DOCSLIB.ORG

1 Reference Sequence Number Gene Symbol Alleles Chromosomal

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

1 Supplemental Table 1. 10,177 non-synonymous single nucleotide polymorphisms on ParAllele panel; the San Francisco Bay Area Adult Glioma Study Minor Allele Minor Allele Reference Sequence Chromosomal Frequency, Frequency, Number Gene Symbol Alleles Location Minor Allele Case Control P-value* rs8289 FUT6, M6PRBP1 A/G 19p A 0.357798165 0.188073394 0.000141 rs10495960 LHCGR, GTF2A1L A/G 02p A 0.102678571 0.245454545 0.000145 rs1195889 GPR133 A/G 12q A 0.339285714 0.495495495 0.000547 rs11076585 C/T 16q T 0.147321429 0.290178571 0.00055 rs10415562 OR7C1 C/T 19p C 0.294642857 0.183035714 0.000805 rs7955866 FGF23 A/G 12p A 0.163636364 0.049549549 0.001078 rs3765083 MFSD1 A/G 03q A 0.486607143 0.339285714 0.001137 rs12455859 G/T 18p G 0.473214286 0.366071429 0.001248 rs3732548 hCG_1813818 A/C 03p C 0.21875 0.357142857 0.001609 rs1047840 EXO1 A/G 01q A 0.321428571 0.468181818 0.002261 rs10817025 SVEP1 C/T 09q C 0.403061224 0.252747253 0.002461 rs1265054 C6orf15 A/G 06p A 0.382882883 0.468468468 0.002688 rs319522 GPC6 A/G 13q G 0.40625 0.455357143 0.003242 rs7522157 CLCC1, C1orf62 C/T 01p T 0.254464286 0.382882883 0.003275 rs2017467 A/G 11q A 0.068181818 0.155963303 0.003282 rs4272850 TMEM132C A/G 12q A 0.294642857 0.178571429 0.003348 rs10490923 ARMS2 A/G 10q A 0.09375 0.196428571 0.003436 rs1129770 CMYA5 A/G 05q A 0.142857143 0.258928571 0.003448 rs2298771 SCN1A A/G 02q G 0.361607143 0.232142857 0.003505 rs6902416 TRDN C/G 06q G 0.1875 0.09009009 0.004266 rs2502601 SYNJ2 C/T 06q T 0.40625 0.459821429 0.0043 rs4691212 G/T 04q G 0.267857143 0.392857143 0.004421 rs3734960 DPP6 C/T 07q C 0.34375 0.218181818 0.004809 rs3817121 CAND2 A/G 03p A 0.245535714 0.138392857 0.005011 rs12610412 ZNF77 C/G 19p G 0.169642857 0.080357143 0.005096 rs2296308 RWDD3 G/T 01p T 0.171171171 0.081081081 0.005159 rs266881 KLK3 A/C 19q A 0.440366973 0.41588785 0.005503 rs1046116 PKP2 C/T 12p C 0.27027027 0.160714286 0.005733 rs2747701 FAM135A A/G 06q A 0.433035714 0.441441441 0.006122 rs4801958 ZNF665 C/T 19q C 0.455357143 0.328828829 0.006323 rs3177253 PECI A/G 06p A 0.223214286 0.339285714 0.006341 rs6949654 tcag7.1314 C/T 07q T 0.178571429 0.089285714 0.006551 Page 1 1 rs3803704 FLJ11171 A/G 16q G 0.321428571 0.205357143 0.006644 rs7022771 A/C 09q A 0.291262136 0.41509434 0.006828 rs10911825 HMCN1 A/G 01q G 0.325892857 0.214285714 0.006939 rs12360890 OR5T1 A/G 11q G 0.459821429 0.325892857 0.007113 rs843971 PGLYRP3 A/G 01q A 0.297297297 0.419642857 0.007251 rs1265053 C6orf15 C/G 06p C 0.341121495 0.476635514 0.007562 rs1657133 A/G 16p G 0.133027523 0.229357798 0.007829 rs10845293 TAS2R44 A/G 12p A 0.416666667 0.462616822 0.007847 rs709564 CCDC54 A/G 03q A 0.196428571 0.299107143 0.008181 rs799661 A/G 14q A 0.068807339 0.138392857 0.008647 rs2862954 ERLIN1 C/T 10q T 0.397321429 0.473214286 0.008824 rs12460170 ZNF665 A/G 19q A 0.45045045 0.330357143 0.009014 rs10896271 OR8K1 A/G 11q G 0.455357143 0.325892857 0.009332 rs998544 OR5R1 C/T 11q T 0.455357143 0.325892857 0.009332 rs511987 A/G 11q G 0.446428571 0.321428571 0.009383 rs10028124 SCLT1 A/T 04q T 0.397321429 0.279279279 0.009603 rs1742429 C16orf73 C/T 16p C 0.126126126 