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Supplementary Table I

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Supplementary Table I TNF-inducible genes (360) identified by the microarrays are listed. These genes were identified by the formula M+T/M+M ≥2, and shown is the log2 induction (mean±SD). The Table contains the gene (alphabetical order), the systematic name, and the probe name. Gene Systematic Name Probe Name log2 induction (mean±SD) 7A5 NM_182762 A_32_P131031 3,06 ± 0,68 ABTB2 NM_145804 A_23_P356616 2,65 ± 0,53 ACSL1 NM_001995 A_23_P110212 2,95 ± 0,36 ACSL5 NM_203380 A_24_P201360 1,97 ± 0,61 ACVR2A NM_001616 A_23_P153930 2,80 ± 0,20 ADA NM_000022 A_23_P210482 1,63 ± 0,30 ADM NM_001124 A_23_P127948 3,15 ± 0,31 ADORA2A NM_000675 A_23_P109436 3,89 ± 0,22 AK3L1 NM_001005353 A_32_P108655 3,81 ± 1,22 AK3L2 NM_001002921 A_23_P200524 3,27 ± 1,40 ALS2CR4 NM_152388 A_23_P370097 1,69 ± 0,40 AMPD3 NM_000480 A_23_P116286 1,77 ± 0,32 AMZ1 NM_133463 A_24_P383649 3,08 ± 0,64 ANKRD15 NM_153186 A_32_P64570 4,34 ± 0,48 ANKRD22 NM_144590 A_23_P161428 1,56 ± 0,65 APOL3 NM_145641 A_24_P416997 2,36 ± 0,69 AQP9 NM_020980 A_23_P106362 2,84 ± 0,94 AREG NM_001657 A_23_P259071 2,62 ± 0,63 ARHGAP20 NM_020809 A_23_P422933 1,69 ± 0,44 ARHGEF7 NM_145735 A_23_P417891 2,01 ± 0,41 ARL5B NM_178815 A_23_P378588 3,64 ± 0,73 ARNTL2 NM_020183 A_23_P53345 2,07 ± 0,40 ARRDC3 NM_020801 A_24_P274615 1,84 ± 0,38 ARRDC4 NM_183376 A_23_P339818 1,89 ± 0,25 ATF5 NM_012068 A_23_P119337 1,66 ± 0,28 ATP2B1 NM_001682 A_23_P128319 2,36 ± 0,20 AXUD1 NM_033027 A_23_P121011 2,03 ± 0,46 B4GALT1 NM_001497 A_24_P103803 2,04 ± 0,20 B4GALT5 NM_004776 A_24_P239731 2,10 ± 0,60 BAZ1A NM_013448 A_23_P76799 1,95 ± 0,33 BCAR3 NM_003567 A_23_P97394 1,35 ± 0,17 BCL2A1 NM_004049 A_23_P152002 3,08 ± 1,08 BCMO1 NM_017429 A_23_P124300 1,37 ± 0,13 BIC NR_001458 A_32_P108156 4,69 ± 1,07 BID NM_197966 A_23_P154929 1,59 ± 0,23 BIRC3 NM_001165 A_23_P98350 2,80 ± 0,55 BLR1 NM_032966 A_24_P252945 2,47 ± 0,83 BRPF3 NM_015695 A_24_P414712 1,31 ± 0,26 BTBD4 NM_025224 A_32_P518489 1,95 ± 0,72 I Supplementary Table I, continued Gene Systematic Name Probe Name log2 induction (mean±SD) BTG1 NM_001731 A_23_P87560 1,88 ± 0,47 BTG2 NM_006763 A_23_P62901 1,64 ± 0,48 BTG3 NM_006806 A_23_P80068 2,92 ± 0,14 BTNL8 NM_024850 A_23_P7412 1,39 ± 0,20 CCL1 NM_002981 A_23_P49759 1,88 ± 0,65 CCL19 NM_006274 A_23_P123853 1,42 ± 0,48 CCL20 NM_004591 A_23_P17065 7,76 ± 0,50 CCL22 NM_002990 A_24_P313418 