA5SP42 STX12 WDTC1 EIF2C4 THEMIS2 SNORA73 EIF2C1 XKR8 SNORA61 AGO3 DNAJC8 U11 RP3-423B22.5 ATPIF1 YTHDF2 MANEAL SESN2 PTPRU C1orf122 MED18 EPB41 NDUFS5 PHACTR4 KHDRBS1 MACF1 GMEB1 COL16A1 OXCT2 OPRD1 SYNC ZFP69 ZCCHC17 HPCA MIR30E SERINC2 TMEM234 CTPS1 TMEM39B BSDC1 GUCA2B KPNA6 ZBTB8A RIMKLA TXLNA ZBTB8OS C1orf50 CCDC28B FNDC5 FAM183A IQCC ADC TMEM125 EIF3I CSMD2 ARTN HDAC1 ZMYM6NB SNORD38B RBBP4 EIF2C3 SNORD46 KIAA1522 GRIK3 SNORD38A S100PBP ZC3H12A TMEM69 ZNF362 OSCP1 DMBX1 ZSCAN20 GJA9 CYP4X1 ZMYM1 MYCL FOXE3 ZMYM4 MAP7D1 RP11-329A14.1 NCDN TEKT2 RP11-183G22.1 AGO4 COL9A2 BTF3L4 AGO1 KIAA0754 ZFYVE9 ADPRHL2 CTPS DMRTB1 THRAP3 DEM1 C1orf191 SH3D21 KCNQ4 RP11-466L17.1 DNALI1 LEPRE1 MGC34796 CDCA8 C1H1ORF50 INADL UTP11L NFYC LAMTOR5P1 AKIRIN1 PTPRF FOXD3 PPIE C1ORF84 PIN1P1 MFSD2A HYI HHLA3 CAP1 PLK3 RP11-42O15.2 RLF EIF2B3 SNORD45C ZMPSTE24 MUTYH TPI1P1 SMAP2 FAAH RNA5SP20 ZFP69B POMGNT1 GIPC2 ZNF642 RNF11 RP4-612B15.2 ZNF684 ELAVL4 LOC339524 PPCS FAM159A HSP90B3P CCDC30 CC2D1B EPHX4 PPIH ECHDC2 BTBD8 YBX1 OSBPL9 KIAA1107 ZNF691 C1H1ORF123 RPL5 CDC20 OMA1 GAPDHP29 KDM4A USP1 SLC44A3 ST3GAL3 ITGB3BP TMEM56 IPO13 LEPROT EEF1A1P11 DPH2 SLC35D1 LPPR4 ATP6V0B LEPR GPR88 B4GALT2 NEGR1 AMY2B CCDC24 ST6GALNAC3 AMY1B DMAP1 TTLL7 AMY1A RNF220 SYDE2 NBPF5P KIF2C PRKACB NBPF4 RPS8 HS2ST1 FNDC7 UROD TGFBR3 SYPL2 HPDL LRRC8D MIR197 TOE1 TMED5 GSTM2 MMACHC BCAR3 GSTM1 AKR1A1 DBT GSTM5 NASP DPYD KCNC4 MAST2 EXTL2 CD53 LURAP1 AGL PIFO RAD54L S1PR1 RP11-426L16.7 NSUN4 OLFM3 AKR7A2P1 CMPK1 VAV3 CD2 PRPF38A AMY2A FAM46C GPX7 ATXN7L2 HSD3BP1 ZYG11B GSTM3 HSD3B1 ZYG11A AMPD2 HSD3BP5 SCP2 AHCYL1 PFN1P9 CPT2 HBXIP FAM72B LRRC42 OVGP1 HIST2H3DP1 TCEANC2 RAP1A HIST2H2BA MRPL37 SLC16A1 SRGAP2C ACOT11 ST7L LINC00328 TTC4 RBM8A SRGAP2B PCSK9 POLR3GL LOC100505630 PRKAA2 GNRHR2 NBPF10 FGGY BOLA1 NBPF9 HOOK1 SF3B4 NBPF15 NFIA PLEKHO1 NBPF24 L1TD1 C1H1ORF51 LOC101060202 ATG4C MTMR11 RP3-377D14.1 ALG6 TARS2 NBPF16 EFCAB7 ECM1 LOC101060531 PGM1 ADAMTSL4 LOC100996517 ROR1 LASS2 NOTCH2NL CACHD1 OAZ3 LOC101060503 RAVER2 S100A13 LOC101060487 DNAJC6 S100A1 LOC101060567 MIER1 CRTC2 LOC101060431 GADD45A ATP8B2 LOC101060478 SRSF11 KCNN3 LOC101060636 CTH FLAD1 GPR89A FPGT DPM3 GPR89C TYW3 C1orf43 RP6-74O6.2 ACADM EFNA1 PDIA3P RABGGTB THBS3 LOC101060601 ST6GALNAC5 TRIM46 LOC101060700 FAM73A MUC1 ABHD17A NEXN ADAM15 LOC101060353 DNAJB4 RUSC1 RNVU1-13 LPHN2 MEX3A LOC100996725 ARID3B BGLAP PPIAL4E SAMD13 ARHGEF2 FLJ37786 RPF1 APOA1BP RP11-14N7.2 CYR61 ISG20L2 LOC101060590 SH3GLB1 MEF2D LOC388692 LMO4 C1H1ORF182 PPIAL4B PKN2 NTRK1 PPIAL4C LRRC8B AIM2 LOC100996721 ZNF326 YY1AP1 HIST2H2AA3 CDC7 CADM3 HIST2H3C RPAP2 IGSF9 HIST2H2AC MTF2 KLHDC9 C1orf51 CCDC18 TSTD1 RP11-235D19.3 DR1 OLFML2B C1orf56 FNBP1L C1ORF226 GABPB2 ABCD3 NIT1 