PCDHA12 Polyclonal Antibody (A01)
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Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like, -
Ep 3039174 B1
(19) TZZ¥Z¥__T (11) EP 3 039 174 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: C12Q 1/6886 (2018.01) C12Q 1/6883 (2018.01) 16.10.2019 Bulletin 2019/42 (86) International application number: (21) Application number: 14840036.9 PCT/US2014/053306 (22) Date of filing: 28.08.2014 (87) International publication number: WO 2015/031694 (05.03.2015 Gazette 2015/09) (54) OLIGONUCLEOTIDE PROBES AND USES THEREOF OLIGONUKLEOTIDSONDEN UND VERWENDUNGEN DAVON SONDES OLIGONUCLÉOTIDIQUES ET LEURS UTILISATIONS (84) Designated Contracting States: (74) Representative: Patent Boutique LLP AL AT BE BG CH CY CZ DE DK EE ES FI FR GB 10A Printing House Yard GR HR HU IE IS IT LI LT LU LV MC MK MT NL NO Hackney Road PL PT RO RS SE SI SK SM TR London E2 7PR (GB) (30) Priority: 28.08.2013 US 201361871107 P (56) References cited: 06.09.2013 US 201361874621 P WO-A1-2011/066589 WO-A2-2010/056337 06.11.2013 US 201361900975 P WO-A2-2011/088226 WO-A2-2013/022995 05.12.2013 US 201361912471 P 06.01.2014 US 201461924192 P • TERESA JANAS ET AL: "The selection of 06.03.2014 US 201461949216 P aptamers specific for membrane molecular 03.04.2014 US 201461974949 P targets", CELLULAR & MOLECULAR BIOLOGY 07.05.2014 US 201461990085 P LETTERS, vol. 16, no. 1, 1 March 2011 16.05.2014 US 201461994704 P (2011-03-01), pages 25-39, XP055001923, ISSN: 14.07.2014 US 201462024436 P 1425-8153, DOI: 10.2478/s11658-010-0023-3 • HENNING ULRICH ET AL: "Disease-specific (43) Date of publication of application: biomarkerdiscovery by aptamers", CYTOMETRY 06.07.2016 Bulletin 2016/27 PART A, vol. -
Role of the Chromosome Architectural Factor SMCHD1 in X-Chromosome Inactivation, Gene Regulation, and Disease in Humans
HIGHLIGHTED ARTICLE | INVESTIGATION Role of the Chromosome Architectural Factor SMCHD1 in X-Chromosome Inactivation, Gene Regulation, and Disease in Humans Chen-Yu Wang,*,† Harrison Brand,‡,§,**,†† Natalie D. Shaw,‡‡,§§ Michael E. Talkowski,‡,§,**,†† and Jeannie T. Lee*,†,1 *Department of Molecular Biology, ††Center for Human Genetic Research, and ‡‡Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, †Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, ‡Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, §Program in Medical and Population Genetics and **Center for Mendelian Genomics, Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, §§National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709 ORCID IDs: 0000-0002-3912-5113 (C.-Y.W.); 0000-0001-7786-8850 (J.T.L.) ABSTRACT Structural maintenance of chromosomes flexible hinge domain-containing 1 (SMCHD1) is an architectural factor critical for X-chromosome inactivation (XCI) and the repression of select autosomal gene clusters. In mice, homozygous nonsense mutations in Smchd1 cause female-specific embryonic lethality due to an XCI defect. However, although human mutations in SMCHD1 are associated with congenital arhinia and facioscapulohumeral muscular dystrophy type 2 (FSHD2), the diseases do not show a sex- specific bias, despite the essential nature of XCI in humans. To investigate whether there is a dosage imbalance for the sex chromo- somes, we here analyze transcriptomic data from arhinia and FSHD2 patient blood and muscle cells. We find that X-linked dosage compensation is maintained in these patients. In mice, SMCHD1 controls not only protocadherin (Pcdh) gene clusters, but also Hox genes critical for craniofacial development. -
Enhancer Hubs and Loop Collisions Identified from Single-Allele Topologies