1,67 ± 0,26 CCL23 NM_005064 A_24_P319088 4,23 ± 0,33 CCL3 D00044 A_23_P373017 3,11 ± 0,18 CCL3L3 NM_001001437 A_23_P321920 3,33 ± 0,86 CCL4 NM_002984 A_23_P207564 5,22 ± 0,30 CCL5 NM_002985 A_23_P152838 4,59 ± 0,34 CCL8 NM_005623 A_23_P207456 3,55 ± 0,48 CCR7 NM_001838 A_23_P343398 2,91 ± 1,22 CCRL2 NM_003965 A_23_P69310 1,84 ± 0,37 CCRN4L NM_012118 A_24_P213794 2,99 ± 0,85 CD274 NM_014143 A_23_P338479 2,70 ± 0,75 CD40 NM_001250 A_23_P57036 3,00 ± 0,46 CD44 NM_000610 A_23_P24870 1,78 ± 0,25 CD58 NM_001779 A_23_P138308 1,59 ± 0,30 CD6 NM_006725 A_23_P311875 3,17 ± 0,46 CD69 NM_001781 A_23_P87879 4,03 ± 1,04 CD80 NM_005191 A_24_P320033 3,88 ± 0,36 CD83 NM_004233 A_23_P70670 2,80 ± 0,58 CDC42EP2 NM_006779 A_23_P1602 3,91 ± 0,42 CDGAP NM_020754 A_24_P349039 1,88 ± 0,17 CDKN2B NM_078487 A_24_P360674 3,93 ± 0,40 CENTD1 NM_015230 A_32_P83784 1,38 ± 0,22 CGN NM_020770 A_24_P45728 2,10 ± 0,54 CH25H NM_003956 A_23_P86470 3,38 ± 1,54 CHML NM_001821 A_23_P46118 2,36 ± 0,52 CHST2 NM_004267 A_23_P40847 3,24 ± 0,48 CIAS1 NM_004895 A_23_P9883 1,83 ± 0,27 CLCF1 NM_013246 A_23_P138760 2,25 ± 0,62 CLEC4D NM_080387 A_23_P25235 2,56 ± 1,00 CLEC4E NM_014358 A_24_P78531 3,20 ± 0,55 CLIC4 NM_013943 A_23_P135494 2,50 ± 0,22 CRIM1 NM_016441 A_23_P51105 3,06 ± 0,77 CSF2 NM_000758 A_23_P133408 4,45 ± 0,52 CSF3 NM_000759 A_23_P501754 4,03 ± 0,46 CSRP2 NM_001321 A_23_P44724 3,06 ± 0,61 CTNND2 NM_001332 A_24_P380196 1,84 ± 0,34 CXCL1 NM_001511 A_23_P7144 6,09 ± 0,70 CXCL2 NM_002089 A_23_P315364 3,58 ± 0,81 CXCL3 NM_002090 A_24_P251764 3,29 ± 0,40 CXCL5 NM_002994 A_23_P110204 3,81 ± 0,82 CXCL6 NM_002993 A_23_P155755 4,29 ± 1,28 II Supplementary Table I, continued Gene Systematic Name Probe Name log2 induction (mean±SD) CYP7B1 NM_004820 A_23_P169092 3,00 ± 1,01 DC-UbP NM_152277 A_23_P19061 1,89 ± 0,37 DDIT4 NM_019058 A_23_P104318 2,21 ± 0,42 DGKH NM_152910 A_23_P502980 1,90 ± 0,73 DLC1 NM_182643 A_24_P940115 2,00 ± 0,20 DNAJB5 NM_012266 A_23_P112241 2,56 ± 0,22 DOC1 NM_182909 A_23_P252052 2,41 ± 0,27 DOT1L NM_032482 A_23_P408768 2,21 ± 0,33 DSU NM_018000 A_23_P108948 1,51 ± 0,44 DUSP1 NM_004417 A_23_P110712 2,11 ± 0,40 DUSP2 NM_004418 A_24_P37409 2,41 ± 0,61 DUSP5 NM_004419 A_23_P150018 3,44 ± 1,03 DUSP6 NM_001946 A_23_P139704 1,87 ± 0,58 DYRK3 NM_001004023 A_24_P345209 2,45 ± 1,05 E2F7 NM_203394 A_32_P210202 3,16 ± 1,29 EBI3 NM_005755 A_24_P370201 3,20 ± 0,26 ECE1 NM_001397 A_24_P154080 1,72 ± 0,50 EDEM1 NM_014674 A_24_P285768 1,53 ± 0,22 EDN1 NM_001955 