TNFAIP8L2-SCNM1 RWDD3 TOMM40L PIP5K1A PTBP2 NR1I3 RIIAD1 SNX7 TRIM17 HMGN3P1 SLC35A3 SNAP47 LCE3B HIAT1 CDC42BPA LCE2B TRMT13 MOSC2 LCE2A RTCA C1ORF115 LCE4A CDC14A C1ORF69 C1orf68 VCAM1 MRPL55 LCE1E SLC30A7 C1H1ORF35 LCE1D RNPC3 SUSD4 SMCP PRMT6 C1ORF227 IVL FAM102B TATDN3 SPRR1A PRPF38B ATF3 SPRR3 STXBP3 PLXNA2 SPRR1B GPSM2 PFKFB2 LELP1 TMEM167B DYRK3 S100A9 SARS IKBKE IL6R CELSR2 ELK4 CHRNB2 CYB561D1 CDK18 CKS1B GNAI3 PLEKHA6 HCN3 GSTM4 DSTYK POU5F1P4 CSF1 TMCC2 RAB25 STRIP1 NFASC SEMA4A RBM15 OPTC PMF1 CEPT1 PPFIA4 PMF1-BGLAP ATP5F1 ARL8A RP11-367J7.4 DDX20 ZBED6 MRPS21P2 CTTNBP2NL PHLDA3 CD1D WNT2B PPP1R12B CD1E CAPZA1 C1ORF106 RNA5SP60 MOV10 TMEM9 FCER1A LRIG2 KIF21B OR10J1 MAGI3 CAMSAP1L1 CASQ1 DCLRE1B FAM5C SUMO1P3 HIPK1 GLRX2 LY9 OLFML3 PLA2G4A PCP4L1 VANGL1 C1ORF27 RGS4 ATP1A1 UCHL5 LRRC52 PTGFRN C1ORF21 LOC100505828 TTF2 GLT25D2 RP11-466F5.6 MAN1A2 ARPC5 RP11-466F5.9 WDR3 IER5 MIR3658 PHGDH STX6 RNA5SP65 SEC22B NPL DUSP27 TXNIP MR1 LOC100128751 LIX1L CACNA1E C1orf112 PEX11B FAM78B FMO4 PIAS3 ILDR2 PRRC2C RNF115 MPZL1 RP4-560B9.4 GPR89B METTL18 DNM3 FAM108A1 C1ORF112 FASLG CHD1L BRP44 GPR52 BCL9 ANKRD45 C1orf220 VOPP1 KLHL20 RNU5F-2P HIST2H2AA4 BAT2L2 LOC100506242 VPS45 BLZF1 VDAC1P4 CA14 C1H1ORF114 RP11-416K24.2 C1orf54 TNN LAMC2 MRPS21 PGBD2 C1orf21 PRPF3 ASTN1 RNF2 RPRD2 FAM5B C1orf27 SETDB1 RABGAP1L OCLM PRUNE ZNF695 RGS21 MLLT11 ZNF124 RPS27A SCNM1 CNST C1orf53 PSMD4 SMYD3 RP11-16L9.1 ZNF687 PPPDE1 NR5A2 PSMB4 OPN3 FAM58BP CGN ACTN2 CAMSAP2 TUFT1 MAP10 RPL34P1 SNX27 C1ORF124 C1orf106 CHTOP FAM89A RP11-134G8.5 SNAPIN TAF5L SHISA4 INTS3 AGT RP11-465N4.2 SLC27A3 CCSAP GPR37L1 CREB3L4 ZNF512B OCR1 RPS27 SAMD10 TMEM183B UBAP2L TCEA2 LINC00260 HAX1 DNAJC5 LOC441155 ZBTB7B C20orf195 LOC284581 EFNA4 BIRC7 FAM72C EFNA3 KCNQ2 FAM72A SLC50A1 ARFRP1 IL24 MTX1 C20ORF20 CR2 FDPS DIDO1 LOC148696 MSTO1 OGFR MIR205 DAP3 MTG2 G0S2 SYT11 PSMA7 RP11-543B16.1 LAMTOR2 SLCO4A1 RP11-543B16.2 LMNA PMEPA1 LINC00467 SLC25A44 NPEPL1 SNORA16B TMEM79 GNAS1 FAM71A GPATCH4 ZFP64 TGFB2 RRNAD1 KCNB1 RNA5SP76 PRCC RTFDC1 C1orf115 KIRREL FAM210B MARC2 IFI16 TMEM189 FAM177B DUSP23 EYA2 RP11-504P24.6 ATP1A2 ZMYND8 CNIH3 PEA15 ZNF335 DNAH14 NCSTN CD40 H3F3A VANGL2 WFDC2 MIXL1 UFC1 DBNDD2 BTF3P9 USP21 C20ORF111 MIR3620 PPOX NEURL2 GJC2 NDUFS2 SNX21 IBA57 SDHC UBE2C HIST3H2BB DUSP12 PKIG RNA5SP19 ATF6 EMILIN3 FTH1P2 NOS1AP L3MBTL1 RNA5SP79 UHMK1 SLC32A1 SPRTN UAP1 ZHX3 RNU5A-5P DDR2 SNORA71 KIAA1383 HSD17B7 7SK KCNK1 NUF2 SOGA1 RPL35P1 PBX1 SRC RYR2 MGST3 CTNNBL1 RP11-193H5.2 UCK2 ROMO1 KRT18P32 POGK DLGAP4 CHRM3 POU2F1 C20ORF132 FMN2 DCAF6 EPB41L1 C1orf100 TIPRL CPNE1 DESI2 SFT2D2 EIF6 NLRP3 ATP1B1 MAP1LC3A OR2W5 GORAB CEP250 OR9H1P PRRX1 GGT7 OR2W3 METTL13 DYNLRB1 TRIM58 SUCO SNTA1 OR2L3 PRDX6 BPIFB3 OR2T34 