ARTICLES https://doi.org/10.1038/s41588-018-0161-5 Enhancer hubs and loop collisions identified from single-allele topologies Amin Allahyar1,2,7, Carlo Vermeulen 3,7, Britta A. M. Bouwman3, Peter H. L. Krijger3, Marjon J. A. M. Verstegen3, Geert Geeven3, Melissa van Kranenburg3, Mark Pieterse3, Roy Straver 1, Judith H. I. Haarhuis4, Kees Jalink5, Hans Teunissen6, Ivo J. Renkens1, Wigard P. Kloosterman1, Benjamin D. Rowland4, Elzo de Wit 6, Jeroen de Ridder 1* and Wouter de Laat3* Chromatin folding contributes to the regulation of genomic processes such as gene activity. Existing conformation capture methods characterize genome topology through analysis of pairwise chromatin contacts in populations of cells but cannot dis- cern whether individual interactions occur simultaneously or competitively. Here we present multi-contact 4C (MC-4C), which applies Nanopore sequencing to study multi-way DNA conformations of individual alleles. MC-4C distinguishes cooperative from random and competing interactions and identifies previously missed structures in subpopulations of cells. We show that individual elements of the β-globin superenhancer can aggregate into an enhancer hub that can simultaneously accommodate two genes. Neighboring chromatin domain loops can form rosette-like structures through collision of their CTCF-bound anchors, as seen most prominently in cells lacking the cohesin-unloading factor WAPL. Here, massive collision of CTCF-anchored chro- matin loops is believed to reflect ‘cohesin traffic jams’. Single-allele topology studies thus help us understand the mechanisms underlying genome folding and functioning. he invention of chromatin conformation capture (3C) tech- matrices cannot distinguish clustered interactions from mutually nology1 and derived methods2 has greatly advanced our exclusive interactions that independently occur in different cells. -
The Pdx1 Bound Swi/Snf Chromatin Remodeling Complex Regulates Pancreatic Progenitor Cell Proliferation and Mature Islet Β Cell
Page 1 of 125 Diabetes The Pdx1 bound Swi/Snf chromatin remodeling complex regulates pancreatic progenitor cell proliferation and mature islet β cell function Jason M. Spaeth1,2, Jin-Hua Liu1, Daniel Peters3, Min Guo1, Anna B. Osipovich1, Fardin Mohammadi3, Nilotpal Roy4, Anil Bhushan4, Mark A. Magnuson1, Matthias Hebrok4, Christopher V. E. Wright3, Roland Stein1,5 1 Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN 2 Present address: Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN 3 Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 4 Diabetes Center, Department of Medicine, UCSF, San Francisco, California 5 Corresponding author: [email protected]; (615)322-7026 1 Diabetes Publish Ahead of Print, published online June 14, 2019 Diabetes Page 2 of 125 Abstract Transcription factors positively and/or negatively impact gene expression by recruiting coregulatory factors, which interact through protein-protein binding. Here we demonstrate that mouse pancreas size and islet β cell function are controlled by the ATP-dependent Swi/Snf chromatin remodeling coregulatory complex that physically associates with Pdx1, a diabetes- linked transcription factor essential to pancreatic morphogenesis and adult islet-cell function and maintenance. Early embryonic deletion of just the Swi/Snf Brg1 ATPase subunit reduced multipotent pancreatic progenitor cell proliferation and resulted in pancreas hypoplasia. In contrast, removal of both Swi/Snf ATPase subunits, Brg1 and Brm, was necessary to compromise adult islet β cell activity, which included whole animal glucose intolerance, hyperglycemia and impaired insulin secretion. Notably, lineage-tracing analysis revealed Swi/Snf-deficient β cells lost the ability to produce the mRNAs for insulin and other key metabolic genes without effecting the expression of many essential islet-enriched transcription factors. -
Thousands of Cpgs Show DNA Methylation Differences in ACPA-Positive Individuals
