DOCSLIB.ORG

Supporting Table 1. Genes Differentially Expressed in Heparg Cells by the Coculture Condition

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Supporting Table 1. Genes Differentially Expressed in HepaRG Cells by the Coculture Condition List of Up-Regulated Genes Gene symbol Description GB acc EntrezID p-value FDR HepaRG HepaRG/LX2 Fold-change CYP1A1 cytochrome P450, family 1, subfamily A, polypeptide 1 NM_000499 1543 0.0000021 0.00591 0.54 8.55 15.87 ENO2 enolase 2 NM_001975 2026 0.0003024 0.0243 0.049 0.32 6.67 C15orf48 chromosome 15 open reading frame 48 NM_032413 84419 0.0000131 0.00851 1.28 6.97 5.56 WISP2 WNT1 inducible signaling pathway protein 2 NM_003881 8839 0.0000395 0.0113 1.94 10.56 5.56 COL13A1 collagen, type XIII, alpha 1 NM_080801 1305 0.0000713 0.0135 0.58 2.55 4.35 C4orf47 chromosome 4 open reading frame 47 NM_001114357 441054 0.000041 0.0113 1.23 5.01 4.00 ZP1 zona pellucida glycoprotein 1 NM_207341 22917 0.0000433 0.0114 0.2 0.8 4.00 DENND2A DENN/MADD domain containing 2A NM_015689 27147 0.0000763 0.0138 0.19 0.73 3.85 SAA2 serum amyloid A2 NM_001127380 6289 0.0002017 0.0204 0.91 3.45 3.85 CP ceruloplasmin NM_000096 1356 0.0000028 0.00591 1.07 3.97 3.70 TXNIP thioredoxin interacting protein NM_006472 10628 0.0001031 0.0155 0.1 0.37 3.57 TEK TEK tyrosine kinase, endothelial NM_000459 7010 0.0000543 0.0119 0.14 0.48 3.45 C3P1 complement component 3 precursor pseudogene NR_027300 388503 0.0003026 0.0243 0.63 2.06 3.33 IL1RL1 interleukin 1 receptor-like 1 NM_016232 9173 0.0000345 0.0111 1.15 3.65 3.13 NDRG1 N-myc downstream regulated 1 NM_006096 10397 0.0001186 0.0164 1.3 4.07 3.13 IL6 interleukin 6 NM_000600 3569 0.0001052 0.0157 0.45 1.36 3.03 S100A8 S100 calcium binding protein A8 NM_002964 6279 0.0001176 0.0164 1.06 3.13 2.94 EREG epiregulin NM_001432 2069 0.0000076 0.00709 1.83 5.21 2.86 RASD1 RAS, dexamethasone-induced 1 NM_016084 51655 0.0000848 0.0142 0.97 2.74 2.86 CA12 carbonic anhydrase XII NM_001218 771 0.0000043 0.00591 2.48 6.81 2.78 SPAG4 sperm associated antigen 4 NM_003116 6676 0.0000186 0.00931 0.57 1.56 2.78 H19 H19, imprinted maternally expressed transcript NR_002196 283120 0.0001937 0.0203 3.02 8.24 2.70 HMHA1 histocompatibility (minor) HA-1 NM_012292 23526 0.0000535 0.0119 4.49 12.07 2.70 IER3 immediate early response 3 NM_003897 8870 0.0000035 0.00591 1.43 3.83 2.70 MT1X metallothionein 1X NM_005952 4501 0.0000062 0.0067 0.93 2.48 2.70 FAM27A family with sequence similarity 27, member A NR_024060 548321 0.0000112 0.00791 1.76 4.59 2.63 protein tyrosine phosphatase, receptor type, f PPFIA4 polypeptide, interacting protein, alpha 4 NM_015053 8497 0.000156 0.0186 0.19 0.5 2.63 solute carrier family 6 (neurotransmitter transporter, SLC6A8 creatine), member 8 NM_005629 6535 0.0003998 0.0279 1.25 3.29 2.63 ALDOC aldolase C, fructose-bisphosphate NM_005165 230 0.0000954 0.0151 0.7 1.78 2.56 SAM domain, SH3 domain and nuclear localization SAMSN1 signals 1 NM_022136 64092 0.0000001 0.00206 2.59 6.71 2.56 IGFBP3 insulin-like growth factor binding protein 3 NM_001013398 3486 0.0000161 0.00908 3.47 8.6 2.50 MUC1 mucin 1, cell surface associated NM_002456 4582 0.0000941 0.0151 0.37 0.91 2.50 TMEM45A transmembrane protein 45A NM_018004 55076 0.0000344 0.0111 0.53 1.3 2.44 BMPER