(Human and Monkey) and Mouse Pscs Mouse Primed

Total Page:16

File Type:pdf, Size:1020Kb

(Human and Monkey) and Mouse Pscs Mouse Primed Comparison of genes expressed in primed states of primates (human and monkey) and mouse PSCs mouse_primed primate_primed primate_primed_AND_mouse_primed GM6123 ISG15 AGRN ATP6V1H GLTPD1 B3GALT6 OPRK1 C1orf86 PUSL1 GM9826 TPRG1L VWA1 GM30414 AJAP1 SKI GM24276 KCNAB2 RER1 GM7445 ZNF593 FAM213B GM6161 CD52 RNF207 SGK3 KIAA1522 PHF13 GM28659 ZNF362 CAMTA1 A830018L16RIK DNALI1 VAMP3 GM7560 ZFP69B PARK7 SULF1 ZNF642 H6PD LOC105243866 ZNF684 SLC25A33 RPL5-PS1 ZNF691 NMNAT1 KCNB2 CCDC24 UBE4B GM7634 MAST2 KIF1B LY96 GPX7 PGD PI15 ZYG11A UBIAD1 TFAP2B PCSK9 FBXO44 GM4849 ST6GALNAC5 DRAXIN MIR133B NEXN AGTRAP IL17A LPHN2 CLCN6 GSTA3 SAMD13 MFN2 LOC101056100 PKN2 MIIP KHDC1C ZNF326 TMEM51 KHDC1B CCDC18 EFHD2 MIR30C-2 VCAM1 DNAJC16 GM19028 CELSR2 PLEKHM2 GM6462 GSTM4 SPEN GM6473 WNT2B NECAP2 GM19680 GPR89B MRTO4 GM7910 FAM108A1 PQLC2 GM25792 HIST2H2AA4 MINOS1 GM23453 CA14 OTUD3 1700001G17RIK C1orf54 PINK1 DST ZNF687 ALPL PRSS39 CGN CDC42 ARHGEF4 LMNA ZBTB40 PLEKHB2 IFI16 EPHB2 GM19430 ATP1A2 KDM1A GM25634 PEA15 TCEB3 HS6ST1 DDR2 PITHD1 ARID5A SUCO SRRM1 N-R5S210 NAV1 CLIC4 VWA3B CD46 TMEM50A CNGA3 HHAT TMEM57 LIPT1 TRAF5 LDLRAP1 MRPL30 FLVCR1 MAN1C1 NPAS2 MARC1 SEPN1 GM24826 ZNF678 PDIK1L CNOT11 KIAA1804 CEP85 SLC9A2 MTR SH3BGRL3 TMEM182 ZNF238 DHDDS GM5267 ZNF672 ARID1A GPR45 NOC2L PIGV AI597479 C1orf174 ZDHHC18 GM8210 MTOR TMEM222 GM29610 FBXO2 GPR3 LOC102632770 HNRNPCL1 TMA7 GM8241 ATP13A2 FAM76A BIVM AKR7A2 STX12 ERCC5 C1orf63 THEMIS2 GULP1 NKAIN1 XKR8 GM8304 SNRNP40 DNAJC8 GM23974 BAI2 ATPIF1 RPL23A-PS1 KIAA0319L SESN2 DNAH7B C1orf216 MED18 N-R5S211 CLSPN PHACTR4 GM8357 INPP5B GMEB1 GM8367 SNORA55 OPRD1 C230029F24RIK HEYL ZCCHC17 GM8384 CCDC23 SERINC2 TMEFF2 CCDC17 TMEM39B STAT4 PPAP2B KPNA6 MOB4 DOCK7 TXLNA RPS24 JAK1 CCDC28B PLCL1 DEPDC1 IQCC 9430016H08RIK USP33 EIF3I SGOL2A AIDA HDAC1 NDUFB3 C1orf52 RBBP4 CBX3-PS7 ZNF644 S100PBP CASP8 ARHGAP29 ZSCAN20 G730003C15RIK LPPR5 ZMYM1 CARF COL11A1 ZMYM4 ICOS HENMT1 NCDN RPL17-PS1 CD58 AGO4 PARD3B ZNF697 AGO1 GM11599 CTSK ADPRHL2 NRP2 DENND4B THRAP3 GM26457 GON4L SH3D21 SNORA41 KIAA0907 CDCA8 CCNYL1 C1orf85 UTP11L CRYGF IQGAP3 AKIRIN1 MAP2 SH2D2A PPIE UNC80 ARHGEF11 MFSD2A SPAG16 TNFSF4 CAP1 GM23422 KCNT2 RLF APOL7D ZNF281 