0.21875 0.009638 rs8097835 A/G 18q A 0.383928571 0.490990991 0.009657 rs7226913 OSBPL1A C/T 18q C 0.40625 0.473214286 0.009687 rs3123101 VIL2, SYTL3 A/T 06q T 0.325892857 0.214285714 0.009707 rs1421217 C/T 08q C 0.482142857 0.396396396 0.009864 rs7000148 C8orf68 C/G 08p C 0.415178571 0.290178571 0.009871 rs6235 PCSK1 C/G 05q C 0.223214286 0.339285714 0.01003 rs4590080 LIMCH1 C/G 04p C 0.072072072 0.013513513 0.010241 rs2014576 SIX5 C/T 19q C 0.387387387 0.490990991 0.010394 rs911391 A/C 16p A 0.133027523 0.227678571 0.010747 rs1056320 MGC24039 A/C 12p A 0.160714286 0.075892857 0.010755 rs2022923 MGC39715 A/G 08q G 0.355855856 0.472972973 0.010953 rs3783941 TSHR G/T 14q G 0.400900901 0.285714286 0.011044 rs10888390 CTSS A/G 01q A 0.303571429 0.424107143 0.011053 rs2242373 FLJ35773 C/T 17p T 0.125 0.214285714 0.011096 rs4555873 C/T 05q T 0.378378378 0.258928571 0.011157 rs3118574 A/G 09q A 0.272321429 0.382882883 0.01122 rs3806692 LOC401068 C/G 03p C 0.129464286 0.058035714 0.011288 rs9639168 ETV1 C/T 07p C 0.294642857 0.410714286 0.01153 rs12115750 LOC402377 A/C 09q A 0.085585586 0.160714286 0.011651 rs1935 JMJD1C C/G 10q G 0.436936937 0.449074074 0.011651 Page 2 1 rs2458236 DUOX1 C/T 15q C 0.413636364 0.296296296 0.012023 rs2898904 A/G 11p G 0.439814815 0.327102804 0.012136 rs5748648 XKR3 A/G 22q A 0.107142857 0.045045045 0.012189 rs12096753 TRIM67 C/T 01q C 0.111607143 0.205357143 0.012308 rs3813636 C1orf49 G/T 01q G 0.469072165 0.403061224 0.012503 rs649058 TNNI3K A/G 01p G 0.491071429 0.397321429 0.012544 rs9806945 C16orf73 A/G 16p G 0.131818182 0.223214286 0.01258 rs1553316 HAVCR1 C/T 05q T 0.09375 0.174107143 0.01259 rs2285374 A/G 11q G 0.450892857 0.333333333 0.012642 rs8030587 STARD9 A/G 15q A 0.265765766 0.169642857 0.012652 rs1291212 ZGPAT C/G 20q C 0.09009009 0.032110092 0.012993 rs1006954 ZZEF1 C/T 17p T 0.081081081 0.15625 0.013052 rs10825269 PCDH15 C/T 10q T 0.080357143 0.15625 0.013123 rs10022054 LOC402175 A/G 04p G 0.125 0.053571429 0.013395 rs8023524 CDAN1 A/G 15q A 0.235576923 0.136792453 0.013523 rs2045571 FCGR2B C/T 01q T 0.089622642 0.164948454 0.013544 rs560389 A/G 01p A 0.263392857 0.370535714 0.013678 rs12568310 FLJ35530 C/T 01q T 0.446428571 0.333333333 0.013762 rs2274756 MMP9 A/G 20q A 0.116071429 0.202702703 0.013772 rs9532758 MTRF1 C/T 13q C 0.108108108 0.040178571 0.013823 rs1065838 C16orf45 C/T 16p C 0.316513761 0.213636364 0.013829 rs2637777 FAT G/T 04q G 0.325892857 0.446428571 0.01394 rs10904481 UCN3 A/G 10p G 0.370535714 0.261261261 0.014251 rs1381657 CENPE C/G 04q G 0.217592593 0.135135135 0.014263 rs6234 PCSK1 C/G 05q G 0.225225225 0.336363636 0.014507 rs10817479 WDR31 A/G 09q A 0.095454545 0.036036036 0.014973 rs2306595 MYOHD1 C/T 17q C 0.086363636 0.03125 0.015081 rs2306175 C4orf26 A/G 04q A 0.169642857 0.263392857 0.015123 rs227787 OR3A3 C/T 17p C 0.205357143 0.301801802 0.015262 rs1801516 ATM A/G 11q A 0.098214286 0.183035714 0.015312 rs2208525 G/T 20q T 0.207207207 0.303571429 0.015664 rs2280544 BET1L C/T 11p T 0.207207207 0.303571429 0.015678 rs6983981 C8orf68 A/C 08p C 0.387387387 0.272321429 0.015777 rs3213831 PZP C/T 12p T 0.385321101 0.5 0.01587 rs12568050 ZNF648 C/G 01q C 0.189189189 0.110091743 0.016023 rs4245199 PVRL1 G/T 11q G 0.117117117 0.054545454 0.016052 rs710187 GCAT