DARS2 ASXL1 FAM138E ZBTB37 C20ORF112 RP11-261C10.2 RASAL2 POFUT1 AP006222.2 RALGPS2 TRIB3 MT-TQ FAM20B SIRPA MT-TA TOR3A PDYN MT-TN SOAT1 C20ORF96 MT-TS1 TOR1AIP1 EBF4 OR4F16 CEP350 SLC4A11 RP4-669L17.10 QSOX1 C10H20ORF194 LINC00115 XPR1 HSPA12B RP11-206L10.13 DHX9 FASTKD5 LOC728690 LAMC1 ADAM33 RP11-181G12.2 SMG7 PROSAPIP1 MORN1 TSEN15 FAM113A RP4-740C4.6 SWT1 VPS16 HES5 HMCN1 PCNA RP1-163G9.1 RGS2 SLC23A1 TP73-AS1 TROVE2 C10H20ORF196 TNFRSF25 CDC73 PLCB4 TNFRSF9 NEK7 LAMP5 ENO1 NAV1 ISM1 RP3-510D11.1 IPO9 SNAP25 NPPB TIMM17A PLCB1 RNU5E-4P RNPEP C10H20ORF72 PRAMEF10 TMEM183A KIF16B RP13-221M14.5 BTG2 PET117 PRAMEF3 ATP2B4 DZANK1 PRAMEF8 ZC3H11A FOXA2 LRRC38 SNRPE TMEM90B TMEM51-AS1 SOX13 C20orf26 C1orf126 MDM4 ACSS1 RP11-169K16.9 NUCKS1 ABHD12 RP11-430L17.1 SRGAP2 BID LOC100132147 MAPKAPK2 CECR2 NBPF1 CD55 HIRA EIF1AXP1 CD46 TRMT2A MST1L DIEXF CLTCL1 RP11-108M9.3 SYT14 C22ORF25 RCC2 SERTAD4 mml-mir-1306 AKR7A3 HHAT TXNRD2 LOC100506730 RCOR3 LZTR1 TMCO4 TRAF5 ARVCF PLA2G2E DTL PPIL2 PLA2G2D PPP2R5A THAP7 PLA2G2C NENF IGLV11-55 PINK1-AS FLVCR1 RAB36 KIF17 RPS6KC1 CRYBB2 NBPF2P PROX1 SGSM1 LUZP1 SMYD2 CRYBB1 ASAP3 CENPF CRYBA4 STPG1 KCTD3 HPS4 RUNX3 RRP15 RHBDD3 AIM1L LYPLAL1 KREMEN1 C1orf172 IARS2 ZMAT5 FAM46B MARK1 CCDC157 MAP3K6 MARC1 NF2 IFI6 MIA3 PLA2G3 RP5-1053E7.1 BROX SMTN SNHG12 DISP1 SEC14L2 SNORA44 CAPN2 C10H22ORF28 SNORA16A FBXO28 PATZ1 TMEM200B DEGS1 PRR14L MATN1 CNIH4 FBXO7 SNORD103B EPHX1 SFI1 FABP3 H3F3B PISD PEF1 PSEN2 FOXRED2 MTMR9LP ADCK3 RBM9 C1orf212 ZNF678 KCTD17 LOC100996496 ARF1 ANKRD54 MRPS15 GUK1 TRIOBP EPHA10 RNF187 KDELR3 POU3F1 RHOU DMC1 GJA9-MYCBP RAB4A PLA2G6 RNA5SP44 URB2 DNAL4 RP1-228H13.1 GALNT2 TAB1 LOC100130557 COG2 SYNGR1 LOC100131756 ARV1 XPNPEP3 C1orf210 GNPAT L3MBTL2 SZT2 TSNAX SGSM3 RP11-570P14.1 NTPCR PPPDE2 RNU5F-1 KIAA1804 C10H22ORF32 RNU5D-1 COA6 CYP2D42 PTCH2 GGPS1 TSPO KNCN TBCE KIAA1644 EFCAB14 GPR137B SULT4A1 KIAA0494 LGALS8 PHF21B TRABD2B MTR PARVB AGBL4 EXO1 NUP50 DMRTA2 SDCCAG8 PRR5 RP11-296A18.5 ZNF238 FBLN1 SELRC1 COX20 TUBGCP6 RP11-159C21.4 EFCAB2 MAPK11 C1orf123 SCCPDH HDAC10 TMEM48 ZNF672 CPT1B USP24 NOC2L NCAPH2 RP11-393I23.2 SDF4 5_8S_rRNA CFL1P3 MXRA8 ARSA RP11-182I10.4 CCNL2 PPAP2A WDR78 MRPL20 RGS3 MIR186 NADK MAPK8IP2 RP4-682C21.2 GNB1 NRF1 RP11-181C21.4 PEX10 C9ORF80 NEXN-AS1 PANK4 GDF9 ELTD1 WRAP73 U2 CTBS LRRC47 SCN4B C1orf180 C1orf174 SNRNP35 LPAR3 RPL22 TPGS1 COL24A1 GPR153 SEPT9 PTGES3P1 NOL9 DDX59 GEMIN8P4 KLHL21 U3 LOC100996620 DNAJC11 ERO1LB RNA45S5 ERRFI1 CBY3 RP11-47K11.2 RERE CNFN RNA5SP53 CLSTN1 FAM125A F3 CTNNBIP1 PNMA2 RPL7 LZIC C14ORF109 C1orf194 DFFA C19ORF70
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  • Protein Identities in Evs Isolated from U87-MG GBM Cells As Determined by NG LC-MS/MS

