Supplementary Table 1. the Clinical Characteristics of SCC Patients Analyzed by RNA 2 Sequencing

Total Page:16

File Type:pdf, Size:1020Kb

Supplementary Table 1. the Clinical Characteristics of SCC Patients Analyzed by RNA 2 Sequencing 1 Supplementary Table 1. The clinical characteristics of SCC patients analyzed by RNA 2 sequencing. 3 Value or number of patients (n = 23) Factor Non-smoker or Heavy smoker** light smoker* (n = 8) (n = 15) Median age (years) Median 70 72 Range 63-86 55-77 Sex Female 3 0 Male 5 15 Pathological T status T1 2 4 T2 3 10 T3 2 1 T4 1 0 Pathological N status N0 5 13 N1 1 2 N2 2 0 Pathological stage I 3 10 II, III 5 5 4 5 * ≤ 30 pack years 6 ** > 30 pack years 7 SCC, squamous cell lung cancer 8 9 1 9 Supplementary Table 2. The list of 234 candidate oncogenes of non-/light smoker squamous 10 cell lung cancer patients. 11 2 FAM136A CHAF1A UBE2K NUDT19 CDCA4 SUSD4 PLD1 CDC45 DSCC1 NDUFB4 SLC38A7 RFC4 TIMELESS CCNB2 MCM2 VANGL2 XPO5 DPP3 FAM192A MRPL30 CLCN2 FBXO45 EPHB3 CLN6 MESDC2 TRMU CDCA3 WDYHV1 MARVELD3 ISY1 DNAH14 EZH2 WDHD1 ALG3 NUP43 CHEK2 NUDT1 PAFAH1B3 TIAL1 SF3B3 KCNMB3 UMPS NUP205 BIRC5 SRRD GGCT MAGEF1 PRC1 NIPSNAP1 RFC2 FAM162A WDR62 CEP250 AK2 GOT2 BCL11A APOBEC3C CKAP4 OLA1 MCM5 EME1 PIGF MTA3 TPI1 NAA50 ACOT11 RNF7 MCM7 ESRP1 NUP37 TP63 TMEM177 LRPPRC PARD6G PREB FAM83H DNAJB11 LIG1 PCYT1A TTC39C VRK1 KIF18B SEC61A1 MOCS3 UGGT1 ABCC5 AVL9 FXYD3 TIMM8A ZNRF1 IQGAP3 TK1 C5orf34 AAGAB UCK2 C1orf112 YIPF4 SH3BP1 DTYMK DLEU1 POLQ RECQL4 LSM5 DCAF4 TBRG4 BLM SPAG5 E2F7 SAE1 MFSD9 PSME4 FEN1 PSMD11 NKRF PLEKHA8 RNASEH2A EFNA4 ABCF3 KIAA1522 SHMT2 DLX5 ASPM EIF4EBP1 XRCC3 GPN1 C8orf44 CPSF3 NUP155 FOXM1 MRPS22 TOP2A C17orf53 RAD51 DSN1 TPX2 AP2M1 LRFN1 C19orf48 SEMA4B DNAJA3 MTIF2 COX16 CDC6 POLE2 CKAP2 ATP6V1C2 PPIL2 STAP2 TMEM189 VOPP1 POLR2H POLA2 CCNE1 ANKRD52 POLR1D FKBP3 FANCI FBXO27 CSE1L MELK 3 GAPDH TRIP13 PARP16 SLC12A8 SDHAP1 SLC5A6 LMNB2 DCAF13 NCBP2 MTBP C2orf68 BCL2L12 GSS KDELR2 DEPDC5 CEP72 MAP7 SNRPD1 SIAH2 EIF2B5 YDJC ESPL1 GTSE1 TDP1 CHAF1B PRIM2 UNC119 ASF1B PLEKHG3 SRD5A1 CENPA FARSB ECE2 DCTN5 SKP2 ALG1L PSMD2 CSNK1G1 OIP5 MRPL47 CDCA7 TRAF3 WDR53 POP5 ACAD9 UBE2T TUBG1 CRIPT TMEM41A SNRPA1 STX6 NIT2 PSMD7 GINS1 PLEKHG6 KPTN MRPL42 EIF2S3 TCF3 ZNF74 NIF3L1 METTL2A CNP CIAO1 HPS4 IRF6 CCDC137 EXO1 RANBP1 PAWR NUF2 CENPO YKT6 GTF2E1 11 12 13 4 13 Supplementary Table 3. The list of 968 candidate oncogenes of heavy smoker squamous cell 14 lung cancer patients 15 16 5 GPATCH1 FKBP3 CDCA3 SNRPD3 SMG5 KIAA0907 RNF187 EZH2 RBM34 WDYHV1 DTNB RPS7 CLPB POLA2 CCNB1IP1 FAM136A GAPDH UBA5 FANCI WDHD1 TNRC6B SLC5A6 TMEM138 TRIP13 PAFAH1B3 FAM118A FUNDC1 ATIC LMNB2 MRPS14 SLC38A7 WDR92 NUDT1 TCF19 SPRYD4 XYLT2 XRCC2 DVL3 GEN1 PA2G4 MLF2 C2orf68 C1orf131 POFUT1 TMEM206 CBX1 AFMID CADM4 FXR1 MPP6 TCF20 FBL COX10 CDK2AP1 RAD51C TCTEX1D2 SMARCD1 UMPS PHF13 FBXL20 HAUS5 RNASEH1 TUBB TOMM34 C17orf75 KLRG2 TMEM17 TRIM28 TTC9C NUP205 CLCN2 GMNN MAGEF1 GNGT1 PDIA4 ABCA5 SIAH2 EDC3 PACSIN3 LIMK2 MOGS GTSE1 NUP85 DNAJC19 LTBR ATP11B ATMIN THUMPD3 GRK7 PRC1 TRMU ZNF3 FETUB TTF2 TMEM106C DNAH14 CLK2 ACBD6 KIF14 UBE2E3 CHEK2 MSI2 CDK4 EIF3B PDXP YEATS2 UNC119 PRPS2 LRRC42 CEP250 PPM1G ARHGAP8 RAD9A BCL2L12 MTA3 SGPL1 CENPA HDGF CEP72 MCM7 TARBP1 STAR STAMBP GNB5 RCC2 KCNMB3 CHD6 WDR62 AARS2 MARS CBFA2T2 ACTL6A FRMD6 MRPL12 NFRKB USP21 NUP50 BCL7A FARSA SNAP47 GGCT B4GALT4 ZNF174 EIF2B5 PDIA3 KAT2A ZNF786 ZNF623 DNMT3A ANKRD13B GCAT SOX4 C12orf73 ACTR3B TOP1MT SMG7 ZCRB1 RNF7 PSPH NOP56 6 PATZ1 DDX11 TMEM177 PIGX CDK16 ZNF18 WNT3 SMOX TDP1 EBPL