A_23_P214821 3,58 ± 0,34 EGR3 NM_004430 A_23_P216225 2,86 ± 1,09 EHD1 NM_006795 A_23_P52647 3,52 ± 0,57 EID3 NM_001008394 A_23_P65068 2,02 ± 0,42 EMP2 NM_001424 A_23_P106682 1,46 ± 0,16 EREG NM_001432 A_23_P41344 5,53 ± 0,71 ESPL1 NM_012291 A_23_P32707 1,84 ± 0,23 ETV3 NM_005240 A_23_P400945 1,96 ± 0,37 EYA3 NM_001990 A_23_P74737 1,60 ± 0,35 EZH2 NM_004456 A_23_P259641 1,73 ± 0,13 F3 NM_001993 A_23_P126782 5,57 ± 1,02 FAM107B NM_031453 A_23_P149975 1,19 ± 0,14 FAM49A NM_030797 A_23_P21560 1,49 ± 0,20 FAM57A NM_024792 A_23_P50000 1,63 ± 0,38 FCAR NM_133280 A_24_P348265 2,15 ± 0,67 FEZ1 NM_005103 A_24_P201552 4,94 ± 0,85 FFAR2 NM_005306 A_23_P397391 1,58 ± 0,20 FJX1 NM_014344 A_23_P150693 1,80 ± 0,49 FMNL3 NM_175736 A_23_P379200 1,73 ± 0,38 FOSL1 NM_005438 A_23_P322519 2,85 ± 0,81 FOSL2 NM_005253 A_23_P348121 2,24 ± 0,59 FPRL1 NM_001462 A_23_P55649 1,46 ± 0,21 FSCN1 NM_003088 A_23_P168532 3,67 ± 0,79 FUT4 NM_002033 A_23_P12965 1,48 ± 0,29 FZD7 NM_003507 A_23_P209449 1,36 ± 0,23 G0S2 NM_015714 A_23_P74609 5,83 ± 0,38 GBP1 NM_002053 A_23_P62890 3,67 ± 0,58 GBP2 NM_004120 A_23_P85693 2,92 ± 0,26 GCH1 NM_000161 A_23_P163079 4,79 ± 0,42 GJB2 NM_004004 A_23_P204947 4,45 ± 0,48 III Supplementary Table I, continued Gene Systematic Name Probe Name log2 induction (mean±SD) GPR109A NM_177551 A_23_P329924 2,15 ± 0,54 GPR109B NM_006018 A_23_P64721 4,33 ± 0,72 GPR132 NM_013345 A_24_P201994 2,66 ± 0,51 GPR35 NM_005301 A_23_P154245 1,51 ± 0,34 GPR84 NM_020370 A_23_P25155 2,76 ± 0,20 GRAMD1A NM_020895 A_23_P56213 2,97 ± 0,54 GRAMD3 NM_023927 A_23_P22350 2,55 ± 0,07 HEY1 NM_012258 A_32_P83845 5,81 ± 1,20 HIVEP1 NM_002114 A_23_P19619 2,38 ± 0,30 HIVEP2 NM_006734 A_23_P214766 3,45 ± 0,34 HSA251708 AJ251708 A_24_P932084 2,80 ± 0,30 HSD11B1 NM_181755 A_23_P63209 2,27 ± 0,77 IBRDC2 NM_182757 A_24_P406060 3,87 ± 0,31 IBRDC3 NM_153341 A_23_P321388 2,54 ± 0,51 ICAM1 NM_000201 A_23_P153320 3,34 ± 0,56 IER3 NM_003897 A_23_P42257 3,30 ± 0,39 IFNB1 NM_002176 A_23_P71774 2,54 ± 0,76 IFNGR2 NM_005534 A_23_P29036 1,69 ± 0,28 IGSF21 NM_032880 A_32_P78101 2,14 ± 0,54 IL12B NM_002187 A_23_P7560 4,53 ± 0,97 IL15RA NM_172200 A_23_P138680 2,90 ± 0,48 IL18 NM_001562 A_23_P104798 2,75 ± 0,16 IL18R1 NM_003855 A_24_P208567 2,58 ± 1,29 IL1A NM_000575 A_23_P72096 8,19 ± 0,63 IL1B NM_000576 A_23_P79518 6,16 ± 0,53 IL1F9 NM_019618 A_23_P17053 4,12 ± 0,90 IL20 NM_018724 A_23_P46482 2,58 ± 1,63 IL23A NM_016584 A_23_P76078 3,91 ± 0,76 IL28A NM_172138 A_23_P409438 1,72 ± 0,25 