BMP binding endothelial regulator NM_133468 168667 0.00018 0.0196 1.37 3.28 2.38 HULC highly up-regulated in liver cancer NR_004855 728655 0.000206 0.0205 0.92 2.17 2.38 solute carrier family 6 (neurotransmitter transporter, SLC6A10P creatine), member 10 NR_003083 386757 0.0001374 0.0174 1.78 4.22 2.38 BNIP3 BCL2/adenovirus E1B 19kDa interacting protein 3 NM_004052 664 0.0000372 0.0111 0.95 2.23 2.33 CA9 carbonic anhydrase IX NM_001216 768 0.0002515 0.022 2.98 6.89 2.33 CD3D CD3d molecule, delta (CD3-TCR complex) NM_000732 915 0.0000211 0.00932 1.94 4.51 2.33 IL1B interleukin 1, beta NM_000576 3553 0.000096 0.0151 0.16 0.38 2.33 PDK1 pyruvate dehydrogenase kinase, isozyme 1 NM_002610 5163 0.0000244 0.00932 0.74 1.72 2.33 THBS2 thrombospondin 2 NM_003247 7058 0.0000372 0.0111 0.037 0.085 2.33 CLEC3B C-type lectin domain family 3, member B NM_003278 7123 0.0002815 0.0235 1.49 3.41 2.27 CPNE5 copine V NM_020939 57699 0.0000065 0.0067 1.05 2.36 2.27 DNER delta/notch-like EGF repeat containing NM_139072 92737 0.0000115 0.00791 3.56 8.11 2.27 SYTL2 synaptotagmin-like 2 NM_206927 54843 0.0000296 0.0103 0.98 2.25 2.27 ADSSL1 adenylosuccinate synthase like 1 NM_199165 122622 0.0000035 0.00591 0.97 2.14 2.22 C1QTNF1 C1q and tumor necrosis factor related protein 1 NM_198594 114897 0.0001349 0.0174 1 2.21 2.22 IGFBP1 insulin-like growth factor binding protein 1 NM_000596 3484 0.0000374 0.0111 1.26 2.78 2.22 MT1E unknown mRNA AF495759 4493 0.0000233 0.00932 0.92 2.01 2.17 APCS amyloid P component, serum NM_001639 325 0.0000074 0.00709 0.98 2.11 2.13 C13orf33 chromosome 13 open reading frame 33 NM_032849 84935 0.0001804 0.0196 0.21 0.45 2.13 C16orf74 chromosome 16 open reading frame 74 NM_206967 404550 0.0000023 0.00591 1.44 3.05 2.13 CCL20 chemokine (C-C motif) ligand 20 NM_004591 6364 0.0000132 0.00851 1.08 2.28 2.13 MX2 myxovirus (influenza virus) resistance 2 NM_002463 4600 0.00005 0.0115 0.31 0.66 2.13 CYP1B1 cytochrome P450, family 1, subfamily B, polypeptide 1 NM_000104 1545 0.0000176 0.00908 1.48 3.09 2.08 GFPT2 glutamine-fructose-6-phosphate transaminase 2 NM_005110 9945 0.0004493 0.0299 0.15 0.32 2.08 C21orf90 chromosome 21 open reading frame 90 NR_026547 114043 0.0000095 0.00726 1.95 3.96 2.04 ITIH3 inter-alpha (globulin) inhibitor H3 NM_002217 3699 0.0003927 0.0277 0.82 1.67 2.04 PLOD2 procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 NM_182943 5352 0.0003379 0.0254 1.02 2.08 2.04 solute carrier family 7 (cationic amino acid transporter, SLC7A5 y+ system), member 5 NM_003486 8140 0.0000446 0.0114 0.45 0.91 2.04 WDR54 WD repeat domain 54 NM_032118 84058 0.0001595 0.0186 0.39 0.78 2.04 ADRBK2 adrenergic, beta, receptor kinase 2 NM_005160 157 0.0000401 0.0113 0.12 0.25 2.00 HOPX HOP homeobox NM_139211 84525 0.0000035 0.00591 1.57 3.16 2.00 LBP lipopolysaccharide binding protein NM_004139 3929 0.0000374 0.0111 1 1.99 2.00 SAA1 serum amyloid A1 NM_000331 6288 0.0000079 0.00709 0.96 1.91 2.00 SOCS1 suppressor of cytokine signaling 1 NM_003745 8651 0.0001437 0.0179 0.4 0.81 2.00 SOCS3 suppressor of cytokine signaling 3 NM_003955 9021 0.0000171 0.00908 1.28 2.58 2.00 ERO1L ERO1-like NM_014584 30001 0.000108 0.016 0.99 1.92 1.96 IL8 interleukin 8 NM_000584 3576 0.0000782 0.0138 1.15 2.24 1.96 KRT6A keratin 6A NM_005554 