ZNF785 BOP1 CEP78 BLCAP PPME1 STON2 DHRS13 STIP1 ASF1B LRPPRC TNK2 PRPSAP1 TRAPPC2 CSNK2A1 MRPL9 FAM162A HOMEZ FAM117B FARSB INTS8 ANKRD16 CCDC77 BRCA1 RPL39L TMEM60 BCL11A MRM1 NIT1 PYCR2 ANAPC1 SOX2 TOR3A DNAJB11 MCM8 PIK3R2 FOXRED2 SKP2 ZNF138 POMT2 HRG EME1 FZR1 FAM83G ALG1L STOML2 MYPOP PARP1 ZNF572 DNMT1 BRIX1 OTX1 PSMG3 PRCC SNRPG FANCF GEMIN6 SNRPF SIGMAR1 BDH1 ZSWIM1 TP63 RUSC1 NUCKS1 P4HB LIG1 KCTD1 ATP5G1 KIF18B MRPL47 SEC61A1 CAD CCDC142 ZWILCH ALG8 UBXN2A SSR3 SLC25A39 SHOX2 EFTUD2 CEBPG LYSMD1 WDR53 SUPT16H LIN9 ANLN NUP133 CENPF CCT3 CRIPT KRBA1 FAM83H TUBG1 AVL9 KDM1A C5orf34 VRK1 PRPSAP2 RPAP1 TFDP2 HDAC1 NCS1 XPNPEP3 ERAL1 NIT2 SH3BP1 CD3EAP SEMA4F MRPL35 GLRX5 LSM5 ZC3H8 TRIB3 RRM2 KPTN FBXO48 ABCC5 CDK5 TK1 ASCC2 MRPL51 IQGAP3 TPRKB RFC5 CHD1L BRIP1 HRASLS STX6 UBE2O COPS7A NRBP1 C1orf112 CASP2 SNRNP200 ZNF74 MED10 CAPN1 PLEKHG6 DBF4B CBX8 LSM2 POLQ OCIAD2 INPP5F PPP2R3A PSMD11 CCDC58 KIF3C ALDOC BICD2 PSMD3 7 LSM14B DERL1 RECQL4 CIAO1 RSRC1 MKKS DDOST CCT7 EXO1 GYS1 ALDH18A1 TLCD1 NAT9 CENPO HNRNPA3 NOL10 HDAC2 SHROOM2 KLHL12 ABCF3 DDX10 RNF43 RBM8A UBE2K ODF2 NCAPD2 CCT4 PGAM1 CDC45 TOMM40 DLG1 TCF3 NPLOC4 GMPS NMNAT3 PDCD5 CNP IDH2 SUMO2 CENPL WDR12 CCDC137 HTATIP2 GTF3C2 CPSF4 BLM NUF2 SPAG5 TIMELESS EIF4EBP1 SUPT7L MRPS16 CUL7 TIMM8B CSNK1E PSME4 CHAF1A YARS DPP3 C1orf74 GTF2F2 DHX35 PARL VPS72 MRPS23 DCAKD PDAP1 FEN1 CAMK2N2 COX5A RARS2 CS USP5 MDH2 RPA1 NUPL2 ZNF251 LANCL2 EPHB3 NUP155 CCHCR1 MORC2 USP39 BLMH MAPK13 KLHL24 QSOX2 ASPM TFR2 LIPT2 TP53BP1 NDC80 METTL8 PRDX4 HSPE1 RNASEH2A RAB40B FBXO46 RANGAP1 LLGL1 PAK1 ATAD5 CBX3 CSTF1 C19orf48 RNF215 PLD1 NACC1 PSMA1 CDC6 TOP2A ZNF133 VPS37D GPR19 DUT DVL2 RFC4 CPSF3 CDC25B ADM2 PHB2 XPO5 FAM189B TUBGCP4 KIF20B ACP1 CDAN1 C17orf53 GINS4 SNRPE AP2M1 FLAD1 LRFN1 TSPAN33 UCHL3 MTIF2 CCT6A COPZ1 TBL2 STAP2 EXOSC3 FKBP4 ECT2 TSSC1 EXOSC2 PVT1 ABHD10 NKIRAS2 RAD51AP1 LIMK1 TMEM99 RCCD1 SMARCD2 SALL4 IGF2BP2 LSM4 TTPAL MSH6 SEC61G ILF2 8 TRAF7 PSMC3IP ZNF367 PNPT1 TBX1 MAP6D1 FBXO45 UBAP2 STRADA DHCR7 POLR2H TMEM81 NAA20 RPF2 SPATA5L1 DTL UBAP2L C12orf65 RNF216 CCNE1 MRPS7 PDCD11 RNPS1 SPATS2 RRM1 ATXN10 CKS2 PRMT3 TRIM37 PRPF19 PDHA1 CDK6 RABIF CENPN ANAPC7 PARP16 USP35 DSG2 DBF4 PREB PPIL1 TMEM5 PARD3 DAP3 DPY30 NAT10 ETFA AAGAB HMBS UGGT1 ZNF212 HCCS DTYMK CDCA7L SLC25A12 MRPS10 DCUN1D5 C12orf66 GPR89A MYBL2 DCAF13 RAE1 NOL8 ABCB9 C1QBP LDHB GRTP1 IPPK PHF5A LRRC28 METTL1 NIF3L1 ACO2 METTL2A TXN WDR5 GTPBP3 SRPRB SMC2 TBC1D7 TSFM HPS4 TIPIN DNAJC9 EPHA1 LSG1 RANBP1 SAE1 CISD1 SLC1A5 IMPA2 TYRO3 TMX2 NANP FSCN1 NOP2 ZNF687 TIMM17A PRMT1 UCK2 SMYD5 ERGIC2 SOX12 TTK PLOD1 MRPS30 GSK3B NKRF FN3KRP EIF2AK1 TIGD2 SAAL1 MRPL45 DDB1 DHX32 PFN2 YKT6 E2F1 CRNKL1 EIF3H UNG NMT1 LAPTM4B CLNS1A PDCD2L L2HGDH NDUFA9 XRCC3 C2orf49 TBRG4 GSS DSCC1 SHCBP1 NEK2 ANP32B MRPL36 RPL22L1 SLC20A2 PDIA6 MFSD9 MRPL13 DDX31 ANAPC5 RNF26 MARCKSL1 DENND1A MAST2 EIF5A2 ENO1 PEX10 CCT5 VPS25 DCTPP1 KIAA1524 PCNA TACO1 TOPBP1 AHCY EPRS SERPINH1 9 ZDHHC13 MCM3 FOXM1 KPNA2 RUVBL1 FIGNL1 PDCL3 PYGO2 TYMS MAPKAP1 MAP7 MITD1 BET1 TPD52 PLEKHA8 GTF2IRD1 RPGRIP1L GNPAT HRAS CORO2A YDJC MRPL18 MEN1 FRMD8 PABPC1 COPB2 PRKAB2 DSN1 POLE3 FOXRED1 MYO19 IMMT KIF18A IMPDH1 OTUB2 NUDT5 POLDIP2 POLE2 UBE2C SHMT2 ZNF706 PRPF4 PFDN4 YARS2 GPN1 CHAF1B MAGOHB SMARCB1 GLI4 RIPK4 PLEKHG3 RPAP2 C12orf29 CKAP5 PNPLA4 FGF12 DTD1 TFB1M CDCA4 RPLP0 EIF4G1 IGSF11 DLGAP5 METTL5 TAF6 RHBDD3 EIF3M PIGU NCAPH MRPS28 VARS2 POLR3K CSE1L COX7A2L WDR77 RAP2B UBE2S TARBP2 FAM57A TPX2 ECE2 SARS2 SSRP1 NDUFB4 PAICS ZNF496 BAIAP2L1 COIL MCM2 DNAJA3 TRIT1 RBM28 SRD5A3 