IL2RA NM_000417 A_23_P127288 4,22 ± 1,10 IL32 NM_001012631 A_23_P15146 1,82 ± 0,19 IL4I1 NM_172374 A_23_P502520 1,59 ± 0,27 IL6 NM_000600 A_23_P71037 6,54 ± 0,50 IL7R NM_002185 A_23_P404494 4,47 ± 0,97 IL8 NM_000584 A_32_P87013 5,80 ± 1,08 INHBA NM_002192 A_23_P122924 2,65 ± 1,38 INSIG1 NM_198336 A_23_P22027 3,08 ± 0,40 IRAK2 NM_001570 A_23_P80635 2,79 ± 0,88 IRAK3 NM_007199 A_23_P162300 2,00 ± 0,20 ITGB8 NM_002214 A_24_P273599 2,93 ± 0,73 JAG1 NM_000214 A_23_P210763 5,20 ± 0,38 JUNB NM_002229 A_23_P4821 1,72 ± 0,25 KCNA3 NM_002232 A_23_P201138 3,68 ± 0,34 KCNJ2 NM_000891 A_23_P329261 3,45 ± 0,45 KCNN4 NM_002250 A_23_P67529 2,14 ± 0,40 KMO NM_003679 A_23_P200838 2,17 ± 0,47 KRT23 NM_015515 A_23_P78248 2,50 ± 0,66 KYNU NM_003937 A_24_P11506 2,24 ± 0,31 IV Supplementary Table I, continued Gene Systematic Name Probe Name log2 induction (mean±SD) LAD1 NM_005558 A_23_P415510 2,98 ± 0,88 LAMB3 NM_001017402 A_23_P86012 3,36 ± 0,52 LAMP3 NM_014398 A_23_P29773 2,38 ± 1,03 LCT NM_002299 A_23_P79217 1,86 ± 0,29 LENG9 NM_198988 A_32_P493225 3,08 ± 0,55 LIMS3 NM_033514 A_23_P365685 1,69 ± 0,50 LINCR NM_001080535 A_23_P328740 3,15 ± 0,61 LITAF NM_004862 A_23_P3532 1,45 ± 0,47 LONRF1 NM_152271 A_23_P94216 1,90 ± 0,39 LRFN5 NM_152447 A_23_P163195 3,11 ± 0,78 LRP12 NM_013437 A_23_P8906 1,92 ± 0,62 LRRC32 NM_005512 A_24_P389916 4,24 ± 1,02 LSS NM_002340 A_24_P110799 1,88 ± 0,29 MAFF NM_012323 A_23_P103110 2,27 ± 0,56 MAP2K3 NM_145109 A_23_P118427 2,28 ± 0,40 MAP3K8 NM_005204 A_23_P23947 3,09 ± 0,46 MARCH3 NM_178450 A_23_P321511 1,92 ± 0,32 MCL1 NM_021960 A_24_P319635 1,92 ± 0,53 MCOLN2 NM_153259 A_23_P23639 2,75 ± 0,55 MCTP1 NM_024717 A_24_P212481 1,79 ± 0,47 MESDC1 NM_022566 A_23_P99891 1,42 ± 0,25 MET NM_000245 A_23_P359245 3,66 ± 1,39 MFSD2 NM_032793 A_23_P43820 2,81 ± 0,33 MN1 NM_002430 A_23_P6381 2,27 ± 0,73 MOBKL2C NM_145279 A_24_P225339 1,87 ± 0,31 MSC NM_005098 A_23_P256948 4,29 ± 0,31 MTF1 NM_005955 A_23_P74241 2,36 ± 0,18 MYC NM_002467 A_23_P215956 2,70 ± 0,87 MYO1G NM_033054 A_23_P257542 1,37 ± 0,37 N4BP3 NM_015111 A_23_P58747 2,03 ± 0,38 NAB1 NM_005966 A_23_P209805 1,80 ± 0,31 NBN NM_002485 A_23_P251480 2,75 ± 0,33 NFE2L3 NM_004289 A_23_P42718 2,20 ± 0,32 NFKB1 NM_003998 A_23_P30024 3,00 ± 0,27 NFKB2 NM_002502 A_23_P202156 2,56 ± 0,25 NFKBIA NM_020529 A_23_P106002 2,45 ± 0,28 NFKBIE NM_004556
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  • The Expression of the Human Apolipoprotein Genes and Their Regulation by Ppars