ZMPSTE24 GM5528 KIF14 SMAP2 GM25360 SYT2 PPCS GM23444 KLHDC8A CCDC30 GM24497 RAB7L1 PPIH GM25939 C1orf74 YBX1 TMEM169 TP53BP2 CDC20 XRCC5 C1orf198 KDM4A GPBAR1 C1orf131 ST3GAL3 MIR26B TARBP1 IPO13 PLCD4 FH DPH2 WNT6 ZNF669 ATP6V0B WNT10A ZNF496 B4GALT2 CDK5R2 ZNF692 DMAP1 INHA AKR1E2 RNF220 SLC4A3 KIAA1217 KIF2C GM33152 ZNF37A RPS8 UTP14B ZNF485 UROD N-R5S213 ZNF22 HPDL MFF STOX1 TOE1 CCL20 KIAA1279 MMACHC FBXO36 C10orf35 AKR1A1 GM15433 FAM149B1 NASP RPL19-PS1 ZSWIM8 LURAP1 GM10553 PLAU RAD54L GM7609 KIF20B NSUN4 G530012D18RIK BTAF1 CMPK1 SP140 SCD PRPF38A SP100 ATRNL1 ZYG11B 4933407L21RIK PPAPDC1A SCP2 2810459M11RIK DOCK1 CPT2 C130036L24RIK DPYSL4 LRRC42 1700019O17RIK ZNF511 TCEANC2 RPL30-PS6 PAOX MRPL37 PTMA ANKRD26 ACOT11 DIS3L2 KIAA1462 TTC4 PRSS56 ZNF33B PRKAA2 CHRNG ZNF32 FGGY 3110079O15RIK SLC16A9 HOOK1 MROH2A HERC4 NFIA GM4753 DLG5 L1TD1 ACKR3 POLR3A ATG4C GM9991 WAPAL ALG6 PRLH HTR7 EFCAB7 RBM44 FRAT2 PGM1 LOC102639127 RRP12 ROR1 FAM132B C10orf76 CACHD1 TWIST2 SORCS1 RAVER2 OLFR1413 KIAA1598 DNAJC6 OLFR1412 C10orf88 MIER1 OLFR1411 RIC8A GADD45A OLFR1410 TRIM22 SRSF11 OLFR12 FXC1 CTH GPR35 ZNF215 FPGT MIR149 ZNF143 TYW3 AQP12 CTR9 ACADM AGXT ANO5 RABGGTB PPP1R7 CD44 FAM73A GM26446 CD82 DNAJB4 GM10550 ZNF408 ARID3B ING5 MADD RPF1 D2HGDH RTN4RL2 CYR61 GAL3ST2 DAK SH3GLB1 GM9994 ALDH3B1 LMO4 RPL18A TPCN2 LRRC8B GM6430 PAAF1 CDC7 GM7952 C11orf30 RPAP2 GM5260 C11orf82 MTF2 CDH20 KIAA1731 DR1 GM10193 SRSF8 FNBP1L ZCCHC2 JRKL ABCD3 GM6651 RAB39A RWDD3 D630008O14RIK C2CD2L PTBP2 SERPINB2 NLRX1 SNX7 CNTNAP5A RNF26 SLC35A3 NIFK ARHGEF12 HIAT1 TFCP2L1 TECTA TRMT13 GM8321 SC5DL RTCA 3110009E18RIK ZNF214 CDC14A C1QL2 STK33 SLC30A7 EN1 DKK3 RNPC3 GM24547 CYP2R1 PRMT6 GPR39 PIK3C2A FAM102B GM23734 IMMP1L PRPF38B ACMSD CD59 STXBP3 GM23902 PAMR1 GPSM2 FCMR LRP4 TMEM167B IL10 UBE2L6 SARS FAM72A STX5 CYB561D1 CTSE B3GNT1 GNAI3 RAB29 C11orf24 CSF1 ELK4 FGF19 STRIP1 MIR135B NUMA1 RBM15 GM7241 C2CD3 CEPT1 DSTYK KCTD14 ATP5F1 GM10538 CCDC82 DDX20 GM29257 USP28 CTTNBP2NL FMOD ZNF259 CAPZA1 CHIL1 PCSK7 MOV10 MYBPH C12orf5 LRIG2 MYOG ZNF384 MAGI3 GM29376 LOH12CR1 DCLRE1B GM10535 KIAA1467 HIPK1 ARL8A PPFIBP1 OLFML3 GM4793 DDX11 VANGL1 PHLDA3 KIAA1551 ATP1A1 TNNI1 DIP2B PTGFRN LAD1 METTL7A TTF2 TMEM9 SCN8A MAN1A2 ASCL5 ZNF740 WDR3 DDX59 ESPL1 PHGDH ZFP281 METTL7B SEC22B GM29718 DGKA TXNIP MIR181B-1 IKZF4 LIX1L DENND1B