C/T 22q C 0.482142857 0.403669725 0.016496 Page 3 1 rs10836399 OR51D1 C/G 11p C 0.165178571 0.258928571 0.016558 rs11230600 OR4C6 C/T 11q C 0.339285714 0.232142857 0.016685 rs1459101 OR4C16 A/G 11q A 0.339285714 0.232142857 0.016685 rs4987236 A/G 08p A 0.072072072 0.022522522 0.016757 rs7811042 CCDC129 A/C 07p C 0.368686869 0.260869565 0.016823 rs2266988 PRAME A/G 22q A 0.352678571 0.464285714 0.016995 rs2280205 SLC2A9 A/G 04p G 0.49537037 0.390909091 0.017326 rs3823430 DNAH8 C/T 06p C 0.111607143 0.191964286 0.017409 rs10816 C13orf28 A/T 13q A 0.45045045 0.342342342 0.017653 rs1051624 CDH17 A/C 08q A 0.473214286 0.405405405 0.01772 rs3817672 TFRC A/G 03q G 0.5 0.391891892 0.017722 rs1805127 KCNE1 A/G 21q A 0.308035714 0.419642857 0.017774 rs9850805 A/C 03q A 0.252252252 0.36036036 0.018056 rs627933 C/T 11q C 0.245535714 0.351351351 0.018572 rs4949211 C/T 01p C 0.477272727 0.405660377 0.019046 rs3798130 KIF3A A/G 05q A 0.118181818 0.200892857 0.019145 rs447802 FAM83E C/T 19q C 0.211711712 0.304545454 0.019167 rs2372536 ATIC C/G 02q G 0.267857143 0.375 0.019415 rs626251 C1orf87 C/T 01p C 0.364864865 0.482142857 0.019488 rs4902695 C/T 14q T 0.223214286 0.321428571 0.019609 rs1151625 LIME1, SLC2A4RG C/T 20q T 0.089285714 0.035714286 0.019707 rs9394866 FLJ90086 A/G 06p G 0.459821429 0.433035714 0.020243 rs3733242 SHROOM3 A/G 04q A 0.357142857 0.46875 0.020391 rs966365 EDARADD C/T 01q C 0.133928571 0.214285714 0.020476 rs10851704 VPS13C C/T 15q T 0.424107143 0.463963964 0.020719 rs2074469 OR10C1 A/G 06p G 0.165178571 0.254464286 0.020745 rs10076911 FLJ13231 A/C 05p C 0.160714286 0.089285714 0.020984 rs648614 TNNI3K C/T 01p C 0.477678571 0.418918919 0.021553 rs2609881 ZNF228 A/C 19q C 0.085585586 0.160714286 0.021965 rs10078391 DNAH5 C/T 05p C 0.160714286 0.245535714 0.022032 rs365990 MYH6 A/G 14q G 0.330357143 0.436363636 0.022069 rs6428538 A/G 01p A 0.071428571 0.138392857 0.022254 rs2799123 C/G 09p G 0.400900901 0.292792793 0.022384 rs2799125 C/T 09p T 0.401785714 0.294642857 0.022399 rs10146482 NEK9 C/T 14q T 0.472972973 0.414414414 0.023071 rs2836662 C21orf24 A/T 21q A 0.279279279 0.376146789 0.023109 rs2276976 NHEDC2 A/C 04q C 0.133928571 0.071428571 0.023197 Page 4 1 rs11230864 C/T 11q T 0.454954955 0.34375 0.023216 rs2293172 GIMAP4 A/C 07q A 0.116071429 0.189189189 0.02336 rs10017772 DCHS2 C/T 04q C 0.459821429 0.433035714 0.023585 rs7032785 JAK2 C/T 09p C 0.4375 0.454954955 0.023589 rs9616310 C/G 22q G 0.330357143 0.433035714 0.023786 rs11024970 MRGPRX2 G/T 11p G 0.080357143 0.03125 0.02381 rs1110627 DLL3 A/G 19q A 0.446428571 0.446428571 0.0247 rs376618 FGFR4 A/G 05q G 0.308411215 0.213636364 0.024724 rs2231926 FLJ10213, PPP4R2 A/G 03p A 0.495454546 0.391891892 0.024789 rs3823603 IQCE C/G 07p C 0.222727273 0.325892857 0.024807 rs2486668 GRHL3 C/G 01p C 0.198198198 0.117117117 0.024937 rs10408247 CEACAM20 A/G 19q A 0.142857143 0.075892857 0.025046 rs3741845 TAS2R9 C/T 12p T 0.444444444 0.341584158 0.02512 rs2748404 FLJ43860 G/T 08q G 0.261261261 0.352678571 0.025268 rs7157977 C/T 14q T 0.352678571 0.450450451 0.025358 rs10120210 ECM2, CENPP G/T 09q T 0.481818182 0.372727273 0.025503 rs11568658 ABCC4 G/T 13q T
Recommended publications
  • Chromatin State Barriers Enforce an Irreversible Mammalian Cell Fate Decision