ANP32A FAM102A PPAT MARVELD3 MRPS33 IPO9 MICALL1 NFS1 TBCE SLC12A8 STEAP1 EMG1 ADCK5 PSMB5 YTHDF1 GARS MTX2 ABHD4 AMZ2 GOSR2 MRPL30 FOXK1 TIMM9 GPI TFG BID NME2 ENTPD6 METAP1 NCBP2 PSMD14 NAE1 TUFT1 RNF121 TMEM147 HARBI1 REPS1 PSMD2 SUB1 METTL13 BUB3 KDELR1 NDUFB3 SKA1 AURKA PSMC4 FBXL18 GANAB APEX1 METTL2B AVEN NUDT21 UAP1L1 NUP62 ARHGEF5 TM9SF4 SH3BP5L MAZ SDCCAG3 NME1 ELMOD2 QPCTL EARS2 HNRNPD ZMYND19 PREP TARS 10 B4GALT2 SEC22A FAM104A CCDC86 MELK TOMM22 PTPRF DNMT3B DENR GTF2E2 LTB4R ZNF606 KDELR2 UBFD1 NDUFB5 DKC1 ZNF343 SAMM50 MMACHC ADSL DARS2 TCFL5 CLDND1 POLR2G CHEK1 NRM RACGAP1 SNRPD1 ISY1 VCP VAPB ALG3 GLG1 DOLPP1 ATP6V1E2 TBL1XR1 PALB2 CDCA5 SNRPD2 MTBP GTPBP8 TSEN15 DIABLO NUP43 CDKN3 TRIM59 TIAL1 TYSND1 SF3B3 MCM5 ELAVL1 SKA2 PRIM2 SLC25A10 RPA3 HYOU1 RAI1 CD276 PCCB DDTL ACAD9 PARP2 AHSG GTPBP10 NAA50 RBL1 ATP5G3 SRD5A1 CYC1 TCP11L1 NAPB RABEPK CKS1B NR2C2AP ATAD2 MSTO1 JAG2 FAM173B RPP30 PWP1 PLEK2 BIRC5 BOLA3 GLE1 NUP37 EIF2A NIPSNAP1 DYRK2 SRRD MTCH2 MPHOSPH9 POLR2D GGH C20orf24 WDR75 AARS EIF2AK2 CSNK1G1 MCM4 OST4 UBE2M OLA1 TTLL12 DHX37 TAF1D ASNS MRPL48 MRPL11 RFC2 PPP1R14B RAD54B RPN1 MRPS24 GOT2 GINS1 MRPS17 TPI1 TRAF3 MIF SRP68 ZP3 AP1S1 UBE2T KLC2 TRUB2 DRG1 ESRP1 PGAM5 THOP1 FANCC SLC25A17 PARD6G SLC37A4 RAN EIF2S3 SS18L1 RCC1 PSMD4 CCDC134 TMEM41A NF2 GLRX3 11 MRPL17 TRAP1 BZW2 PSMD7 MRPL42 FANCG SNRPB CLTCL1 SERBP1 UBE2Z RPN2 MRPL3 INTS7 FBXO22 PCYT1A DUS4L PYCR1 MOCS3 HNRNPL SMYD3 PHB NCBP1 NIPA1 WNT7B MTHFD1 SNRPA1 16 17 12 17 18 19 20 21 Supplementary Table 4. The list of 188 candidate oncogenes which are common to non-/light 22 and heavy smoker SCC patients and the results of log rank test of median overall survival (OS) 23 and recurrence free survival (RFS) based on The Cancer Genome Atlas dataset. 24 25 Prognosis Effect of high- Gene expression on OS RFS prognosis (p-value) (p-value) FAM136A 0.002 0.411 SLC38A7 0.004 0.019 Poor CLCN2 0.006 0.049 Good TRMU 0.008 0.096 DNAH14 0.008 0.636 CHEK2 0.008 0.036 Good KCNMB3 0.011 0.744 GGCT 0.018 0.111 FAM162A 0.024 0.006 Good BCL11A 0.025 0.123 EME1 0.026 0.427 TP63 0.028 0.205 FAM83H 0.033 0.734 VRK1 0.033 0.028 Good ABCC5 0.035 0.090 IQGAP3 0.035 0.583 C1orf112 0.037 0.297 POLQ 0.038 0.043 Good BLM 0.044 0.189 PSME4 0.045 0.756 RNASEH2A 0.050 0.027 13 TOP2A 0.052 0.529 AP2M1 0.056 0.032 MTIF2 0.056 0.894 POLR2H 0.061 0.014 FKBP3 0.063 0.457 GAPDH 0.065 0.417 SLC5A6 0.065 0.859 C2orf68 0.067 0.174 SIAH2 0.072 0.041 GTSE1 0.076 0.907 UNC119 0.077 0.002 CENPA 0.079 0.978 SKP2 0.096 0.045 WDR53 0.103 0.297 TUBG1 0.104 0.354 STX6 0.114 0.537 PLEKHG6 0.115 0.526 TCF3 0.120 0.499 CNP 0.124 0.130 CCDC137 0.124 0.313 NUF2 0.126 0.740 CHAF1A 0.127 0.068 PLD1 0.136 0.681 RFC4 0.138 0.223 XPO5 0.139 0.278 FBXO45 0.145 0.627 CDCA3 0.146 0.705 EZH2 0.149 0.068
Recommended publications
  • Translational Control in Cancer Etiology
    Downloaded from http://cshperspectives.cshlp.org/ on October 1, 2021 - Published by Cold Spring Harbor Laboratory Press Translational Control in Cancer Etiology Davide Ruggero Helen Diller Cancer Center, School of Medicine, University of California, San Francisco, California 94158 Correspondence: [email protected] The link between perturbations in translational control and cancer etiology is becoming a primary focus in cancer research. It has now been established that genetic alterations in several components of the translational apparatus underlie spontaneous cancers as well as an entire class of inherited syndromes known as “ribosomopathies” associated with in- creased