ESYT1 PEX11B GLRX2 HSD17B6 PIAS3 UCHL5 SRGAP1 RNF115 GM5262 ALX1 CHD1L GM5263 C12orf45 BCL9 PTGS2 KIAA1033 VOPP1 PDC POLR3B VPS45 SKA2L-PS SDSL MRPS21 ARPC5 ZNF664 PRPF3 NMNAT2 PXMP2 RPRD2 RNASEL ZNF26 SETDB1 STX6 ZNF140 PRUNE GM10031 ZNF10 MLLT11 GM15428 KDM5A SCNM1 2810025M15RIK C12orf4 PSMD4 BC026585 C1RL PSMB4 GM37713 CD163 TUFT1 ASTN1 CSDA SNX27 GM31256 C2CD5 CHTOP TNR ITPR2 SNAPIN GM10530 IPO8 INTS3 GM6177 KIF21A SLC27A3 RC3H1 SLC2A13 CREB3L4 SERPINC1 ZNF641 RPS27 GAS5 FMNL3 UBAP2L SNORD80 ITGA5 HAX1 SNORD47 WIBG ZBTB7B GM25789 PMEL EFNA4 TNFSF18 TIMELESS EFNA3 RPSA-PS1 TAC3 SLC50A1 METTL18 TMEM194A MTX1 CCDC181 R3HDM2 FDPS MPC2 KITLG MSTO1 GM18186 EEA1 DAP3 CD247 CCDC41 SYT11 ILDR2 C12orf76 LAMTOR2 FAM78B IQCD SLC25A44 RXRG RBM19 TMEM79 LMX1A MED13L GPATCH4 CCDC190 TESC RRNAD1 1700015E13RIK ABCB9 PRCC GM7299 MPHOSPH9 KIRREL OLFML2B DHX37 DUSP23 GM9929 TMEM132D NCSTN GM26620 ZNF605 VANGL2 GM39701 MEDAG UFC1 LOC102638466 B3GALTL USP21 FCGR4 BRCA2 PPOX GM26110 FREM2 NDUFS2 CFAP126 DGKH SDHC MPZ PHF11 DUSP12 NR1I3 TPP2 ATF6 ALYREF2 COL4A2 NOS1AP CD48 ATP11A UHMK1 CD84 PARP4 UAP1 GM10521 CDX2 HSD17B7 DCAF8 SUPT20H NUF2 KCNJ10 VWA8 PBX1 SLAMF9 ABCC4 MGST3 IGSF9 COL4A1 UCK2 VSIG8 SRP54 POGK OLFR16 FAM177A1 POU2F1 OLFR1407-PS1 FRMD6 DCAF6 OLFR218 ARID4A TIPRL OLFR1404 KIAA0586 SFT2D2 OLFR418 DAAM1 ATP1B1 AIM2 PLEKHH1 GORAB PYDC3 KIAA0247 PRRX1 OLFR433 PCNX METTL13 OLFR432 ZNF410 PRDX6 OLFR430 CCDC176 DARS2 OLFR429 YLPM1 ZBTB37 OLFR427 FLVCR2 RASAL2 OLFR424 KIAA1737 RALGPS2 OLFR258-PS1 SAMD15 FAM20B OLFR420 PPP4R4 TOR3A MPTX1 TNFAIP2 SOAT1 OLFR414 INF2 TOR1AIP1 OLFR220 PACS2 CEP350 FMN2 ZNF219 QSOX1 ZBTB18 SUPT16H XPR1 DESI2 CHD8 DHX9 GM24405 RBM23 LAMC1 KIF26B HEATR5A SMG7 CNST RALGAPA1 TSEN15 ITPKB SLC25A21 SWT1 G370120E05RIK METTL21D HMCN1 LEFTY1 NIN RGS2 A430110L20RIK PYGL TROVE2 GM8146 CNIH CDC73 CNIH3 GCH1 NEK7 DNAH14 ZFYVE26 IPO9 TRP53BP2 KIAA0317 TIMM17A CAPN8 CEP128 RNPEP SUSD4 CCDC88C TMEM183A DUSP10 NDUFB1 BTG2 RPL21-PS1 IFI27L2 ATP2B4 SNORA36B CLMN ZC3H11A MIR194-1 SLC25A29 SNRPE MIR215 C14orf2 SOX13 SLC30A10 TUBGCP5 MDM4 GM26169 EIF2AK4 NUCKS1 GM3809 EIF3J SRGAP2 D1PAS1 FOXB1 MAPKAPK2 ESRRG TLN2 CD55 A230020J21RIK ZNF609 DIEXF SPATA45 PTPLAD1 SYT14 BATF3 C15orf61 SERTAD4 D730003I15RIK LOXL1 RCOR3 RD3 C15orf39 DTL GM32460 FAM154B PPP2R5A GM10516 ZNF592 NENF GM22265 AKAP13 RPS6KC1 IRF6 