3853 0.0000083 0.00713 10.69 20.88 1.96 PCOLCE2 procollagen C-endopeptidase enhancer 2 NM_013363 26577 0.0001182 0.0164 1.72 3.37 1.96 BNIP3L BCL2/adenovirus E1B 19kDa interacting protein 3-like NM_004331 665 0.0000258 0.0095 0.42 0.81 1.92 C13orf15 chromosome 13 open reading frame 15 NM_014059 28984 0.000143 0.0179 1.96 3.77 1.92 MT1H metallothionein 1H NM_005951 4496 0.0001139 0.0164 0.54 1.02 1.92 PTGFR prostaglandin F receptor NM_000959 5737 0.0000138 0.00863 0.83 1.59 1.92 AREG amphiregulin NM_001657 374 0.0000866 0.0143 0.91 1.7 1.89 C3orf59 chromosome 3 open reading frame 59 NM_178496 151963 0.0000753 0.0137 0.44 0.83 1.89 MAP7D2 MAP7 domain containing 2 NM_152780 256714 0.000006 0.0067 5.58 10.55 1.89 MT1B metallothionein 1B NM_005947 4490 0.0000087 0.00718 0.54 1.02 1.89 PGK1 phosphoglycerate kinase 1 NM_000291 5230 0.0001202 0.0164 0.76 1.44 1.89 PTTG1IP pituitary tumor-transforming 1 interacting protein NM_004339 754 0.0000225 0.00932 1.03 1.96 1.89 ANGPTL4 angiopoietin-like 4 NM_139314 51129 0.0000172 0.00908 1.47 2.71 1.85 CHI3L1 chitinase 3-like 1 NM_001276 1116 0.0000352 0.0111 0.96 1.78 1.85 FGA fibrinogen alpha chain NM_000508 2243 0.0000743 0.0137 0.96 1.77 1.85 HS3ST3B1 heparan sulfate (glucosamine) 3-O-sulfotransferase 3B1 AK023723 9953 0.0000665 0.0131 1.33 2.45 1.85 LPCAT1 lysophosphatidylcholine acyltransferase 1 NM_024830 79888 0.0000146 0.00886 1 1.86 1.85 MUCL1 mucin-like 1 NM_058173 118430 0.0006771 0.0354 1.03 1.91 1.85 TLR2 toll-like receptor 2 NM_003264 7097 0.0000467 0.0115 1.12 2.08 1.85 ITGA5 integrin, alpha 5 NM_002205 3678 0.0000162 0.00908 0.67 1.22 1.82 NXPH4 neurexophilin 4 NM_007224 11247 0.0001534 0.0186 1.7 3.07 1.82 PTX3 pentraxin 3, long NM_002852 5806 0.0000449 0.0114 0.13 0.24 1.82 TGFBI transforming growth factor, beta-induced, 68kDa NM_000358 7045 0.0000312 0.0107 0.56 1.02 1.82 TMEM158 transmembrane protein 158 NM_015444 25907 0.0000243 0.00932 0.34 0.63 1.82 DNAH5 dynein, axonemal, heavy chain 5 NM_001369 1767 0.0001766 0.0194 1.06 1.9 1.79 F3 coagulation factor III NM_001993 2152 0.0000662 0.0131 0.37 0.67 1.79 G protein-coupled receptor, family C, group 5, member GPRC5A A NM_003979 9052 0.0001754 0.0194 0.85 1.52 1.79 HAPLN3 hyaluronan and proteoglycan link protein 3 NM_178232 145864 0.0002865 0.0235 0.52 0.93 1.79 LDHA lactate dehydrogenase A NM_005566 3939 0.0000549 0.0119 0.92 1.66 1.79 LRP1B low density lipoprotein receptor-related protein 1B NM_018557 53353 0.0001566 0.0186 1.07 1.92 1.79 solute carrier family 29 (nucleoside transporters), SLC29A4 member 4 NM_001040661 222962 0.0000321 0.0109 1.47 2.66 1.79 APOL1 apolipoprotein L, 1 NM_145343 8542 0.0001888 0.0202 1.16 2.02 1.75 CDCP1 CUB domain containing protein 1 NM_022842 64866 0.000021 0.00932 0.39 0.69 1.75 CXCL2 chemokine NM_002089 2920 0.000071 0.0135 1.02 1.8 1.75 DCN decorin NM_001920 1634 0.0000724 0.0135 0.35 0.61 1.75 MASP1 mannan-binding lectin serine peptidase 1 NM_001031849 5648 0.0002039 0.0204 1.53 2.68 1.75 P4HA1 prolyl 4-hydroxylase, alpha polypeptide I NM_001142595 5033 0.0001688 0.0191 0.41 0.71 1.75 AFAP1L1 actin filament associated protein 1-like 1 NM_152406 134265 0.0001709 0.0192 1.18 2.04 1.72 BIRC3 baculoviral IAP repeat-containing
Recommended publications
  • Supplementary Information