cancer susceptibility. These discoveries have illuminated the importance of dereg- ulations in translational control to very specific cellular processes that contribute to cancer etiology. In addition, a growing body of evidence supports the view that deregulation of translational control is a common mechanism by which diverse oncogenic pathways promote cellular transformation and tumor development. Indeed, activation of these key oncogenic pathways induces rapid and dramatic translational reprogramming both by in- creasing overall protein synthesis and by modulating specific mRNA networks. These trans- lational changes promote cellular transformation, impacting almost every phase of tumor development. This paradigm represents a new frontier in the multihit model of cancer for- mation and offers significant promise for innovative cancer therapies. Current research,
    [Show full text]
  • Title a New Centrosomal Protein Regulates Neurogenesis By
    Title A new centrosomal protein regulates neurogenesis by microtubule organization Authors: Germán Camargo Ortega1-3†, Sven Falk1,2†, Pia A. Johansson1,2†, Elise Peyre4, Sanjeeb Kumar Sahu5, Loïc Broic4, Camino De Juan Romero6, Kalina Draganova1,2, Stanislav Vinopal7, Kaviya Chinnappa1‡, Anna Gavranovic1, Tugay Karakaya1, Juliane Merl-Pham8, Arie Geerlof9, Regina Feederle10,11, Wei Shao12,13, Song-Hai Shi12,13, Stefanie M. Hauck8, Frank Bradke7, Victor Borrell6, Vijay K. Tiwari§, Wieland B. Huttner14, Michaela Wilsch- Bräuninger14, Laurent Nguyen4 and Magdalena Götz1,2,11* Affiliations: 1. Institute of Stem Cell Research, Helmholtz Center Munich, German Research Center for Environmental Health, Munich, Germany. 2. Physiological Genomics, Biomedical Center, Ludwig-Maximilian University Munich, Germany. 3. Graduate School of Systemic Neurosciences, Biocenter, Ludwig-Maximilian University Munich, Germany. 4. GIGA-Neurosciences, Molecular regulation of neurogenesis, University of Liège, Belgium 5. Institute of Molecular Biology (IMB), Mainz, Germany. 6. Instituto de Neurociencias, Consejo Superior de Investigaciones Científicas and Universidad Miguel Hernández, Sant Joan d’Alacant, Spain. 7. Laboratory for Axon Growth and Regeneration, German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany. 8. Research Unit Protein Science, Helmholtz Centre Munich, German Research Center for Environmental Health, Munich, Germany. 9. Protein Expression and Purification Facility, Institute of Structural Biology, Helmholtz Center Munich, German Research Center for Environmental Health, Munich, Germany. 10. Institute for Diabetes and Obesity, Monoclonal Antibody Core Facility, Helmholtz Center Munich, German Research Center for Environmental Health, Munich, Germany. 11. SYNERGY, Excellence Cluster of Systems Neurology, Biomedical Center, Ludwig- Maximilian University Munich, Germany. 12. Developmental Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, USA 13.
    [Show full text]
  • Isoform-Specific Monobody Inhibitors of Small Ubiquitin-Related Modifiers Engineered Using Structure-Guided Library Design