ZNF710 PROX1 A130010J15RIK TTLL13 SMYD2 GM21362 CHD2 CENPF CD34 LRRK1 KCTD3 A330023F24RIK HERC2 RRP15 XKR4 FAM189A1 LYPLAL1 GM6085 ZNF770 IARS2 RGS20 RASGRP1 MARK1 NPBWR1 GPR176 MIA3 4732440D04RIK FAM82A2 BROX GM19026 RPAP1 DISP1 GM23358 CDAN1 CAPN2 GM6152 TP53BP1 FBXO28 MYBL1 MFAP1 DEGS1 GM6195 FBN1 CNIH4 SNORD87 CEP152 EPHX1 TCF24 MYO5C H3F3B PPP1R42 MYO1E PSEN2 GM25253 NARG2 ADCK3 GM7593 VPS13C ARF1 GM5523 HERC1 GUK1 EYA1 KIAA0101 RNF187 SMT3H2-PS4 LCTL RHOU GM10566 LARP6 RAB4A SBSPON THAP10 URB2 4930444P10RIK PARP6 GALNT2 RPL7 HCN4 COG2 GM7654 SEMA7A ARV1 GM5828 SCAPER GNPAT GM6075 CTSH TSNAX CRISP4 RPS17L NTPCR DEFB18 SOLH COA6 GM10075 MAPK8IP3 GGPS1 GM28341 C16orf59 TBCE IL17F ZNF205 GPR137B KCNQ5 ZNF213 LGALS8 GM7658 ZNF263 EXO1 GM5696 ABCC1 SDCCAG8 SDHAF4 C16orf62 COX20 FAM135A IQCK EFCAB2 ND4L C16orf52 SCCPDH ATP6 TNRC6A SDF4 ATP8 IL4R MXRA8 COX2 KIAA0556 CCNL2 4931408C20RIK MVP MRPL20 GM5697 ZNF48 NADK GM9898 ZNF771 GNB1 PTP4A1 STX4 PEX10 GM5698 ZNF646 PANK4 GM9458 ZNF267 WRAP73 4931428L18RIK PHKB LRRC47 GM25814 TMEM188 RPL22 GM9839 MT1B GPR153 GM5415 MT1X NOL9 ZFP451 MMP15 KLHL21 GM15455 CCDC113 DNAJC11 BEND6 EDC4 ERRFI1 CCDC115 DUS2L RERE PRSS40 GABARAPL2 CLSTN1 1700101I19RIK NECAB2 CTNNBIP1 ANKRD23 KIAA0513 LZIC RPL12-PS1 ZNF276 DFFA COA5 WASH4P CASZ1 2010300C02RIK TMEM8A SRM TSGA10 C16orf13 EXOSC10 LYG1 CLCN7 MAD2L2 TXNDC9 IFT140 MTHFR AFF3 ZNF598 CASP9 GM23722 ZNF597 AGMAT RFX8 ZNF500 UQCRH MFSD9 GRIN2A EPHA2 GM5973 PARN ARHGEF19 METTL21E KIAA0430 RSG1 TXN-PS1 ZNF768 FBXO42 GM5526 ZNF764 MFAP2 SLC40A1 ZNF688 SDHB STK-PS2 ZNF689 IFFO2 GM4852 ZNF629 UBR4 GM8354 ZNF423 EMC1 GM28388 RPGRIP1L CAPZB NABP1 ZNF319 CAMK2N1 GM27607 FTSJD1 MUL1 GM8420 ZNF19 DDOST GM5976 TMEM170A SH2D5 MFSD6 CHST6 HP1BP3 INPP1 ZZEF1 EIF4G3 1700019D03RIK PLD2 USP48 1700019A02RIK C17orf49 HSPG2 DNAH7A CHD3 HTR1D HECW2 SLC47A1 HNRNPR GM34066 SUPT6H ID3 GM5147 TP53I13 HMGCL GM6822 ZNF207 FUCA1 BOLL ZNF830 SYF2 GM6644 TCAP AUNIP GM5254 RAPGEFL1 STMN1 GM8581 CNTNAP1 PAFAH2 GM29389 C17orf53 GPN2 GM33589 DBF4B GPATCH3 ICA1L TBKBP1 WASF2 WDR12 BCAS3 AHDC1 GM23448 METTL2A PPP1R8 GM11605 PRKCA RPA2 GM13751 C17orf80 EYA3 KLF7 FAM100B TAF12 METTL21A MYO1C SRSF4 FZD5 CLUH MECR D630023F18RIK SHPK SDC3 IDH1 ZNF232 PUM1 KANSL1L KIAA0753 PTP4A2 ACADL TP53 MARCKSL1 RPL31-PS14 LSMD1 YARS GM8840 KRBA2 TMEM54 IKZF2 ZNF18 RNF19B GM8870 