    Chromatin State Barriers Enforce an Irreversible Mammalian Cell Fate Decision

    bioRxiv preprint doi: https://doi.org/10.1101/2021.05.12.443709; this version posted May 14, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Chromatin state barriers… Blanco et al. 2021 Chromatin state barriers enforce an irreversible mammalian cell fate decision M. Andrés Blanco1,19,*,†,, David B. Sykes6,8,19, Lei Gu2,15,17,18,19, Mengjun Wu2,4,15, Ricardo Petroni1, Rahul Karnik7,8,9, Mathias Wawer10, Joshua Rico1, Haitao Li1, William D. Jacobus2,12,15, Ashwini Jambhekar2,15,11, Sihem Cheloufi5, Alexander Meissner7,8,9,13, Konrad Hochedlinger6,7,8,14, David T. Scadden6,8,9,*, and Yang Shi2,3,* 1 Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104 USA 2 Division of Newborn Medicine, Boston Children’s Hospital, Boston, MA 02115, USA 3 Ludwig Institute for Cancer Research, Oxford Branch, Oxford University, UK 4 Current address: The Bioinformatics Centre, Department of Biology and Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark 5 Department of Biochemistry, Stem Cell Center, University of California, Riverside, Riverside, CA 92521, USA. 6 Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA, 02114, USA. 7 Broad Institute of MIT and Harvard, Cambridge, MA, USA 8 Harvard Stem Cell Institute, Cambridge, Massachusetts,
  • ZNF354C Is a Transcriptional Repressor That Inhibits Endothelial Angiogenic Sprouting James A