    Isoform-specific monobody inhibitors of small ubiquitin-related modifiers engineered using structure-guided library design Ryan N. Gilbretha, Khue Truongb, Ikenna Madub, Akiko Koidea, John B. Wojcika, Nan-Sheng Lia, Joseph A. Piccirillia,c, Yuan Chenb, and Shohei Koidea,1 aDepartment of Biochemistry and Molecular Biology, and cDepartment of Chemistry, University of Chicago, 929 East 57th Street, Chicago, IL 60637; and bDepartment of Molecular Medicine, Beckman Research Institute of the City of Hope, 1450 East Duarte Road, Duarte, CA 91010 Edited by David Baker, University of Washington, Seattle, WA, and approved March 16, 2011 (received for review February 10, 2011) Discriminating closely related molecules remains a major challenge which SUMOylation alters protein function appears to be in the engineering of binding proteins and inhibitors. Here we through SUMO-mediated interactions with other proteins con- report the development of highly selective inhibitors of small ubi- taining a short peptide motif known as a SUMO-interacting motif quitin-related modifier (SUMO) family proteins. SUMOylation is (SIM) (4, 7, 8). involved in the regulation of diverse cellular processes. Functional There are few inhibitors of SUMO/SIM interactions, a defi- differences between two major SUMO isoforms in humans, SUMO1 ciency that limits our ability to finely dissect SUMO biology. In and SUMO2∕3, are thought to arise from distinct interactions the only reported example of such an inhibitor, a SIM-containing mediated by each isoform with other proteins containing SUMO- linear peptide was used to inhibit SUMO/SIM interactions, estab- interacting motifs (SIMs). However, the roles of such isoform- lishing their importance in coordinating DNA repair by nonho- specific interactions are largely uncharacterized due in part to the mologous end joining (9).
    [Show full text]
  • Computational Genome-Wide Identification of Heat Shock Protein Genes in the Bovine Genome [Version 1; Peer Review: 2 Approved, 1 Approved with Reservations]
    F1000Research 2018, 7:1504 Last updated: 08 AUG 2021 RESEARCH ARTICLE Computational genome-wide identification of heat shock protein genes in the bovine genome [version 1; peer review: 2 approved, 1 approved with reservations] Oyeyemi O. Ajayi1,2, Sunday O. Peters3, Marcos De Donato2,4, Sunday O. Sowande5, Fidalis D.N. Mujibi6, Olanrewaju B. Morenikeji2,7, Bolaji N. Thomas 8, Matthew A. Adeleke 9, Ikhide G. Imumorin2,10,11 1Department of Animal Breeding and Genetics, Federal University of Agriculture, Abeokuta, Nigeria 2International Programs, College of Agriculture and Life Sciences, Cornell University, Ithaca, NY, 14853, USA 3Department of Animal Science, Berry College, Mount Berry, GA, 30149, USA 4Departamento Regional de Bioingenierias, Tecnologico de Monterrey, Escuela de Ingenieria y Ciencias, Queretaro, Mexico 5Department of Animal Production and Health, Federal University of Agriculture, Abeokuta, Nigeria 6Usomi Limited, Nairobi, Kenya 7Department of Animal Production and Health, Federal University of Technology, Akure, Nigeria 8Department of Biomedical Sciences, Rochester Institute of Technology, Rochester, NY, 14623, USA 9School of Life Sciences, University of KwaZulu-Natal, Durban, 4000, South Africa 10School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA, 30032, USA 11African Institute of Bioscience Research and Training, Ibadan, Nigeria v1 First published: 20 Sep 2018, 7:1504 Open Peer Review https://doi.org/10.12688/f1000research.16058.1 Latest published: 20 Sep 2018, 7:1504 https://doi.org/10.12688/f1000research.16058.1 Reviewer Status Invited Reviewers Abstract Background: Heat shock proteins (HSPs) are molecular chaperones 1 2 3 known to bind and sequester client proteins under stress. Methods: To identify and better understand some of these proteins, version 1 we carried out a computational genome-wide survey of the bovine 20 Sep 2018 report report report genome.