TRIM16 AK2 GM6947 FAM211A TRIM62 FN1 ZNF287 PHC2 GM5829 FLII SFPQ GM5256 ULK2 PSMB2 MREG CORO6 TRAPPC3 MARCH4 MYO19 EVA1B TNS1 ACACA STK40 CXCR1 ACLY LSM10 ZFP142 PTGES3L-AARSD1 MEAF6 FEV MPP2 SNIP1 CRYBA2 HDAC5 GNL2 MIR375 ZNF652 YRDC IHH COL1A1 MTF1 CNPPD1 TRIM25 SF3A3 ABCB6 SUPT4H1 FHL3 PTPRN TRIM37 RRAGC OBSL1 HELZ PABPC4 GM26263 SDK2 TRIT1 PAX3 C17orf70 PPT1 BC035947 SIRT7 RIMS3
Recommended publications
  • Responses of Bats to White-Nose Syndrome and Implications for Conservation
    University of New Hampshire University of New Hampshire Scholars' Repository Doctoral Dissertations Student Scholarship Spring 2020 Responses of Bats to White-Nose Syndrome and Implications for Conservation Meghan Stark University of New Hampshire, Durham Follow this and additional works at: https://scholars.unh.edu/dissertation Recommended Citation Stark, Meghan, "Responses of Bats to White-Nose Syndrome and Implications for Conservation" (2020). Doctoral Dissertations. 2518. https://scholars.unh.edu/dissertation/2518 This Dissertation is brought to you for free and open access by the Student Scholarship at University of New Hampshire Scholars' Repository. It has been accepted for inclusion in Doctoral Dissertations by an authorized administrator of University of New Hampshire Scholars' Repository. For more information, please contact [email protected]. RESPONSES OF BATS TO WHITE-NOSE SYNDROME AND IMPLICATIONS FOR CONSERVATION BY MEGHAN A. STARK B.S., University of Alabama at Birmingham, 2013 DISSERTATION Submitted to the University of New Hampshire in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy In Genetics May 2020 i This dissertation was examined and approved in partial fulfillment of the requirements for the degree of Ph.D. in Genetics by: Dissertation Director, Matthew MacManes, Assoc. Prof. UNH MCBS Jeffrey T. Foster, Associate Professor, NAU PMI W. Kelley Thomas, Professor, UNH MCBS Rebecca Rowe, Associate Professor, UNH NREN Thomas Lee, Associate Professor Emeritus, UNH NREN On April 6, 2020 Approval signatures are on file with the University of New Hampshire Graduate School. ii DEDICATION I dedicate this work to all of the strong women in my life: Myra Michele Ange Heather Michelle Coons Kaitlyn Danielle Cagle Brindlee Michelle Coons Patricia Gail Miller Sarah Jean Lane “Here’s to strong women.