    Supplementary Information

    doi: 10.1038/nature08795 SUPPLEMENTARY INFORMATION Supplementary Discussion Population naming In some contexts, the indigenous hunter-gatherer and pastoralist peoples of southern Africa are referred to collectively as the Khoisan (Khoi-San) or more recently Khoesan (Khoe-San) people. This grouping is based on the unique linguistic use of click-consonants1. Many names, often country-specific, have been used by Bantu pastoralists and European settlers to describe the hunter-gatherers, including San, Saan, Sonqua, Soaqua, Souqua, Sanqua, Kwankhala, Basarwa, Batwa, Abathwa, Baroa, Bushmen, Bossiesmans, Bosjemans, or Bosquimanos. In addition, group-specific names such as !Kung and Khwe are often used for the broader population. The two most commonly used names, “San” and “Bushmen”, have both been associated with much controversy due to derogatory connotations2. “San” has become the more popular term used in Western literature, although “Bushmen” is arguably the more commonly recognized term within the communities. Since they have no collective name for themselves, the term Bushmen was selected for use in this paper as the term most familiar to the participants themselves. Regarding identification of individuals The five men identified in this study have all elected to have their identity made public knowledge. Thus we present two complete personal genomes (KB1 and ABT), a low-coverage personal genome (NB1), and personal exomes for all five men. On a scientific level, identification allows for current and future correlation of genetic data with demographic and medical histories. On a social level, identification allows for maximizing community benefit. For !Gubi, G/aq’o, D#kgao and !Aî, their name represents not only themselves, but importantly their extended family unit and a way of life severely under threat.
  • IDF Patient & Family Handbook

    IDF Patient & Family Handbook

    Immune Deficiency Foundation Patient & Family Handbook for Primary Immunodeficiency Diseases This book contains general medical information which cannot be applied safely to any individual case. Medical knowledge and practice can change rapidly. Therefore, this book should not be used as a substitute for professional medical advice. FIFTH EDITION COPYRIGHT 1987, 1993, 2001, 2007, 2013 IMMUNE DEFICIENCY FOUNDATION Copyright 2013 by Immune Deficiency Foundation, USA. REPRINT 2015 Readers may redistribute this article to other individuals for non-commercial use, provided that the text, html codes, and this notice remain intact and unaltered in any way. The Immune Deficiency Foundation Patient & Family Handbook may not be resold, reprinted or redistributed for compensation of any kind without prior written permission from the Immune Deficiency Foundation. If you have any questions about permission, please contact: Immune Deficiency Foundation, 110 West Road, Suite 300, Towson, MD 21204, USA; or by telephone at 800-296-4433. Immune Deficiency Foundation Patient & Family Handbook for Primary Immunodeficency Diseases 5th Edition This publication has been made possible through a generous grant from Baxalta Incorporated Immune Deficiency Foundation 110 West Road, Suite 300 Towson, MD 21204 800-296-4433 www.primaryimmune.org [email protected] EDITORS R. Michael Blaese, MD, Executive Editor Francisco A. Bonilla, MD, PhD Immune Deficiency Foundation Boston Children’s Hospital Towson, MD Boston, MA E. Richard Stiehm, MD M. Elizabeth Younger, CPNP, PhD University of California Los Angeles Johns Hopkins Los Angeles, CA Baltimore, MD CONTRIBUTORS Mark Ballow, MD Joseph Bellanti, MD R. Michael Blaese, MD William Blouin, MSN, ARNP, CPNP State University of New York Georgetown University Hospital Immune Deficiency Foundation Miami Children’s Hospital Buffalo, NY Washington, DC Towson, MD Miami, FL Francisco A.
  • Small Cell Ovarian Carcinoma: Genomic Stability and Responsiveness to Therapeutics

    Small Cell Ovarian Carcinoma: Genomic Stability and Responsiveness to Therapeutics