    [Show full text]
  • Mutations in DCPS and EDC3 in Autosomal Recessive Intellectual
    Human Molecular Genetics, 2015, Vol. 24, No. 11 3172–3180 doi: 10.1093/hmg/ddv069 Advance Access Publication Date: 20 February 2015 Original Article Downloaded from ORIGINAL ARTICLE Mutations in DCPS and EDC3 in autosomal recessive intellectual disability indicate a crucial role for mRNA http://hmg.oxfordjournals.org/ decapping in neurodevelopment Iltaf Ahmed1,2,†, Rebecca Buchert3,†, Mi Zhou5,†, Xinfu Jiao5,†, Kirti Mittal1, Taimoor I. Sheikh1, Ute Scheller3, Nasim Vasli1, Muhammad Arshad Rafiq1, 6 1 7 2 M. Qasim Brohi , Anna Mikhailov , Muhammad Ayaz , Attya Bhatti , at Universitaet Erlangen-Nuernberg, Wirtschafts- und Sozialwissenschaftliche Z on August 15, 2016 Heinrich Sticht4, Tanveer Nasr8,9, Melissa T. Carter10, Steffen Uebe3, André Reis3, Muhammad Ayub7,11, Peter John2, Megerditch Kiledjian5,*, John B. Vincent1,12,13,* and Rami Abou Jamra3,* 1Molecular Neuropsychiatry and Development Lab, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, 250 College Street, Toronto, Ontario, Canada M5T 1R8, 2Atta-ur-Rehman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST), Islamabad 44000, Pakistan, 3Institute of Human Genetics and 4Bioinformatics, Institute of Biochemistry, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen 91054, Germany, 5Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854, USA, 6Sir Cowasji Jehangir Institute of Psychiatry, Hyderabad, Sindh 71000, Pakistan, 7Lahore Institute of Research and Development,
    [Show full text]
  • Organ Level Protein Networks As a Reference for the Host Effects of the Microbiome
    Downloaded from genome.cshlp.org on October 6, 2021 - Published by Cold Spring Harbor Laboratory Press 1 Organ level protein networks as a reference for the host effects of the microbiome 2 3 Robert H. Millsa,b,c,d, Jacob M. Wozniaka,b, Alison Vrbanacc, Anaamika Campeaua,b, Benoit 4 Chassainge,f,g,h, Andrew Gewirtze, Rob Knightc,d, and David J. Gonzaleza,b,d,# 5 6 a Department of Pharmacology, University of California, San Diego, California, USA 7 b Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, 8 California, USA 9 c Department of Pediatrics, and Department of Computer Science and Engineering, University of 10 California, San Diego California, USA 11 d Center for Microbiome Innovation, University of California, San Diego, California, USA 12 e Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State 13 University, Atlanta, GA, USA 14 f Neuroscience Institute, Georgia State University, Atlanta, GA, USA 15 g INSERM, U1016, Paris, France. 16 h Université de Paris, Paris, France. 17 18 Key words: Microbiota, Tandem Mass Tags, Organ Proteomics, Gnotobiotic Mice, Germ-free Mice, 19 Protein Networks, Proteomics 20 21 # Address Correspondence to: 22 David J. Gonzalez, PhD 23 Department of Pharmacology and Pharmacy 24 University of California, San Diego 25 La Jolla, CA 92093 26 E-mail: [email protected] 27 Phone: 858-822-1218 28 1 Downloaded from genome.cshlp.org on October 6, 2021 - Published by Cold Spring Harbor Laboratory Press 29 Abstract 30 Connections between the microbiome and health are rapidly emerging in a wide range of 31 diseases.