    Protein Identities in Evs Isolated from U87-MG GBM Cells As Determined by NG LC-MS/MS

    Protein identities in EVs isolated from U87-MG GBM cells as determined by NG LC-MS/MS. No. Accession Description Σ Coverage Σ# Proteins Σ# Unique Peptides Σ# Peptides Σ# PSMs # AAs MW [kDa] calc. pI 1 A8MS94 Putative golgin subfamily A member 2-like protein 5 OS=Homo sapiens PE=5 SV=2 - [GG2L5_HUMAN] 100 1 1 7 88 110 12,03704523 5,681152344 2 P60660 Myosin light polypeptide 6 OS=Homo sapiens GN=MYL6 PE=1 SV=2 - [MYL6_HUMAN] 100 3 5 17 173 151 16,91913397 4,652832031 3 Q6ZYL4 General transcription factor IIH subunit 5 OS=Homo sapiens GN=GTF2H5 PE=1 SV=1 - [TF2H5_HUMAN] 98,59 1 1 4 13 71 8,048185945 4,652832031 4 P60709 Actin, cytoplasmic 1 OS=Homo sapiens GN=ACTB PE=1 SV=1 - [ACTB_HUMAN] 97,6 5 5 35 917 375 41,70973209 5,478027344 5 P13489 Ribonuclease inhibitor OS=Homo sapiens GN=RNH1 PE=1 SV=2 - [RINI_HUMAN] 96,75 1 12 37 173 461 49,94108966 4,817871094 6 P09382 Galectin-1 OS=Homo sapiens GN=LGALS1 PE=1 SV=2 - [LEG1_HUMAN] 96,3 1 7 14 283 135 14,70620005 5,503417969 7 P60174 Triosephosphate isomerase OS=Homo sapiens GN=TPI1 PE=1 SV=3 - [TPIS_HUMAN] 95,1 3 16 25 375 286 30,77169764 5,922363281 8 P04406 Glyceraldehyde-3-phosphate dehydrogenase OS=Homo sapiens GN=GAPDH PE=1 SV=3 - [G3P_HUMAN] 94,63 2 13 31 509 335 36,03039959 8,455566406 9 Q15185 Prostaglandin E synthase 3 OS=Homo sapiens GN=PTGES3 PE=1 SV=1 - [TEBP_HUMAN] 93,13 1 5 12 74 160 18,68541938 4,538574219 10 P09417 Dihydropteridine reductase OS=Homo sapiens GN=QDPR PE=1 SV=2 - [DHPR_HUMAN] 93,03 1 1 17 69 244 25,77302971 7,371582031 11 P01911 HLA class II histocompatibility antigen,
  • Browsing Genes and Genomes with Ensembl