    Gamwell et al. Orphanet Journal of Rare Diseases 2013, 8:33 http://www.ojrd.com/content/8/1/33 RESEARCH Open Access Small cell ovarian carcinoma: genomic stability and responsiveness to therapeutics Lisa F Gamwell1,2, Karen Gambaro3, Maria Merziotis2, Colleen Crane2, Suzanna L Arcand4, Valerie Bourada1,2, Christopher Davis2, Jeremy A Squire6, David G Huntsman7,8, Patricia N Tonin3,4,5 and Barbara C Vanderhyden1,2* Abstract Background: The biology of small cell ovarian carcinoma of the hypercalcemic type (SCCOHT), which is a rare and aggressive form of ovarian cancer, is poorly understood. Tumourigenicity, in vitro growth characteristics, genetic and genomic anomalies, and sensitivity to standard and novel chemotherapeutic treatments were investigated in the unique SCCOHT cell line, BIN-67, to provide further insight in the biology of this rare type of ovarian cancer. Method: The tumourigenic potential of BIN-67 cells was determined and the tumours formed in a xenograft model was compared to human SCCOHT. DNA sequencing, spectral karyotyping and high density SNP array analysis was performed. The sensitivity of the BIN-67 cells to standard chemotherapeutic agents and to vesicular stomatitis virus (VSV) and the JX-594 vaccinia virus was tested. Results: BIN-67 cells were capable of forming spheroids in hanging drop cultures. When xenografted into immunodeficient mice, BIN-67 cells developed into tumours that reflected the hypercalcemia and histology of human SCCOHT, notably intense expression of WT-1 and vimentin, and lack of expression of inhibin. Somatic mutations in TP53 and the most common activating mutations in KRAS and BRAF were not found in BIN-67 cells by DNA sequencing.
  • Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse

    Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse

    Welcome to More Choice CD Marker Handbook For more information, please visit: Human bdbiosciences.com/eu/go/humancdmarkers Mouse bdbiosciences.com/eu/go/mousecdmarkers Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse CD3 CD3 CD (cluster of differentiation) molecules are cell surface markers T Cell CD4 CD4 useful for the identification and characterization of leukocytes. The CD CD8 CD8 nomenclature was developed and is maintained through the HLDA (Human Leukocyte Differentiation Antigens) workshop started in 1982. CD45R/B220 CD19 CD19 The goal is to provide standardization of monoclonal antibodies to B Cell CD20 CD22 (B cell activation marker) human antigens across laboratories. To characterize or “workshop” the antibodies, multiple laboratories carry out blind analyses of antibodies. These results independently validate antibody specificity. CD11c CD11c Dendritic Cell CD123 CD123 While the CD nomenclature has been developed for use with human antigens, it is applied to corresponding mouse antigens as well as antigens from other species. However, the mouse and other species NK Cell CD56 CD335 (NKp46) antibodies are not tested by HLDA. Human CD markers were reviewed by the HLDA. New CD markers Stem Cell/ CD34 CD34 were established at the HLDA9 meeting held in Barcelona in 2010. For Precursor hematopoetic stem cell only hematopoetic stem cell only additional information and CD markers please visit www.hcdm.org. Macrophage/ CD14 CD11b/ Mac-1 Monocyte CD33 Ly-71 (F4/80) CD66b Granulocyte CD66b Gr-1/Ly6G Ly6C CD41 CD41 CD61 (Integrin b3) CD61 Platelet CD9 CD62 CD62P (activated platelets) CD235a CD235a Erythrocyte Ter-119 CD146 MECA-32 CD106 CD146 Endothelial Cell CD31 CD62E (activated endothelial cells) Epithelial Cell CD236 CD326 (EPCAM1) For Research Use Only.
  • Viewed Under 23 (B) Or 203 (C) fi M M Male Cko Mice, and Largely Unaffected Magni Cation; Scale Bars, 500 M (B) and 50 M (C)

    Viewed Under 23 (B) Or 203 (C) fi M M Male Cko Mice, and Largely Unaffected Magni Cation; Scale Bars, 500 M (B) and 50 M (C)

    BRIEF COMMUNICATION www.jasn.org Renal Fanconi Syndrome and Hypophosphatemic Rickets in the Absence of Xenotropic and Polytropic Retroviral Receptor in the Nephron Camille Ansermet,* Matthias B. Moor,* Gabriel Centeno,* Muriel Auberson,* † † ‡ Dorothy Zhang Hu, Roland Baron, Svetlana Nikolaeva,* Barbara Haenzi,* | Natalya Katanaeva,* Ivan Gautschi,* Vladimir Katanaev,*§ Samuel Rotman, Robert Koesters,¶ †† Laurent Schild,* Sylvain Pradervand,** Olivier Bonny,* and Dmitri Firsov* BRIEF COMMUNICATION *Department of Pharmacology and Toxicology and **Genomic Technologies Facility, University of Lausanne, Lausanne, Switzerland; †Department of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, Boston, Massachusetts; ‡Institute of Evolutionary Physiology and Biochemistry, St. Petersburg, Russia; §School of Biomedicine, Far Eastern Federal University, Vladivostok, Russia; |Services of Pathology and ††Nephrology, Department of Medicine, University Hospital of Lausanne, Lausanne, Switzerland; and ¶Université Pierre et Marie Curie, Paris, France ABSTRACT Tight control of extracellular and intracellular inorganic phosphate (Pi) levels is crit- leaves.4 Most recently, Legati et al. have ical to most biochemical and physiologic processes. Urinary Pi is freely filtered at the shown an association between genetic kidney glomerulus and is reabsorbed in the renal tubule by the action of the apical polymorphisms in Xpr1 and primary fa- sodium-dependent phosphate transporters, NaPi-IIa/NaPi-IIc/Pit2. However, the milial brain calcification disorder.5 How- molecular identity of the protein(s) participating in the basolateral Pi efflux remains ever, the role of XPR1 in the maintenance unknown. Evidence has suggested that xenotropic and polytropic retroviral recep- of Pi homeostasis remains unknown. Here, tor 1 (XPR1) might be involved in this process. Here, we show that conditional in- we addressed this issue in mice deficient for activation of Xpr1 in the renal tubule in mice resulted in impaired renal Pi Xpr1 in the nephron.
  • Metallothionein Monoclonal Antibody, Clone N11-G