    [Show full text]
  • Mouse Germ Line Mutations Due to Retrotransposon Insertions Liane Gagnier1, Victoria P
    Gagnier et al. Mobile DNA (2019) 10:15 https://doi.org/10.1186/s13100-019-0157-4 REVIEW Open Access Mouse germ line mutations due to retrotransposon insertions Liane Gagnier1, Victoria P. Belancio2 and Dixie L. Mager1* Abstract Transposable element (TE) insertions are responsible for a significant fraction of spontaneous germ line mutations reported in inbred mouse strains. This major contribution of TEs to the mutational landscape in mouse contrasts with the situation in human, where their relative contribution as germ line insertional mutagens is much lower. In this focussed review, we provide comprehensive lists of TE-induced mouse mutations, discuss the different TE types involved in these insertional mutations and elaborate on particularly interesting cases. We also discuss differences and similarities between the mutational role of TEs in mice and humans. Keywords: Endogenous retroviruses, Long terminal repeats, Long interspersed elements, Short interspersed elements, Germ line mutation, Inbred mice, Insertional mutagenesis, Transcriptional interference Background promoter and polyadenylation motifs and often a splice The mouse and human genomes harbor similar types of donor site [10, 11]. Sequences of full-length ERVs can TEs that have been discussed in many reviews, to which encode gag, pol and sometimes env, although groups of we refer the reader for more in depth and general infor- LTR retrotransposons with little or no retroviral hom- mation [1–9]. In general, both human and mouse con- ology also exist [6–9]. While not the subject of this re- tain ancient families of DNA transposons, none view, ERV LTRs can often act as cellular enhancers or currently active, which comprise 1–3% of these genomes promoters, creating chimeric transcripts with genes, and as well as many families or groups of retrotransposons, have been implicated in other regulatory functions [11– which have caused all the TE insertional mutations in 13].
    [Show full text]
  • An Order Estimation Based Approach to Identify Response Genes
    AN ORDER ESTIMATION BASED APPROACH TO IDENTIFY RESPONSE GENES FOR MICRO ARRAY TIME COURSE DATA A Thesis Presented to The Faculty of Graduate Studies of The University of Guelph by ZHIHENG LU In partial fulfilment of requirements for the degree of Doctor of Philosophy September, 2008 © Zhiheng Lu, 2008 Library and Bibliotheque et 1*1 Archives Canada Archives Canada Published Heritage Direction du Branch Patrimoine de I'edition 395 Wellington Street 395, rue Wellington Ottawa ON K1A0N4 Ottawa ON K1A0N4 Canada Canada Your file Votre reference ISBN: 978-0-494-47605-5 Our file Notre reference ISBN: 978-0-494-47605-5 NOTICE: AVIS: The author has granted a non­ L'auteur a accorde une licence non exclusive exclusive license allowing Library permettant a la Bibliotheque et Archives and Archives Canada to reproduce, Canada de reproduire, publier, archiver, publish, archive, preserve, conserve, sauvegarder, conserver, transmettre au public communicate to the public by par telecommunication ou par Plntemet, prefer, telecommunication or on the Internet, distribuer et vendre des theses partout dans loan, distribute and sell theses le monde, a des fins commerciales ou autres, worldwide, for commercial or non­ sur support microforme, papier, electronique commercial purposes, in microform, et/ou autres formats. paper, electronic and/or any other formats. The author retains copyright L'auteur conserve la propriete du droit d'auteur ownership and moral rights in et des droits moraux qui protege cette these. this thesis. Neither the thesis Ni la these ni des extraits substantiels de nor substantial extracts from it celle-ci ne doivent etre imprimes ou autrement may be printed or otherwise reproduits sans son autorisation.
    [Show full text]
  • Efficacy and Mechanistic Evaluation of Tic10, a Novel Antitumor Agent
    University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2012 Efficacy and Mechanisticv E aluation of Tic10, A Novel Antitumor Agent Joshua Edward Allen University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Oncology Commons Recommended Citation Allen, Joshua Edward, "Efficacy and Mechanisticv E aluation of Tic10, A Novel Antitumor Agent" (2012). Publicly Accessible Penn Dissertations. 488. https://repository.upenn.edu/edissertations/488 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/488 For more information, please contact [email protected]. Efficacy and Mechanisticv E aluation of Tic10, A Novel Antitumor Agent Abstract TNF-related apoptosis-inducing ligand (TRAIL; Apo2L) is an endogenous protein that selectively induces apoptosis in cancer cells and is a critical effector in the immune surveillance of cancer. Recombinant TRAIL and TRAIL-agonist antibodies are in clinical trials for the treatment of solid malignancies due to the cancer-specific cytotoxicity of TRAIL. Recombinant TRAIL has a short serum half-life and both recombinant TRAIL and TRAIL receptor agonist antibodies have a limited capacity to perfuse to tissue compartments such as the brain, limiting their efficacy in certain malignancies. To overcome such limitations, we searched for small molecules capable of inducing the TRAIL gene using a high throughput luciferase reporter gene assay. We selected TRAIL-inducing compound 10 (TIC10) for further study based on its induction of TRAIL at the cell surface and its promising therapeutic index. TIC10 is a potent, stable, and orally active antitumor agent that crosses the blood-brain barrier and transcriptionally induces TRAIL and TRAIL-mediated cell death in a p53-independent manner.