G C A T T A C G G C A T genes Article Thousands of CpGs Show DNA Methylation Differences in ACPA-Positive Individuals Yixiao Zeng 1,2, Kaiqiong Zhao 2,3, Kathleen Oros Klein 2, Xiaojian Shao 4, Marvin J. Fritzler 5, Marie Hudson 2,6,7, Inés Colmegna 6,8, Tomi Pastinen 9,10, Sasha Bernatsky 6,8 and Celia M. T. Greenwood 1,2,3,9,11,* 1 PhD Program in Quantitative Life Sciences, Interfaculty Studies, McGill University, Montréal, QC H3A 1E3, Canada; [email protected] 2 Lady Davis Institute for Medical Research, Jewish General Hospital, Montréal, QC H3T 1E2, Canada; [email protected] (K.Z.); [email protected] (K.O.K.); [email protected] (M.H.) 3 Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montréal, QC H3A 1A2, Canada 4 Digital Technologies Research Centre, National Research Council Canada, Ottawa, ON K1A 0R6, Canada; [email protected] 5 Cumming School of Medicine, University of Calgary, Calgary, AB T2N 1N4, Canada; [email protected] 6 Department of Medicine, McGill University, Montréal, QC H4A 3J1, Canada; [email protected] (I.C.); [email protected] (S.B.) 7 Division of Rheumatology, Jewish General Hospital, Montréal, QC H3T 1E2, Canada 8 Division of Rheumatology, McGill University, Montréal, QC H3G 1A4, Canada 9 Department of Human Genetics, McGill University, Montréal, QC H3A 0C7, Canada; [email protected] 10 Center for Pediatric Genomic Medicine, Children’s Mercy, Kansas City, MO 64108, USA 11 Gerald Bronfman Department of Oncology, McGill University, Montréal, QC H4A 3T2, Canada * Correspondence: [email protected] Citation: Zeng, Y.; Zhao, K.; Oros Abstract: High levels of anti-citrullinated protein antibodies (ACPA) are often observed prior to Klein, K.; Shao, X.; Fritzler, M.J.; Hudson, M.; Colmegna, I.; Pastinen, a diagnosis of rheumatoid arthritis (RA). -
Full Text (PDF)
medRxiv preprint doi: https://doi.org/10.1101/2020.12.29.20248986; this version posted January 4, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . Insights into the molecular mechanism of anticancer drug ruxolitinib repurposable in COVID-19 therapy Manisha Mandal Department of Physiology, MGM Medical College, Kishanganj-855107, India Email: [email protected], ORCID: https://orcid.org/0000-0002-9562-5534 Shyamapada Mandal* Department of Zoology, University of Gour Banga, Malda-732103, India Email: [email protected], ORCID: https://orcid.org/0000-0002-9488-3523 *Corresponding author: Email: [email protected]; [email protected] Abstract Due to non-availability of specific therapeutics against COVID-19, repurposing of approved drugs is a reasonable option. Cytokines imbalance in COVID-19 resembles cancer; exploration of anti-inflammatory agents, might reduce COVID-19 mortality. The current study investigates the effect of ruxolitinib treatment in SARS-CoV-2 infected alveolar cells compared to the uninfected one from the GSE5147507 dataset. The protein-protein interaction network, biological process and functional enrichment of differentially expressed genes were studied using STRING App of the Cytoscape software and R programming tools. The present study indicated that ruxolitinib treatment elicited similar response equivalent to that of SARS-CoV-2 uninfected situation by inducing defense response in host against virus infection by RLR and NOD like receptor pathways. Further, the effect of ruxolitinib in SARS- CoV-2 infection was mainly caused by significant suppression of IFIH1, IRF7 and MX1 genes as well as inhibition of DDX58/IFIH1-mediated induction of interferon- I and -II signalling. -
Table S1. 103 Ferroptosis-Related Genes Retrieved from the Genecards