    Metallothionein Monoclonal Antibody, Clone N11-G

    Metallothionein monoclonal antibody, clone N11-G Catalog # : MAB9787 規格 : [ 50 uL ] List All Specification Application Image Product Rabbit monoclonal antibody raised against synthetic peptide of MT1A, Western Blot (Recombinant protein) Description: MT1B, MT1E, MT1F, MT1G, MT1H, MT1IP, MT1L, MT1M, MT2A. Immunogen: A synthetic peptide corresponding to N-terminus of human MT1A, MT1B, MT1E, MT1F, MT1G, MT1H, MT1IP, MT1L, MT1M, MT2A. Host: Rabbit enlarge Reactivity: Human, Mouse Immunoprecipitation Form: Liquid Enzyme-linked Immunoabsorbent Assay Recommend Western Blot (1:1000) Usage: ELISA (1:5000-1:10000) The optimal working dilution should be determined by the end user. Storage Buffer: In 20 mM Tris-HCl, pH 8.0 (10 mg/mL BSA, 0.05% sodium azide) Storage Store at -20°C. Instruction: Note: This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only. Datasheet: Download Applications Western Blot (Recombinant protein) Western blot analysis of recombinant Metallothionein protein with Metallothionein monoclonal antibody, clone N11-G (Cat # MAB9787). Lane 1: 1 ug. Lane 2: 3 ug. Lane 3: 5 ug. Immunoprecipitation Enzyme-linked Immunoabsorbent Assay ASSP5 MT1A MT1B MT1E MT1F MT1G MT1H MT1M MT1L MT1IP Page 1 of 5 2021/6/2 Gene Information Entrez GeneID: 4489 Protein P04731 (Gene ID : 4489);P07438 (Gene ID : 4490);P04732 (Gene ID : Accession#: 4493);P04733 (Gene ID : 4494);P13640 (Gene ID : 4495);P80294 (Gene ID : 4496);P80295 (Gene ID : 4496);Q8N339 (Gene ID : 4499);Q86YX0 (Gene ID : 4490);Q86YX5
  • ZMYND10 Functions in a Chaperone Relay During Axonemal Dynein Assembly

    ZMYND10 Functions in a Chaperone Relay During Axonemal Dynein Assembly

    bioRxiv preprint doi: https://doi.org/10.1101/233718; this version posted December 13, 2017. 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. 1 ZMYND10 functions in a chaperone relay during axonemal dynein assembly. 2 3 Girish R Mali1,9 , Patricia Yeyati1, Seiya Mizuno2, Margaret A Keighren1, Petra zur Lage3, Amaya 4 Garcia-Munoz4, Atsuko Shimada5, Hiroyuki Takeda5, Frank Edlich6, Satoru Takahashi2,7, Alex von 5 Kreigsheim4,8, Andrew Jarman3 and Pleasantine Mill1,*. 6 7 1. MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of 8 Edinburgh, Edinburgh, UK, EH4 2XU 9 2. Laboratory Animal Resource Centre, University of Tsukuba, Tsukuba, Japan, 305-8575 10 3. Centre for Integrative Physiology, University of Edinburgh, Edinburgh, UK, EH8 9XD 11 4. Systems Biology Ireland, University College Dublin, Dublin, Ireland 12 5. Department of Biological Sciences, University of Tokyo, Tokyo, Japan, 113-0033 13 6. Institute for Biochemistry and Molecular Biology, University of Freiburg, Freiburg, Germany, 14 79104 15 7. Department of Anatomy and Embryology, Faculty of Medicine, University of Tsukuba, Tsukuba, 16 Japan, 305-8575 17 8. Edinburgh Cancer Research UK Centre, Institute of Genetics and Molecular Medicine, University 18 of Edinburgh, Edinburgh, UK, EH4 2XU 19 9. Current address: MRC Laboratory of Molecular Biology, Cambridge, UK, CB2 0QH 20 * Corresponding author: [email protected] 21 22 23 24 25 26 27 28 29 30 31 1 bioRxiv preprint doi: https://doi.org/10.1101/233718; this version posted December 13, 2017.
  • An Autocrine Activinb Mechanism Drives TGF /Activin Signaling In