    [Show full text]
  • Molecular Mechanisms Involved Involved in the Interaction Effects of HCV and Ethanol on Liver Cirrhosis
    Virginia Commonwealth University VCU Scholars Compass Theses and Dissertations Graduate School 2010 Molecular Mechanisms Involved Involved in the Interaction Effects of HCV and Ethanol on Liver Cirrhosis Ryan Fassnacht Virginia Commonwealth University Follow this and additional works at: https://scholarscompass.vcu.edu/etd Part of the Physiology Commons © The Author Downloaded from https://scholarscompass.vcu.edu/etd/2246 This Thesis is brought to you for free and open access by the Graduate School at VCU Scholars Compass. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of VCU Scholars Compass. For more information, please contact [email protected]. Ryan C. Fassnacht 2010 All Rights Reserved Molecular Mechanisms Involved in the Interaction Effects of HCV and Ethanol on Liver Cirrhosis A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science at Virginia Commonwealth University. by Ryan Christopher Fassnacht, B.S. Hampden Sydney University, 2005 M.S. Virginia Commonwealth University, 2010 Director: Valeria Mas, Ph.D., Associate Professor of Surgery and Pathology Division of Transplant Department of Surgery Virginia Commonwealth University Richmond, Virginia July 9, 2010 Acknowledgement The Author wishes to thank his family and close friends for their support. He would also like to thank the members of the molecular transplant team for their help and advice. This project would not have been possible with out the help of Dr. Valeria Mas and her endearing
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • 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,
    [Show full text]
  • Sequence Analysis of Familial Neurodevelopmental Disorders
    SEQUENCE ANALYSIS OF FAMILIAL NEURODEVELOPMENTAL DISORDERS by Joseph Mark Tilghman A dissertation submitted to Johns Hopkins University in conformity with the requirements for the degree of Doctor of Philosophy Baltimore, Maryland December 2020 © 2020 Joseph Tilghman All Rights Reserved Abstract: In the practice of human genetics, there is a gulf between the study of Mendelian and complex inheritance. When diagnosis of families affected by presumed monogenic syndromes is undertaken by genomic sequencing, these families are typically considered to have been solved only when a single gene or variant showing apparently Mendelian inheritance is discovered. However, about half of such families remain unexplained through this approach. On the other hand, common regulatory variants conferring low risk of disease still predominate our understanding of individual disease risk in complex disorders, despite rapidly increasing access to rare variant genotypes through sequencing. This dissertation utilizes primarily exome sequencing across several developmental disorders (having different levels of genetic complexity) to investigate how to best use an individual’s combination of rare and common variants to explain genetic risk, phenotypic heterogeneity, and the molecular bases of disorders ranging from those presumed to be monogenic to those known to be highly complex. The study described in Chapter 2 addresses putatively monogenic syndromes, where we used exome sequencing of four probands having syndromic neurodevelopmental disorders from an Israeli-Arab founder population to diagnose recessive and dominant disorders, highlighting the need to consider diverse modes of inheritance and phenotypic heterogeneity. In the study described in Chapter 3, we address the case of a relatively tractable multifactorial disorder, Hirschsprung disease.
    [Show full text]
  • Transcriptional Control of Tissue-Resident Memory T Cell Generation
    Transcriptional control of tissue-resident memory T cell generation Filip Cvetkovski Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Graduate School of Arts and Sciences COLUMBIA UNIVERSITY 2019 © 2019 Filip Cvetkovski All rights reserved ABSTRACT Transcriptional control of tissue-resident memory T cell generation Filip Cvetkovski Tissue-resident memory T cells (TRM) are a non-circulating subset of memory that are maintained at sites of pathogen entry and mediate optimal protection against reinfection. Lung TRM can be generated in response to respiratory infection or vaccination, however, the molecular pathways involved in CD4+TRM establishment have not been defined. Here, we performed transcriptional profiling of influenza-specific lung CD4+TRM following influenza infection to identify pathways implicated in CD4+TRM generation and homeostasis. Lung CD4+TRM displayed a unique transcriptional profile distinct from spleen memory, including up-regulation of a gene network induced by the transcription factor IRF4, a known regulator of effector T cell differentiation. In addition, the gene expression profile of lung CD4+TRM was enriched in gene sets previously described in tissue-resident regulatory T cells. Up-regulation of immunomodulatory molecules such as CTLA-4, PD-1, and ICOS, suggested a potential regulatory role for CD4+TRM in tissues. Using loss-of-function genetic experiments in mice, we demonstrate that IRF4 is required for the generation of lung-localized pathogen-specific effector CD4+T cells during acute influenza infection. Influenza-specific IRF4−/− T cells failed to fully express CD44, and maintained high levels of CD62L compared to wild type, suggesting a defect in complete differentiation into lung-tropic effector T cells.