    The Expression of the Human Apolipoprotein Genes and Their Regulation by Ppars

    CORE Metadata, citation and similar papers at core.ac.uk Provided by UEF Electronic Publications The expression of the human apolipoprotein genes and their regulation by PPARs Juuso Uski M.Sc. Thesis Biochemistry Department of Biosciences University of Kuopio June 2008 Abstract The expression of the human apolipoprotein genes and their regulation by PPARs. UNIVERSITY OF KUOPIO, the Faculty of Natural and Environmental Sciences, Curriculum of Biochemistry USKI Juuso Oskari Thesis for Master of Science degree Supervisors Prof. Carsten Carlberg, Ph.D. Merja Heinäniemi, Ph.D. June 2008 Keywords: nuclear receptors; peroxisome proliferator-activated receptor; PPAR response element; apolipoprotein; lipid metabolism; high density lipoprotein; low density lipoprotein. Lipids are any fat-soluble, naturally-occurring molecules and one of their main biological functions is energy storage. Lipoproteins carry hydrophobic lipids in the water and salt-based blood environment for processing and energy supply in liver and other organs. In this study, the genomic area around the apolipoprotein genes was scanned in silico for PPAR response elements (PPREs) using the in vitro data-based computer program. Several new putative REs were found in surroundings of multiple lipoprotein genes. The responsiveness of those apolipoprotein genes to the PPAR ligands GW501516, rosiglitazone and GW7647 in the HepG2, HEK293 and THP-1 cell lines were tested with real-time PCR. The APOA1, APOA2, APOB, APOD, APOE, APOF, APOL1, APOL3, APOL5 and APOL6 genes were found to be regulated by PPARs in direct or secondary manners. Those results provide new insights in the understanding of lipid metabolism and so many lifestyle diseases like atherosclerosis, type 2 diabetes, heart disease and stroke.
  • AK3L1 (AK4) Mouse Monoclonal Antibody [Clone ID: OTI3A9] Product Data

    AK3L1 (AK4) Mouse Monoclonal Antibody [Clone ID: OTI3A9] Product Data

    OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for TA503371 AK3L1 (AK4) Mouse Monoclonal Antibody [Clone ID: OTI3A9] Product data: Product Type: Primary Antibodies Clone Name: OTI3A9 Applications: FC, WB Recommended Dilution: WB 1:2000, FLOW 1:100 Reactivity: Human, Mouse, Rat Host: Mouse Isotype: IgG2b Clonality: Monoclonal Immunogen: Full length human recombinant protein of human AK4(NP_037542) produced in HEK293T cell. Formulation: PBS (PH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide. Concentration: 1 mg/ml Purification: Purified from mouse ascites fluids or tissue culture supernatant by affinity chromatography (protein A/G) Conjugation: Unconjugated Storage: Store at -20°C as received. Stability: Stable for 12 months from date of receipt. Predicted Protein Size: 25.1 kDa Gene Name: adenylate kinase 4 Database Link: NP_037542 Entrez Gene 11639 MouseEntrez Gene 29223 RatEntrez Gene 205 Human P27144 This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 3 AK3L1 (AK4) Mouse Monoclonal Antibody [Clone ID: OTI3A9] – TA503371 Background: This gene encodes a member of the adenylate kinase family of enzymes. The encoded protein is localized to the mitochondrial matrix. Adenylate kinases regulate the adenine and guanine nucleotide compositions within a cell by catalyzing the reversible transfer of phosphate group among these nucleotides. Five isozymes of adenylate kinase have been identified in vertebrates.
  • 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.
  • AK3L1 Antibody - Middle Region Rabbit Polyclonal Antibody Catalog # AI12098