    An Autocrine Activinb Mechanism Drives TGF /Activin Signaling In

    An autocrine ActivinB mechanism drives TGF β/Activin signaling in Group 3 medulloblastoma Morgane Morabito, Magalie Larcher, Florence M G Cavalli, Chloé Foray, Antoine Forget, Liliana Mirabal-ortega, Mamy Andrianteranagna, Sabine Druillennec, Alexandra Garancher, Julien Masliah-planchon, et al. To cite this version: Morgane Morabito, Magalie Larcher, Florence M G Cavalli, Chloé Foray, Antoine Forget, et al.. An autocrine ActivinB mechanism drives TGF β/Activin signaling in Group 3 medulloblastoma. EMBO Molecular Medicine, Wiley Open Access, 2019, 6, pp.e9830. 10.15252/emmm.201809830. hal-02347105 HAL Id: hal-02347105 https://hal.archives-ouvertes.fr/hal-02347105 Submitted on 5 Nov 2019 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Article An autocrine ActivinB mechanism drives TGFb/ Activin signaling in Group 3 medulloblastoma Morgane Morabito1,2,3,4,5, Magalie Larcher1,2,3,4,5, Florence MG Cavalli6,7, Chloé Foray1,2,3,4,5, Antoine Forget1,2,3,4,5, Liliana Mirabal-Ortega1,2,3,4,5, Mamy Andrianteranagna5,8,9,10,11,12,13, Sabine Druillennec1,2,3,4,5,
  • Harnessing Gene Expression Profiles for the Identification of Ex Vivo Drug

    Harnessing Gene Expression Profiles for the Identification of Ex Vivo Drug

    cancers Article Harnessing Gene Expression Profiles for the Identification of Ex Vivo Drug Response Genes in Pediatric Acute Myeloid Leukemia David G.J. Cucchi 1 , Costa Bachas 1 , Marry M. van den Heuvel-Eibrink 2,3, Susan T.C.J.M. Arentsen-Peters 3, Zinia J. Kwidama 1, Gerrit J. Schuurhuis 1, Yehuda G. Assaraf 4, Valérie de Haas 3 , Gertjan J.L. Kaspers 3,5 and Jacqueline Cloos 1,* 1 Hematology, Cancer Center Amsterdam, Amsterdam UMC, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands; [email protected] (D.G.J.C.); [email protected] (C.B.); [email protected] (Z.J.K.); [email protected] (G.J.S.) 2 Department of Pediatric Oncology/Hematology, Erasmus MC–Sophia Children’s Hospital, 3015 CN Rotterdam, The Netherlands; [email protected] 3 Princess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands; [email protected] (S.T.C.J.M.A.-P.); [email protected] (V.d.H.); [email protected] (G.J.L.K.) 4 The Fred Wyszkowski Cancer Research, Laboratory, Department of Biology, Technion-Israel Institute of Technology, 3200003 Haifa, Israel; [email protected] 5 Emma’s Children’s Hospital, Amsterdam UMC, Vrije Universiteit Amsterdam, Pediatric Oncology, 1081 HV Amsterdam, The Netherlands * Correspondence: [email protected] Received: 21 April 2020; Accepted: 12 May 2020; Published: 15 May 2020 Abstract: Novel treatment strategies are of paramount importance to improve clinical outcomes in pediatric AML. Since chemotherapy is likely to remain the cornerstone of curative treatment of AML, insights in the molecular mechanisms that determine its cytotoxic effects could aid further treatment optimization.
  • BMC Genomics Biomed Central

    BMC Genomics Biomed Central

    BMC Genomics BioMed Central Research article Open Access Functional annotation of the human retinal pigment epithelium transcriptome Judith C Booij1, Simone van Soest1, Sigrid MA Swagemakers2,3, Anke HW Essing1, Annemieke JMH Verkerk2, Peter J van der Spek2, Theo GMF Gorgels1 and Arthur AB Bergen*1,4 Address: 1Department of Molecular Ophthalmogenetics, Netherlands Institute for Neuroscience (NIN), an institute of the Royal Netherlands Academy of Arts and Sciences (KNAW), Meibergdreef 47, 1105 BA Amsterdam, the Netherlands (NL), 2Department of Bioinformatics, Erasmus Medical Center, 3015 GE Rotterdam, the Netherlands, 3Department of Genetics, Erasmus Medical Center, 3015 GE Rotterdam, the Netherlands and 4Department of Clinical Genetics, Academic Medical Centre Amsterdam, the Netherlands Email: Judith C Booij - [email protected]; Simone van Soest - [email protected]; Sigrid MA Swagemakers - [email protected]; Anke HW Essing - [email protected]; Annemieke JMH Verkerk - [email protected]; Peter J van der Spek - [email protected]; Theo GMF Gorgels - [email protected]; Arthur AB Bergen* - [email protected] * Corresponding author Published: 20 April 2009 Received: 10 July 2008 Accepted: 20 April 2009 BMC Genomics 2009, 10:164 doi:10.1186/1471-2164-10-164 This article is available from: http://www.biomedcentral.com/1471-2164/10/164 © 2009 Booij et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
  • Two Locus Inheritance of Non-Syndromic Midline Craniosynostosis Via Rare SMAD6 and 4 Common BMP2 Alleles 5 6 Andrew T