    ZNF354C Is a Transcriptional Repressor That Inhibits Endothelial Angiogenic Sprouting James A

    www.nature.com/scientificreports OPEN ZNF354C is a transcriptional repressor that inhibits endothelial angiogenic sprouting James A. Oo1,3, Barnabas Irmer1, Stefan Günther2, Timothy Warwick1, Katalin Pálf1, Judit Izquierdo Ponce1, Tom Teichmann1, Beatrice Pfüger‑Müller1,3, Ralf Gilsbach1,3, Ralf P. Brandes1,3 & Matthias S. Leisegang1,3* Zinc fnger proteins (ZNF) are a large group of transcription factors with diverse functions. We recently discovered that endothelial cells harbour a specifc mechanism to limit the action of ZNF354C, whose function in endothelial cells is unknown. Given that ZNF354C has so far only been studied in bone and tumour, its function was determined in endothelial cells. ZNF354C is expressed in vascular cells and localises to the nucleus and cytoplasm. Overexpression of ZNF354C in human endothelial cells results in a marked inhibition of endothelial sprouting. RNA‑sequencing of human microvascular endothelial cells with and without overexpression of ZNF354C revealed that the protein is a potent transcriptional repressor. ZNF354C contains an active KRAB domain which mediates this suppression as shown by mutagenesis analysis. ZNF354C interacts with dsDNA, TRIM28 and histones, as observed by proximity ligation and immunoprecipitation. Moreover, chromatin immunoprecipitation revealed that the ZNF binds to specifc endothelial‑relevant target‑gene promoters. ZNF354C suppresses these genes as shown by CRISPR/Cas knockout and RNAi. Inhibition of endothelial sprouting by ZNF354C is dependent on the amino acids DV and MLE of the KRAB domain. These results demonstrate that ZNF354C is a repressive transcription factor which acts through a KRAB domain to inhibit endothelial angiogenic sprouting. Te vascular system is controlled by numerous signaling pathways and growth factors which all contribute to the regulation of gene expression.
  • Trastuzumab Modulates the Protein Cargo of Extracellular Vesicles Released by ERBB2+ Breast Can‐ Cer Cells

    Trastuzumab Modulates the Protein Cargo of Extracellular Vesicles Released by ERBB2+ Breast Can‐ Cer Cells

    Supplementary Material: Trastuzumab Modulates the Protein Cargo of Extracellular Vesicles Released by ERBB2+ Breast Can‐ cer Cells Silvia Marconi, Sara Santamaria, Martina Bartolucci, Sara Stigliani, Cinzia Aiello, Maria Cristina Gagliani, Grazia Bellese, Andrea Petretto, Katia Cortese and Patrizio Castagnola Table S1. Antibodies used in the study. Antibody Catalog number Manufacturer Anti‐ALIX sc‐271975 Santa Cruz1 Anti‐CD9 PA5‐85955 Thermofisher Scientific2 Anti‐CD63 sc‐15363 Santa Cruz Anti‐ErbB2 (9G6) sc‐08 Santa Cruz Anti‐GAPDH 14C10 Cell signaling3 Anti‐HSP90 sc‐13119 Santa Cruz 1 Dallas, TX, USA; 2 Waltham, MA, USA; 3 Danvers, MA, USA. Table S2. Differentially regulated proteins by trastuzumab Tz treatment in extracellular vesicles EVs purified from SKBR‐ 3 cells with a statistically significant p‐value resulted from Studentʹs T‐test. The gene symbols coding for proteins downregulated by Tz (and hence upregulated in IgG treated cells) are highlighted in red while proteins upregulated by Tz are highlighted in blue. Official Gene Symbol 1 Gene product (Protein name) ACVR1B Activin A receptor type 1B ANO1 Anoctamin 1 ARFGEF2 ADP Ribosylation Factor Guanine Nucleotide Exchange Factor 2 BTN2A1 Butyrophilin subfamily 2 member A1 CIAPIN1 Cytokine Induced Apoptosis Inhibitor 1 CIT Citron Rho‐Interacting Serine/Threonine Kinase CPPED1 Calcineurin Like Phosphoesterase Domain Containing 1 DNAH7 Dynein Axonemal Heavy Chain 7 EIF3F Eukaryotic translation initiation factor 3 subunit F ESD Esterase D ESYT2 Extended Synaptotagmin 2 F2RL1 F2R Like Trypsin Receptor 1 RIPOR3 RIPOR Family Member 3 FZD6 Frizzled‐6 GAN Gigaxonin GTPBP2 GTP‐binding protein 2 GUCD1 Guanylyl Cyclase Domain Containing 1 HNRNPM Heterogeneous nuclear ribonucleoprotein M LMAN2 Lectin, Mannose Binding 2 LRRC8A Volume‐regulated anion channel subunit LRRC8A NOTCH4 Notch Receptor 4 NT5C2 5ʹ‐Nucleotidase, Cytosolic II PCID2 PCI domain‐containing 2 PDCD5 Programmed cell death 5 PHLDB3 Pleckstrin homology like domain family B member 3 PLAA Phospholipase A2 activating protein Membranes 2021, 11, 199.
  • Mouse Germ Line Mutations Due to Retrotransposon Insertions Liane Gagnier1, Victoria P