    [Show full text]
  • Ailanthone Inhibits Non-Small Cell Lung Cancer Cell Growth Through Repressing DNA Replication Via Downregulating RPA1
    FULL PAPER British Journal of Cancer (2017) 117, 1621–1630 | doi: 10.1038/bjc.2017.319 Keywords: ailanthone; non-small cell lung cancer; DNA replication; RPA1; Chinese medicine Ailanthone inhibits non-small cell lung cancer cell growth through repressing DNA replication via downregulating RPA1 Zhongya Ni1, Chao Yao1, Xiaowen Zhu1, Chenyuan Gong1, Zihang Xu2, Lixin Wang3, Suyun Li4, Chunpu Zou2 and Shiguo Zhu*,1,3 1Laboratory of Integrative Medicine, School of Basic Medical Sciences, Shanghai University of Traditional Chinese Medicine, 1200 Cai Lun Rd, Shanghai 201203, PR China; 2Department of Internal Classic of Medicine, School of Basic Medical Sciences, Shanghai University of Traditional Chinese Medicine, 1200 Cai Lun Rd, Shanghai 201203, PR China; 3Department of Immunology and Pathogenic Biology, School of Basic Medical Sciences, Shanghai University of Traditional Chinese Medicine, 1200 Cai Lun Rd, Shanghai 201203, PR China and 4Department of Pathology, School of Basic Medical Sciences, Shanghai University of Traditional Chinese Medicine, 1200 Cai Lun Rd, Shanghai 201203, PR China Background: The identification of bioactive compounds from Chinese medicine plays a crucial role in the development of novel reagents against non-small cell lung cancer (NSCLC). Methods: High throughput screening assay and analyses of cell growth, cell cycle, apoptosis, cDNA microarray, BrdU incorporation and gene expression were performed. Results: Ailanthone (Aila) suppressed NSCLC cell growth and colony formation in vitro and inhibited NSCLC tumour growth in subcutaneously xenografted and orthotopic lung tumour models, leading to prolonged survival of tumour-bearing mice. Moreover, Aila induced cell cycle arrest in a dose-independent manner but did not induce apoptosis in all NSCLC cells.
    [Show full text]
  • Table S1 the Four Gene Sets Derived from Gene Expression Profiles of Escs and Differentiated Cells
    Table S1 The four gene sets derived from gene expression profiles of ESCs and differentiated cells Uniform High Uniform Low ES Up ES Down EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol 269261 Rpl12 11354 Abpa 68239 Krt42 15132 Hbb-bh1 67891 Rpl4 11537 Cfd 26380 Esrrb 15126 Hba-x 55949 Eef1b2 11698 Ambn 73703 Dppa2 15111 Hand2 18148 Npm1 11730 Ang3 67374 Jam2 65255 Asb4 67427 Rps20 11731 Ang2 22702 Zfp42 17292 Mesp1 15481 Hspa8 11807 Apoa2 58865 Tdh 19737 Rgs5 100041686 LOC100041686 11814 Apoc3 26388 Ifi202b 225518 Prdm6 11983 Atpif1 11945 Atp4b 11614 Nr0b1 20378 Frzb 19241 Tmsb4x 12007 Azgp1 76815 Calcoco2 12767 Cxcr4 20116 Rps8 12044 Bcl2a1a 219132 D14Ertd668e 103889 Hoxb2 20103 Rps5 12047 Bcl2a1d 381411 Gm1967 17701 Msx1 14694 Gnb2l1 12049 Bcl2l10 20899 Stra8 23796 Aplnr 19941 Rpl26 12096 Bglap1 78625 1700061G19Rik 12627 Cfc1 12070 Ngfrap1 12097 Bglap2 21816 Tgm1 12622 Cer1 19989 Rpl7 12267 C3ar1 67405 Nts 21385 Tbx2 19896 Rpl10a 12279 C9 435337 EG435337 56720 Tdo2 20044 Rps14 12391 Cav3 545913 Zscan4d 16869 Lhx1 19175 Psmb6 12409 Cbr2 244448 Triml1 22253 Unc5c 22627 Ywhae 12477 Ctla4 69134 2200001I15Rik 14174 Fgf3 19951 Rpl32 12523 Cd84 66065 Hsd17b14 16542 Kdr 66152 1110020P15Rik 12524 Cd86 81879 Tcfcp2l1 15122 Hba-a1 66489 Rpl35 12640 Cga 17907 Mylpf 15414 Hoxb6 15519 Hsp90aa1 12642 Ch25h 26424 Nr5a2 210530 Leprel1 66483 Rpl36al 12655 Chi3l3 83560 Tex14 12338 Capn6 27370 Rps26 12796 Camp 17450 Morc1 20671 Sox17 66576 Uqcrh 12869 Cox8b 79455 Pdcl2 20613 Snai1 22154 Tubb5 12959 Cryba4 231821 Centa1 17897
    [Show full text]
  • Defining Functional Interactions During Biogenesis of Epithelial Junctions
    ARTICLE Received 11 Dec 2015 | Accepted 13 Oct 2016 | Published 6 Dec 2016 | Updated 5 Jan 2017 DOI: 10.1038/ncomms13542 OPEN Defining functional interactions during biogenesis of epithelial junctions J.C. Erasmus1,*, S. Bruche1,*,w, L. Pizarro1,2,*, N. Maimari1,3,*, T. Poggioli1,w, C. Tomlinson4,J.Lees5, I. Zalivina1,w, A. Wheeler1,w, A. Alberts6, A. Russo2 & V.M.M. Braga1 In spite of extensive recent progress, a comprehensive understanding of how actin cytoskeleton remodelling supports stable junctions remains to be established. Here we design a platform that integrates actin functions with optimized phenotypic clustering and identify new cytoskeletal proteins, their functional hierarchy and pathways that modulate E-cadherin adhesion. Depletion of EEF1A, an actin bundling protein, increases E-cadherin levels at junctions without a corresponding reinforcement of cell–cell contacts. This unexpected result reflects a more dynamic and mobile junctional actin in EEF1A-depleted cells. A partner for EEF1A in cadherin contact maintenance is the formin DIAPH2, which interacts with EEF1A. In contrast, depletion of either the endocytic regulator TRIP10 or the Rho GTPase activator VAV2 reduces E-cadherin levels at junctions. TRIP10 binds to and requires VAV2 function for its junctional localization. Overall, we present new conceptual insights on junction stabilization, which integrate known and novel pathways with impact for epithelial morphogenesis, homeostasis and diseases. 1 National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London SW7 2AZ, UK. 2 Computing Department, Imperial College London, London SW7 2AZ, UK. 3 Bioengineering Department, Faculty of Engineering, Imperial College London, London SW7 2AZ, UK. 4 Department of Surgery & Cancer, Faculty of Medicine, Imperial College London, London SW7 2AZ, UK.