    AK3L1 Antibody - Middle Region Rabbit Polyclonal Antibody Catalog # AI12098

    10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 AK3L1 antibody - middle region Rabbit Polyclonal Antibody Catalog # AI12098 Specification AK3L1 antibody - middle region - Product Information Application WB Primary Accession P27144 Other Accession NM_001005353, NP_001005353 Reactivity Human, Mouse, Rat, Rabbit, Zebrafish, Pig, Horse, Bovine, Guinea Pig, Dog Predicted Pig, Dog WB Suggested Anti-AK3L1 Antibody Titration: Host Rabbit 2.5μg/ml Clonality Polyclonal Positive Control: Jurkat cell lysate Calculated MW 25kDa KDa AK3L1 antibody - middle region - Additional Information AK3L1 antibody - middle region - References Gene ID 205 Noma,T.,Biochem.J.358(PT1),225-232(2001)Re Alias Symbol AK3, AK4, AK3L1, constitutionandStorage:Forshorttermuse,storea AK3L2 t2-8Cupto1week.Forlongtermstorage,storeat-2 Other Names 0Cinsmallaliquotstopreventfreeze-thawcycles. Adenylate kinase 4, mitochondrial {ECO:0000255|HAMAP-Rule:MF_03170}, AK 4 {ECO:0000255|HAMAP-Rule:MF_03170}, 2.7.4.10 {ECO:0000255|HAMAP-Rule:MF_03170}, 2.7.4.6 {ECO:0000255|HAMAP-Rule:MF_03170}, Adenylate kinase 3-like {ECO:0000255|HAMAP-Rule:MF_03170}, GTP:AMP phosphotransferase AK4 {ECO:0000255|HAMAP-Rule:MF_03170}, AK4 {ECO:0000255|HAMAP-Rule:MF_03170} Format Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose. Reconstitution & Storage Add 100 ul of distilled water. Final anti-AK3L1 antibody concentration is 1 Page 1/3 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 mg/ml in PBS buffer with 2% sucrose. For longer periods of storage, store at 20°C. Avoid repeat freeze-thaw cycles. Precautions AK3L1 antibody - middle region is for research use only and not for use in diagnostic or therapeutic procedures.
  • A Genomic Approach to Study Down Syndrome and Cancer Inverse Comorbidity: Untangling the Chromosome 21

    A Genomic Approach to Study Down Syndrome and Cancer Inverse Comorbidity: Untangling the Chromosome 21

    PERSPECTIVE ARTICLE published: 04 February 2015 doi: 10.3389/fphys.2015.00010 A genomic approach to study down syndrome and cancer inverse comorbidity: untangling the chromosome 21 Jaume Forés-Martos , Raimundo Cervera-Vidal , Enrique Chirivella , Alberto Ramos-Jarero and Joan Climent* Genomics and Systems Biology (InGSB) Lab, Oncology and Hematology Department, Biomedical Research Institute INCLIVA, Valencia, Spain Edited by: Down syndrome (DS), one of the most common birth defects and the most widespread Anaïs Baudot, Centre National de la genetic cause of intellectual disabilities, is caused by extra genetic material on Recherche Scientifique, France chromosome 21 (HSA21). The increased genomic dosage of trisomy 21 is thought to Reviewed by: be responsible for the distinct DS phenotypes, including an increased risk of developing Cristian Bellodi, Lund University, Sweden some types of childhood leukemia and germ cell tumors. Patients with DS, however, have Jian-Hua Mao, Lawrence Berkeley a strikingly lower incidence of many other solid tumors. We hypothesized that the third National Laboratory, USA copy of genes located in HSA21 may have an important role on the protective effect *Correspondence: that DS patients show against most types of solid tumors. Focusing on Copy Number Joan Climent, Genomics and Variation (CNV) array data, we have generated frequencies of deleted regions in HSA21 in Systems Biology (InGSB) Lab, Oncology and Hematology four different tumor types from which DS patients have been reported to be protected. Department, Biomedical Research We describe three different regions of deletion pointing to a set of candidate genes Institute INCLIVA, Avda Blasco that could explain the inverse comorbidity phenomenon between DS and solid tumors.
  • Targeted Resequencing Identifies Genes with Recurrent Variation In