    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].
  • Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model

    Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model

    Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 T + is online at: average * The Journal of Immunology , 34 of which you can access for free at: 2016; 197:1477-1488; Prepublished online 1 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600589 http://www.jimmunol.org/content/197/4/1477 Molecular Profile of Tumor-Specific CD8 Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. Waugh, Sonia M. Leach, Brandon L. Moore, Tullia C. Bruno, Jonathan D. Buhrman and Jill E. Slansky J Immunol cites 95 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2016/07/01/jimmunol.160058 9.DCSupplemental This article http://www.jimmunol.org/content/197/4/1477.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 25, 2021. The Journal of Immunology Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A.
  • Molecular Mechanisms Involved Involved in the Interaction Effects of HCV and Ethanol on Liver Cirrhosis

    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
  • 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

    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
  • Selectin Ligand Sialyl-Lewis X Antigen Drives Metastasis of Hormone-Dependent Breast Cancers

    Selectin Ligand Sialyl-Lewis X Antigen Drives Metastasis of Hormone-Dependent Breast Cancers

    Published OnlineFirst October 24, 2011; DOI: 10.1158/0008-5472.CAN-11-1139 Cancer Tumor and Stem Cell Biology Research Selectin Ligand Sialyl-Lewis x Antigen Drives Metastasis of Hormone-Dependent Breast Cancers Sylvain Julien1, Aleksandar Ivetic2, Anita Grigoriadis3, Ding QiZe1, Brian Burford1, Daisy Sproviero1, Gianfranco Picco1, Cheryl Gillett4, Suzanne L. Papp5, Lana Schaffer5, Andrew Tutt3, Joyce Taylor-Papadimitriou1, Sarah E. Pinder4, and Joy M. Burchell1 Abstract The glycome acts as an essential interface between cells and the surrounding microenvironment. However, changes in glycosylation occur in nearly all breast cancers, which can alter this interaction. Here, we report that profiles of glycosylation vary between ER-positive and ER-negative breast cancers. We found that genes involved in the synthesis of sialyl-Lewis x (sLex; FUT3, FUT4, and ST3GAL6) are significantly increased in estrogen receptor alpha-negative (ER-negative) tumors compared with ER-positive ones. SLex expression had no influence on the survival of patients whether they had ER-negative or ER-positive tumors. However, high expression of sLex in ER- positive tumors was correlated with metastasis to the bone where sLex receptor E-selectin is constitutively expressed. The ER-positive ZR-75-1 and the ER-negative BT20 cell lines both express sLex but only ZR-75-1 cells could adhere to activated endothelial cells under dynamic flow conditions in a sLex and E-selectin–dependent manner. Moreover, L/P-selectins bound strongly to ER-negative MDA-MB-231 and BT-20 cell lines in a heparan sulfate (HS)–dependent manner that was independent of sLex expression. Expression of glycosylation genes involved in heparan biosynthesis (EXT1 and HS3ST1) was increased in ER-negative tumors.
  • Broad and Thematic Remodeling of the Surface Glycoproteome on Isogenic

    Broad and Thematic Remodeling of the Surface Glycoproteome on Isogenic

    bioRxiv preprint doi: https://doi.org/10.1101/808139; this version posted October 17, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Broad and thematic remodeling of the surface glycoproteome on isogenic cells transformed with driving proliferative oncogenes Kevin K. Leung1,5, Gary M. Wilson2,5, Lisa L. Kirkemo1, Nicholas M. Riley2,4, Joshua J. Coon2,3, James A. Wells1* 1Department of Pharmaceutical Chemistry, UCSF, San Francisco, CA, USA Departments of Chemistry2 and Biomolecular Chemistry3, University of Wisconsin- Madison, Madison, WI, 53706, USA 4Present address Department of Chemistry, Stanford University, Stanford, CA, 94305, USA 5These authors contributed equally *To whom correspondence should be addressed bioRxiv preprint doi: https://doi.org/10.1101/808139; this version posted October 17, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Abstract: The cell surface proteome, the surfaceome, is the interface for engaging the extracellular space in normal and cancer cells. Here We apply quantitative proteomics of N-linked glycoproteins to reveal how a collection of some 700 surface proteins is dramatically remodeled in an isogenic breast epithelial cell line stably expressing any of six of the most prominent proliferative oncogenes, including the receptor tyrosine kinases, EGFR and HER2, and downstream signaling partners such as KRAS, BRAF, MEK and AKT.
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus

    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.
  • Location Analysis of Estrogen Receptor Target Promoters Reveals That

    Location Analysis of Estrogen Receptor Target Promoters Reveals That

    Location analysis of estrogen receptor ␣ target promoters reveals that FOXA1 defines a domain of the estrogen response Jose´ e Laganie` re*†, Genevie` ve Deblois*, Ce´ line Lefebvre*, Alain R. Bataille‡, Franc¸ois Robert‡, and Vincent Gigue` re*†§ *Molecular Oncology Group, Departments of Medicine and Oncology, McGill University Health Centre, Montreal, QC, Canada H3A 1A1; †Department of Biochemistry, McGill University, Montreal, QC, Canada H3G 1Y6; and ‡Laboratory of Chromatin and Genomic Expression, Institut de Recherches Cliniques de Montre´al, Montreal, QC, Canada H2W 1R7 Communicated by Ronald M. Evans, The Salk Institute for Biological Studies, La Jolla, CA, July 1, 2005 (received for review June 3, 2005) Nuclear receptors can activate diverse biological pathways within general absence of large scale functional data linking these putative a target cell in response to their cognate ligands, but how this binding sites with gene expression in specific cell types. compartmentalization is achieved at the level of gene regulation is Recently, chromatin immunoprecipitation (ChIP) has been used poorly understood. We used a genome-wide analysis of promoter in combination with promoter or genomic DNA microarrays to occupancy by the estrogen receptor ␣ (ER␣) in MCF-7 cells to identify loci recognized by transcription factors in a genome-wide investigate the molecular mechanisms underlying the action of manner in mammalian cells (20–24). This technology, termed 17␤-estradiol (E2) in controlling the growth of breast cancer cells. ChIP-on-chip or location analysis, can therefore be used to deter- We identified 153 promoters bound by ER␣ in the presence of E2. mine the global gene expression program that characterize the Motif-finding algorithms demonstrated that the estrogen re- action of a nuclear receptor in response to its natural ligand.
  • Transcriptomic Analysis of Native Versus Cultured Human and Mouse Dorsal Root Ganglia Focused on Pharmacological Targets Short

    Transcriptomic Analysis of Native Versus Cultured Human and Mouse Dorsal Root Ganglia Focused on Pharmacological Targets Short

    bioRxiv preprint doi: https://doi.org/10.1101/766865; this version posted September 12, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-ND 4.0 International license. Transcriptomic analysis of native versus cultured human and mouse dorsal root ganglia focused on pharmacological targets Short title: Comparative transcriptomics of acutely dissected versus cultured DRGs Andi Wangzhou1, Lisa A. McIlvried2, Candler Paige1, Paulino Barragan-Iglesias1, Carolyn A. Guzman1, Gregory Dussor1, Pradipta R. Ray1,#, Robert W. Gereau IV2, # and Theodore J. Price1, # 1The University of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, 800 W Campbell Rd. Richardson, TX, 75080, USA 2Washington University Pain Center and Department of Anesthesiology, Washington University School of Medicine # corresponding authors [email protected], [email protected] and [email protected] Funding: NIH grants T32DA007261 (LM); NS065926 and NS102161 (TJP); NS106953 and NS042595 (RWG). The authors declare no conflicts of interest Author Contributions Conceived of the Project: PRR, RWG IV and TJP Performed Experiments: AW, LAM, CP, PB-I Supervised Experiments: GD, RWG IV, TJP Analyzed Data: AW, LAM, CP, CAG, PRR Supervised Bioinformatics Analysis: PRR Drew Figures: AW, PRR Wrote and Edited Manuscript: AW, LAM, CP, GD, PRR, RWG IV, TJP All authors approved the final version of the manuscript. 1 bioRxiv preprint doi: https://doi.org/10.1101/766865; this version posted September 12, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.