    Two Locus Inheritance of Non-Syndromic Midline Craniosynostosis Via Rare SMAD6 and 4 Common BMP2 Alleles 5 6 Andrew T

    1 2 3 Two locus inheritance of non-syndromic midline craniosynostosis via rare SMAD6 and 4 common BMP2 alleles 5 6 Andrew T. Timberlake1-3, Jungmin Choi1,2, Samir Zaidi1,2, Qiongshi Lu4, Carol Nelson- 7 Williams1,2, Eric D. Brooks3, Kaya Bilguvar1,5, Irina Tikhonova5, Shrikant Mane1,5, Jenny F. 8 Yang3, Rajendra Sawh-Martinez3, Sarah Persing3, Elizabeth G. Zellner3, Erin Loring1,2,5, Carolyn 9 Chuang3, Amy Galm6, Peter W. Hashim3, Derek M. Steinbacher3, Michael L. DiLuna7, Charles 10 C. Duncan7, Kevin A. Pelphrey8, Hongyu Zhao4, John A. Persing3, Richard P. Lifton1,2,5,9 11 12 1Department of Genetics, Yale University School of Medicine, New Haven, CT, USA 13 2Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, USA 14 3Section of Plastic and Reconstructive Surgery, Department of Surgery, Yale University School of Medicine, New Haven, CT, USA 15 4Department of Biostatistics, Yale University School of Medicine, New Haven, CT, USA 16 5Yale Center for Genome Analysis, New Haven, CT, USA 17 6Craniosynostosis and Positional Plagiocephaly Support, New York, NY, USA 18 7Department of Neurosurgery, Yale University School of Medicine, New Haven, CT, USA 19 8Child Study Center, Yale University School of Medicine, New Haven, CT, USA 20 9The Rockefeller University, New York, NY, USA 21 22 ABSTRACT 23 Premature fusion of the cranial sutures (craniosynostosis), affecting 1 in 2,000 24 newborns, is treated surgically in infancy to prevent adverse neurologic outcomes. To 25 identify mutations contributing to common non-syndromic midline (sagittal and metopic) 26 craniosynostosis, we performed exome sequencing of 132 parent-offspring trios and 59 27 additional probands.
  • Supplementary Information Integrative Analyses of Splicing in the Aging Brain: Role in Susceptibility to Alzheimer’S Disease

    Supplementary Information Integrative Analyses of Splicing in the Aging Brain: Role in Susceptibility to Alzheimer’S Disease

    Supplementary Information Integrative analyses of splicing in the aging brain: role in susceptibility to Alzheimer’s Disease Contents 1. Supplementary Notes 1.1. Religious Orders Study and Memory and Aging Project 1.2. Mount Sinai Brain Bank Alzheimer’s Disease 1.3. CommonMind Consortium 1.4. Data Availability 2. Supplementary Tables 3. Supplementary Figures Note: Supplementary Tables are provided as separate Excel files. 1. Supplementary Notes 1.1. Religious Orders Study and Memory and Aging Project Gene expression data1. Gene expression data were generated using RNA- sequencing from Dorsolateral Prefrontal Cortex (DLPFC) of 540 individuals, at an average sequence depth of 90M reads. Detailed description of data generation and processing was previously described2 (Mostafavi, Gaiteri et al., under review). Samples were submitted to the Broad Institute’s Genomics Platform for transcriptome analysis following the dUTP protocol with Poly(A) selection developed by Levin and colleagues3. All samples were chosen to pass two initial quality filters: RNA integrity (RIN) score >5 and quantity threshold of 5 ug (and were selected from a larger set of 724 samples). Sequencing was performed on the Illumina HiSeq with 101bp paired-end reads and achieved coverage of 150M reads of the first 12 samples. These 12 samples will serve as a deep coverage reference and included 2 males and 2 females of nonimpaired, mild cognitive impaired, and Alzheimer's cases. The remaining samples were sequenced with target coverage of 50M reads; the mean coverage for the samples passing QC is 95 million reads (median 90 million reads). The libraries were constructed and pooled according to the RIN scores such that similar RIN scores would be pooled together.