Table S1. 103 ferroptosis-related genes retrieved from the GeneCards. Gene Symbol Description Category GPX4 Glutathione Peroxidase 4 Protein Coding AIFM2 Apoptosis Inducing Factor Mitochondria Associated 2 Protein Coding TP53 Tumor Protein P53 Protein Coding ACSL4 Acyl-CoA Synthetase Long Chain Family Member 4 Protein Coding SLC7A11 Solute Carrier Family 7 Member 11 Protein Coding VDAC2 Voltage Dependent Anion Channel 2 Protein Coding VDAC3 Voltage Dependent Anion Channel 3 Protein Coding ATG5 Autophagy Related 5 Protein Coding ATG7 Autophagy Related 7 Protein Coding NCOA4 Nuclear Receptor Coactivator 4 Protein Coding HMOX1 Heme Oxygenase 1 Protein Coding SLC3A2 Solute Carrier Family 3 Member 2 Protein Coding ALOX15 Arachidonate 15-Lipoxygenase Protein Coding BECN1 Beclin 1 Protein Coding PRKAA1 Protein Kinase AMP-Activated Catalytic Subunit Alpha 1 Protein Coding SAT1 Spermidine/Spermine N1-Acetyltransferase 1 Protein Coding NF2 Neurofibromin 2 Protein Coding YAP1 Yes1 Associated Transcriptional Regulator Protein Coding FTH1 Ferritin Heavy Chain 1 Protein Coding TF Transferrin Protein Coding TFRC Transferrin Receptor Protein Coding FTL Ferritin Light Chain Protein Coding CYBB Cytochrome B-245 Beta Chain Protein Coding GSS Glutathione Synthetase Protein Coding CP Ceruloplasmin Protein Coding PRNP Prion Protein Protein Coding SLC11A2 Solute Carrier Family 11 Member 2 Protein Coding SLC40A1 Solute Carrier Family 40 Member 1 Protein Coding STEAP3 STEAP3 Metalloreductase Protein Coding ACSL1 Acyl-CoA Synthetase Long Chain Family Member 1 Protein -
Name Aliases Binding Partner Physiology / Oncology References
Name Aliases Binding partner Physiology / Oncology References AJAP1 Adherens junction associated protein 1, ? PHY : Expressed in uterus and pancreas. [1] http://www.uniprot.org/uniprot/Q9UKB5. [2] SHREW1 Plays a role in cell adhesion and migration. McDonald JM, Cancer Biol Ther 2006, 5:300-4 Forms a complex with CDH1 and beta-catenin at adherens junctions [1] ONC : Frequently deleted in oligodendrogliomas, functions to inhibit cell adhesion and migration [2] ALCAM Activated leukocyte cell adhesion CD6 PHY : Adhesion of activated leukocytes and [1] Ofori-Acquah SF, Transl Res 2008, 151:122- molecule, CD166, MEMD (melanoma neurons 8. [2] van Kilsdonk JW, Cancer Res 2008, metastasis clone D) 68:3671-9 ONC : Expressed by different tumor types including melanoma; mediates cancer/ melanoma invasiveness [1,2] AMICA1 Adhesion molecule interacting with CXADR PHY : Expression is restricted to the [1] http://www.uniprot.org/uniprot/Q86YT9. [2] CXADR antigen 1, JAML (junctional hematopoietic tissues with the exception of Moog-Lutz C, Blood 2003, 102:3371-8 adhesion molecule-like) liver. May function in transmigration of leukocytes through epithelial and endothelial tissues. Mediates adhesive interactions with CXADR, a protein of the junctional complex of epithelial cells [1] ONC : Enhances myeloid leukemia cell adhesion to endothelial cells [2] AMIGO1 Amphoterin-induced gene and open AMIGO PHY : May be involved in fasciculation as well [1] http://www.uniprot.org/uniprot/Q86WK6 reading frame 1, Alivin-2 as myelination of developing neural axons. May have a role in regeneration as well as neural plasticity in the adult nervous system. May mediate homophilic as well as heterophilic cell-cell interaction and contribute to signal transduction through its intracellular domain [1] ONC : - AMIGO2 Amphoterin-induced gene and open AMIGO PHY : Highest levels in breast, ovary, cervix, [1] http://www.uniprot.org/uniprot/Q86SJ2. -
Antisense Lncrna Transcription Drives Stochastic Protocadherin Α Promoter Choice
bioRxiv preprint doi: https://doi.org/10.1101/360206; this version posted July 1, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Antisense lncRNA transcription drives stochastic Protocadherin α promoter choice Daniele Canzio1,2,*, Chiamaka L. Nwakeze1,2,*, Adan Horta1,2, Sandy M. Rajkumar 1,2, Eliot L. Coffey3, Erin E. Duffy4, Rachel Duffié1,2, Matthew D. Simon4, Stavros Lomvardas1,2, Tom Maniatis1,2,5,# 1. Department of Biochemistry and Molecular Biophysics, Columbia University, New York, NY, 10032 2. Mortimer B. Zuckerman Mind Brain and Behavior Institute, Columbia University, New York, NY, 10027 3. Whitehead Institute for Biomedical Research, Cambridge, 02142 4. Department of Molecular Biophysics and Biochemistry, Yale University, 06516 5. New York Genome Center, New York, NY 10013 * These authors contributed equally to the work # To whom correspondence should be addressed: [email protected] The authors declare no competing financial interests. 