    Browsing Genes and Genomes with Ensembl

    The Bioinformatics Roadshow Tórshavn, The Faroe Islands 28-29 November 2012 BROWSING GENES AND GENOMES WITH ENSEMBL EXERCISES AND ANSWERS 1 BROWSER 3 BIOMART 8 VARIATION 13 COMPARATIVE GENOMICS 18 2 Note: These exercises are based on Ensembl version 69 (October 2012). After in future a new version has gone live, version 69 will still be available at http://e69.ensembl.org/. If your answer doesn’t correspond with the given answer, please consult the instructor. ______________________________________________________________ BROWSER ______________________________________________________________ Exercise 1 – Exploring a gene (a) Find the human F9 (coagulation factor IX) gene. On which chromosome and which strand of the genome is this gene located? How many transcripts (splice variants) have been annotated for it? (b) What is the longest transcript? How long is the protein it encodes? Has this transcript been annotated automatically (by Ensembl) or manually (by Havana)? How many exons does it have? Are any of the exons completely or partially untranslated? (c) Have a look at the external references for ENST00000218099. What is the function of F9? (d) Is it possible to monitor expression of ENST00000218099 with the ILLUMINA HumanWG_6_V2 microarray? If so, can it also be used to monitor expression of the other two transcripts? (e) In which part (i.e. the N-terminal or C-terminal half) of the protein encoded by ENST00000218099 does its peptidase activity reside? (f) Have any missense variants been discovered for the protein encoded by ENST00000218099? (g) Is there a mouse orthologue predicted for the human F9 gene? (h) If you have yourself a gene of interest, explore what information Ensembl displays about it! ______________________________________________________________ Answer (a) 8 Go to the Ensembl homepage (http://www.ensembl.org/).
  • Increased ACTL6A Occupancy Within Mswi/SNF Chromatin Remodelers