    Targeted Resequencing Identifies Genes with Recurrent Variation In

    www.nature.com/npjgenmed ARTICLE OPEN Targeted resequencing identifies genes with recurrent variation in cerebral palsy C. L. van Eyk 1,2, M. A. Corbett 1,2, M. S. B. Frank 1,2, D. L. Webber1,2, M. Newman3, J. G. Berry 1,2, K. Harper1,2, B. P. Haines1,2, G. McMichael1,2, J. A. Woenig1,2, A. H. MacLennan1,2 and J. Gecz 1,2,4* A growing body of evidence points to a considerable and heterogeneous genetic aetiology of cerebral palsy (CP). To identify recurrently variant CP genes, we designed a custom gene panel of 112 candidate genes. We tested 366 clinically unselected singleton cases with CP, including 271 cases not previously examined using next-generation sequencing technologies. Overall, 5.2% of the naïve cases (14/271) harboured a genetic variant of clinical significance in a known disease gene, with a further 4.8% of individuals (13/271) having a variant in a candidate gene classified as intolerant to variation. In the aggregate cohort of individuals from this study and our previous genomic investigations, six recurrently hit genes contributed at least 4% of disease burden to CP: COL4A1, TUBA1A, AGAP1, L1CAM, MAOB and KIF1A. Significance of Rare VAriants (SORVA) burden analysis identified four genes with a genome-wide significant burden of variants, AGAP1, ERLIN1, ZDHHC9 and PROC, of which we functionally assessed AGAP1 using a zebrafish model. Our investigations reinforce that CP is a heterogeneous neurodevelopmental disorder with known as well as novel genetic determinants. npj Genomic Medicine (2019) ; https://doi.org/10.1038/s41525-019-0101-z4:27 1234567890():,; INTRODUCTION is likely also due in part to the stringent criteria used to select Cerebral palsy (CP) is the most common motor disability of causative variants.
  • Synthetic Lethal Screen Demonstrates That a JAK2 Inhibitor Suppresses a BCL6 Dependent IL10RA/JAK2/STAT3 Pathway in High Grade B-Cell Lymphoma

    Synthetic Lethal Screen Demonstrates That a JAK2 Inhibitor Suppresses a BCL6 Dependent IL10RA/JAK2/STAT3 Pathway in High Grade B-Cell Lymphoma

    BCL6 suppresses an IL10RA/JAK2/STAT3 pathway Synthetic lethal screen demonstrates that a JAK2 inhibitor suppresses a BCL6 dependent IL10RA/JAK2/STAT3 pathway in high grade B-cell lymphoma. Daniel Beck1,6, Jenny Zobel3,6, Ruth Barber1,2,6, Sian Evans1, Larissa Lezina1, Rebecca L. Allchin1, Matthew Blades4, Richard Elliott5, Christopher J. Lord5, Alan Ashworth5, Andrew C.G. Porter3, Simon D. Wagner1 1Department of Cancer Studies, Ernest and Helen Scott Haematology Research Institute and, 2 Leicester Diagnostic and Drug Development (LD3) Centre, University of Leicester, Lancaster Road, Leicester LE1 7HB, UK, 3Department of Haematology, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK. 4Bioinformatics and Biostatistics Analysis Support Hub (B/BASH), University of Leicester, Lancaster Road, Leicester LE1 9HN and 5The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, 237 Fulham Road, London, SW3 6JB, UK. 6The first three authors contributed equally to this work Running title: BCL6 suppresses an IL10RA/JAK2/STAT3 pathway. To whom correspondence should be addressed: Simon D. Wagner, Department of Cancer Studies, Room 104, Hodgkin Building, University of Leicester, Lancaster Road, Leicester LE1 7HB, UK. Tel: 0441162525584, Fax: 0441162525616, Email: [email protected] Keywords: cancer therapy, Janus kinase (JAK), lymphocyte, lymphoma, transcription factor, B-cell lymphoma 6 (BCL-6), synthetic lethal screen. ABSTRACT which shows higher levels of IL10RA, JAK2 and We demonstrate the usefulness of synthetic lethal STAT3 but lower levels of BCL6 than GC- screening of a conditionally BCL6 deficient DLBCL and might be usefully combined with Burkitt lymphoma cell line, DG75-AB7, with a novel approaches such as inhibition of IL10RA.