    [Show full text]
  • Supplementary Table 1. Primer Sequences Used in RT-PCR Analysis
    Supplementary Table 1. Primer sequences used in RT-PCR analysis L32 Forward TGAAGCAGGCATCTGAGGG Reverse CGAAGGTGGAAGAG TGGGAG LIFR Forward CTCTCAGGCCAGAGTTGAGC Reverse GCTGTTCAGTCAGCCCTCTC CCR2 Forward TGTCTTCCCTGAATTGAGCC Reverse AAACGCATTAGTGGACAGGG IL12R Forward CGCAATACGTCGTGCGCTGC Reverse CACTCTGACTCCCACGCGCC CSF1R Forward GCTGGTGCGGATTCGAGGGG Reverse TTCGGCGTTAGTGGCCGAGC TGFbR1 Forward ACGCGCTGACATCTATGCAA Reverse CGTCGAGCAATTTCCCAGAA TGFbR2 Forward GCGCATCGCCAGCACGATCC Reverse TGGGCTTCCATTTCCACATCCGA CXCR1 Forward TCCTCCTGCCGCTGCTCACT Reverse CATGCGCAGTGTGAGCCCGT CXCR2 Forward CCTCGTGCCGCTGCTCATCA Reverse GGTGCGCAGTGTGAACCCGT CXCR3 Forward GGTCGCACTGCTCTGCGTGT Reverse GGGGCAGCAGGAAACCAGCC CXCR4 Forward GAGGCGTTTGGTGCTCCGGT Reverse TCGGTTCCATGGCAACACTCGC VEGFR1 (Flt1) Forward CGCGTGAAGAGTGGGTCCT Reverse CACATGCACGGAGGTGTTG VEGFR2 (Flk1) Forward AGCCCAGACTGTGTCCCGCA Reverse GGTGTCCGCGGAATCGGGTC VEGFR3 (Flt4) Forward GCCCGAGGACGAGGGTGACT Reverse CCTGGCTGCGCCTATCCTGC human Flt1 Forward GCACGTCAGCGAAGGCAAGC Reverse CCAGCTCAGCGTGGTCGTAGG Supplementary Table 2. List of putative miR-200 target genes amplified in human cancers amplified in cancers (Tumorscape)a Gene Symbol Title various cancers NSCLC PCT Errfi1 ERBB receptor feedback inhibitor 1 - yes 0.94 D11Bwg0517e DNA segment, Chr 11, Brigham & Women's Genetics 0517 expressed - yes 0.91 Pvrl4 poliovirus receptor-related 4 yes - 0.91 Mecp2 methyl CpG binding protein 2 yes yes 0.9 Jun Jun oncogene yes - 0.88 Prdm16 PR domain containing 16 - yes 0.88 Flt1 FMS-like tyrosine kinase 1 yes
    [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]
  • Roles of Ubiquitination and Sumoylation in the Regulation of Angiogenesis
    Curr. Issues Mol. Biol. (2020) 35: 109-126. Roles of Ubiquitination and SUMOylation in the Regulation of Angiogenesis Andrea Rabellino1*, Cristina Andreani2 and Pier Paolo Scaglioni2 1QIMR Berghofer Medical Research Institute, Brisbane City, Queensland, Australia. 2Department of Internal Medicine, Hematology and Oncology; University of Cincinnati, Cincinnati, OH, USA. *Correspondence: [email protected] htps://doi.org/10.21775/cimb.035.109 Abstract is tumorigenesis-induced angiogenesis, during Te generation of new blood vessels from the which hypoxic and starved cancer cells activate existing vasculature is a dynamic and complex the molecular pathways involved in the formation mechanism known as angiogenesis. Angiogenesis of novel blood vessels, in order to supply nutri- occurs during the entire lifespan of vertebrates and ents and oxygen required for the tumour growth. participates in many physiological processes. Fur- Additionally, more than 70 diferent disorders have thermore, angiogenesis is also actively involved been associated to de novo angiogenesis including in many human diseases and disorders, including obesity, bacterial infections and AIDS (Carmeliet, cancer, obesity and infections. Several inter-con- 2003). nected molecular pathways regulate angiogenesis, At the molecular level, angiogenesis relays on and post-translational modifcations, such as phos- several pathways that cooperate in order to regulate phorylation, ubiquitination and SUMOylation, in a precise spatial and temporal order the process. tightly regulate these mechanisms and play a key In this context, post-translational modifcations role in the control of the process. Here, we describe (PTMs) play a central role in the regulation of these in detail the roles of ubiquitination and SUMOyla- events, infuencing the activation and stability of tion in the regulation of angiogenesis.
    [Show full text]