    Increased ACTL6A Occupancy Within Mswi/SNF Chromatin Remodelers

    bioRxiv preprint doi: https://doi.org/10.1101/2021.03.22.435873; this version posted March 22, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Increased ACTL6A Occupancy Within mSWI/SNF Chromatin Remodelers Drives Human Squamous Cell Carcinoma Chiung-Ying Chang1,2,7, Zohar Shipony3,7, Ann Kuo1,2, Kyle M. Loh4,5, William J. Greenleaf3,6, Gerald R. Crabtree1,2,5* 1Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305, USA. 2Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA. 3Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA. 4Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. 5Department of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305, USA. 6Department of Applied Physics, Stanford University, Stanford, California 94305, USA. 7These authors contributed equally. *Corresponding author: Gerald R. Crabtree, [email protected] Summary Mammalian SWI/SNF (BAF) chromatin remodelers play dosage-sensitive roles in many human malignancies and neurologic disorders. The gene encoding the BAF subunit, ACTL6A, is amplified at an early stage in the development of squamous cell carcinomas (SCCs), but its oncogenic role remains unclear. Here we demonstrate that ACTL6A overexpression leads to its stoichiometric assembly into BAF complexes and drives its interaction and engagement with specific regulatory regions in the genome. In normal epithelial cells, ACTL6A was sub-stoichiometric to other BAF subunits. However, increased ACTL6A levels by ectopic expression or in SCC cells led to near-saturation of ACTL6A within BAF complexes.
  • Open Full Page

    Open Full Page

    Published OnlineFirst August 15, 2016; DOI: 10.1158/1078-0432.CCR-16-0290 Biology of Human Tumors Clinical Cancer Research Recurrent TRIO Fusion in Nontranslocation– Related Sarcomas Lucile Delespaul1,2, Tom Lesluyes1,2,Gaelle€ Perot 1,3,Celine Brulard1, Lydia Lartigue1,2, Jessica Baud1,2, Pauline Lagarde1, Sophie Le Guellec4,Agnes Neuville1,3, Philippe Terrier5, Dominique Vince-Ranchere 6, Susanne Schmidt7, Anne Debant7, Jean-Michel Coindre1,2,3, and Fred eric Chibon1,3 Abstract Purpose: Despite various differences, nontranslocation-related with various partners, was identified in 5.1% of cases. TRIO sarcomas (e.g., comprising undifferentiated pleomorphic sarcoma, translocations are either intrachromosomal with TERT or inter- leiomyosarcoma, myxofibrosarcoma) are unified by their complex chromosomal with LINC01504 or ZNF558. Our results suggest genetics. Extensive analysis of the tumor genome using molecular that all translocations led to a truncated TRIO protein either cytogenetic approaches showed many chromosomal gains, losses, directly or indirectly by alternative splicing. TRIO rearrangement and translocations per cell. Genomic quantitative alterations and is associated with a modified transcriptomic program to immu- expression variations have been extensively studied by adapted nity/inflammation, proliferation and migration, and an increase high-throughput approaches, yet translocations still remained in proliferation. unscreened. We therefore analyzed 117 nontranslocation-related Conclusions: TRIO fusions have been identified in four
  • Supplementary Table S4. FGA Co-Expressed Gene List in LUAD

    Supplementary Table S4. FGA Co-Expressed Gene List in LUAD

    Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase
  • Expressed Gene Fusions As Frequent Drivers of Poor Outcomes in Hormone Receptor–Positive Breast Cancer

    Expressed Gene Fusions As Frequent Drivers of Poor Outcomes in Hormone Receptor–Positive Breast Cancer