    [Show full text]
  • The Relevance of Clinical, Genetic and Serological Markers
    AUTREV-01901; No of Pages 18 Autoimmunity Reviews xxx (2016) xxx–xxx Contents lists available at ScienceDirect Autoimmunity Reviews journal homepage: www.elsevier.com/locate/autrev Review Cardiovascular risk assessment in patients with rheumatoid arthritis: The relevance of clinical, genetic and serological markers Raquel López-Mejías a, Santos Castañeda b, Carlos González-Juanatey c,AlfonsoCorralesa, Iván Ferraz-Amaro d, Fernanda Genre a, Sara Remuzgo-Martínez a, Luis Rodriguez-Rodriguez e, Ricardo Blanco a,JavierLlorcaf, Javier Martín g, Miguel A. González-Gay a,h,i,⁎ a Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IDIVAL, Santander, Spain b Division of Rheumatology, Hospital Universitario la Princesa, IIS-IPrincesa, Madrid, Spain c Division of Cardiology, Hospital Lucus Augusti, Lugo, Spain d Rheumatology Division, Hospital Universitario de Canarias, Santa Cruz de Tenerife, Spain e Division of Rheumatology, Hospital Clínico San Carlos, Madrid, Spain f Division of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, and CIBER Epidemiología y Salud Pública (CIBERESP), IDIVAL, Santander, Spain g Institute of Parasitology and Biomedicine López-Neyra, IPBLN-CSIC, Granada, Spain h School of Medicine, University of Cantabria, Santander, Spain i Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa article info abstract Article history: Cardiovascular disease (CV) is the most common cause of premature mortality in patients with rheumatoid ar- Received 7 July 2016 thritis (RA). This is the result of an accelerated atherosclerotic process. Adequate CV risk stratification has special Accepted 9 July 2016 relevance in RA to identify patients at risk of CV disease.
    [Show full text]
  • Supp Material.Pdf
    Simon et al. Supplementary information: Table of contents p.1 Supplementary material and methods p.2-4 • PoIy(I)-poly(C) Treatment • Flow Cytometry and Immunohistochemistry • Western Blotting • Quantitative RT-PCR • Fluorescence In Situ Hybridization • RNA-Seq • Exome capture • Sequencing Supplementary Figures and Tables Suppl. items Description pages Figure 1 Inactivation of Ezh2 affects normal thymocyte development 5 Figure 2 Ezh2 mouse leukemias express cell surface T cell receptor 6 Figure 3 Expression of EZH2 and Hox genes in T-ALL 7 Figure 4 Additional mutation et deletion of chromatin modifiers in T-ALL 8 Figure 5 PRC2 expression and activity in human lymphoproliferative disease 9 Figure 6 PRC2 regulatory network (String analysis) 10 Table 1 Primers and probes for detection of PRC2 genes 11 Table 2 Patient and T-ALL characteristics 12 Table 3 Statistics of RNA and DNA sequencing 13 Table 4 Mutations found in human T-ALLs (see Fig. 3D and Suppl. Fig. 4) 14 Table 5 SNP populations in analyzed human T-ALL samples 15 Table 6 List of altered genes in T-ALL for DAVID analysis 20 Table 7 List of David functional clusters 31 Table 8 List of acquired SNP tested in normal non leukemic DNA 32 1 Simon et al. Supplementary Material and Methods PoIy(I)-poly(C) Treatment. pIpC (GE Healthcare Lifesciences) was dissolved in endotoxin-free D-PBS (Gibco) at a concentration of 2 mg/ml. Mice received four consecutive injections of 150 μg pIpC every other day. The day of the last pIpC injection was designated as day 0 of experiment.
    [Show full text]
  • 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
    [Show full text]