    Published OnlineFirst December 14, 2017; DOI: 10.1158/2159-8290.CD-17-0535 RESEARCH ARTICLE Expressed Gene Fusions as Frequent Drivers of Poor Outcomes in Hormone Receptor–Positive Breast Cancer Karina J. Matissek1,2, Maristela L. Onozato3, Sheng Sun1,2, Zongli Zheng2,3,4, Andrew Schultz1, Jesse Lee3, Kristofer Patel1, Piiha-Lotta Jerevall2,3, Srinivas Vinod Saladi1,2, Allison Macleay3, Mehrad Tavallai1,2, Tanja Badovinac-Crnjevic5, Carlos Barrios6, Nuran Beşe7, Arlene Chan8, Yanin Chavarri-Guerra9, Marcio Debiasi6, Elif Demirdögen10, Ünal Egeli10, Sahsuvar Gökgöz10, Henry Gomez11, Pedro Liedke6, Ismet Tasdelen10, Sahsine Tolunay10, Gustavo Werutsky6, Jessica St. Louis1, Nora Horick12, Dianne M. Finkelstein2,12, Long Phi Le2,3, Aditya Bardia1,2, Paul E. Goss1,2, Dennis C. Sgroi2,3, A. John Iafrate2,3, and Leif W. Ellisen1,2 ABSTRACT We sought to uncover genetic drivers of hormone receptor–positive (HR+) breast cancer, using a targeted next-generation sequencing approach for detecting expressed gene rearrangements without prior knowledge of the fusion partners. We identified inter- genic fusions involving driver genes, including PIK3CA, AKT3, RAF1, and ESR1, in 14% (24/173) of unselected patients with advanced HR+ breast cancer. FISH confirmed the corresponding chromo- somal rearrangements in both primary and metastatic tumors. Expression of novel kinase fusions in nontransformed cells deregulates phosphoprotein signaling, cell proliferation, and survival in three- dimensional culture, whereas expression in HR+ breast cancer models modulates estrogen-dependent growth and confers hormonal therapy resistance in vitro and in vivo. Strikingly, shorter overall survival was observed in patients with rearrangement-positive versus rearrangement-negative tumors. Cor- respondingly, fusions were uncommon (<5%) among 300 patients presenting with primary HR+ breast cancer.
  • Nuclear PTEN Safeguards Pre-Mrna Splicing to Link Golgi Apparatus for Its Tumor Suppressive Role

    Nuclear PTEN Safeguards Pre-Mrna Splicing to Link Golgi Apparatus for Its Tumor Suppressive Role

    ARTICLE DOI: 10.1038/s41467-018-04760-1 OPEN Nuclear PTEN safeguards pre-mRNA splicing to link Golgi apparatus for its tumor suppressive role Shao-Ming Shen1, Yan Ji2, Cheng Zhang1, Shuang-Shu Dong2, Shuo Yang1, Zhong Xiong1, Meng-Kai Ge1, Yun Yu1, Li Xia1, Meng Guo1, Jin-Ke Cheng3, Jun-Ling Liu1,3, Jian-Xiu Yu1,3 & Guo-Qiang Chen1 Dysregulation of pre-mRNA alternative splicing (AS) is closely associated with cancers. However, the relationships between the AS and classic oncogenes/tumor suppressors are 1234567890():,; largely unknown. Here we show that the deletion of tumor suppressor PTEN alters pre-mRNA splicing in a phosphatase-independent manner, and identify 262 PTEN-regulated AS events in 293T cells by RNA sequencing, which are associated with significant worse outcome of cancer patients. Based on these findings, we report that nuclear PTEN interacts with the splicing machinery, spliceosome, to regulate its assembly and pre-mRNA splicing. We also identify a new exon 2b in GOLGA2 transcript and the exon exclusion contributes to PTEN knockdown-induced tumorigenesis by promoting dramatic Golgi extension and secretion, and PTEN depletion significantly sensitizes cancer cells to secretion inhibitors brefeldin A and golgicide A. Our results suggest that Golgi secretion inhibitors alone or in combination with PI3K/Akt kinase inhibitors may be therapeutically useful for PTEN-deficient cancers. 1 Department of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai 200025, China. 2 Institute of Health Sciences, Shanghai Institutes for Biological Sciences of Chinese Academy of Sciences and SJTU-SM, Shanghai 200025, China.