1 bioRxiv preprint doi: https://doi.org/10.1101/360206; this version posted July 1, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. SUMMARY Stochastic and combinatorial activation of clustered Protocadherin (Pcdh) α, β, and γ gene promoters generates a cell-surface identity code in individual neurons that functions in neural circuit assembly. Here we show that Pcdhα promoter choice requires transcription of a long noncoding RNA (lncRNA) initiated from newly identified promoters located in the protein coding sequence of each Pcdhα exon. -
Genomic Profiling of Primary Histiocytic Sarcoma Reveals Two Molecular
Hystiocyte DIsordes SUPPLEMENTARY APPENDIX Genomic profiling of primary histiocytic sarcoma reveals two molecular subgroups Caoimhe Egan, 1 Alina Nicolae, 1 Justin Lack, 2 Hye-Jung Chung, 1 Shannon Skarshaug, 1 Thu Anh Pham, 1 Winnifred Navarro, 1 Zied Abdullaev, 1 Nadine S. Aguilera, 3 Liqiang Xi, 1 Svetlana Pack, 1 Stefania Pittaluga, 1 Elaine S. Jaffe 1 and Mark Raffeld 1 1Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD; 2NIAID Collaborative Bioinformatics Resource (NCBR), National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD and 3University of Virginia Health System, Charlottesville, VA, USA ©2020 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol. 2019.230375 Received: June 25, 2019. Accepted: August 21, 2019. Pre-published: August 22, 2019. Correspondence: MARK RAFFELD - [email protected] Supplementary Material: Genomic profiling of primary histiocytic sarcoma reveals two molecular subgroups Caoimhe Egan1, Alina Nicolae1, Justin Lack2, Hye-Jung Chung1, Shannon Skarshaug1, Thu Anh Pham1, Winnifred Navarro1, Zied Abdullaev1, Nadine S Aguilera3, Liqiang Xi1, Svetlana Pack1, Stefania Pittaluga1, Elaine S Jaffe1 and Mark Raffeld1. 1Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. 2NIAID Collaborative Bioinformatics Resource (NCBR), National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. 3 University of Virginia Health System, 1215 Lee Street, Box 800214, Charlottesville, VA, USA. 1 Supplementary Methods Case selection. Twenty-one cases of primary histiocytic sarcoma (pHS) with a tumor content of at least 40% were identified from the files of the Hematopathology Section of the National Cancer Institute under an IRB approved protocol. -
Disease-Associated Mutations of Claudin-19 Disrupt Retinal Neurogenesis and Visual Function
ARTICLE https://doi.org/10.1038/s42003-019-0355-0 OPEN Disease-associated mutations of claudin-19 disrupt retinal neurogenesis and visual function Shao-Bin Wang1,2,4, Tao Xu1,2,3, Shaomin Peng3, Deepti Singh1,2,5, Maryam Ghiassi-Nejad1,2, Ron A. Adelman2 & Lawrence J. Rizzolo 1,2 1234567890():,; Mutations of claudin-19 cause Familial Hypomagnesaemia and Hypercalciuria, Nephrocalci- nosis with Ocular Involvement. To study the ocular disease without the complications of the kidney disease, naturally occurring point mutations of human CLDN19 were recreated in human induced pluripotent cells or overexpressed in the retinae of newborn mice. In human induced pluripotent cells, we show that the mutation affects retinal neurogenesis and maturation of retinal pigment epithelium (RPE). In mice, the mutations diminish the P1 wave of the electroretinogram, activate apoptosis in the outer nuclear layer, and alter the mor- phology of bipolar cells. If mice are given 9-cis-retinal to counter the loss of retinal isomerase, the P1 wave is partially restored. The ARPE19 cell line fails to express claudin-19. Exogenous expression of wild type, but not mutant claudin-19, increases the expression of RPE signature genes. Mutated claudin-19 affects multiple stages of RPE and retinal differentiation through its effects on multiple functions of the RPE. 1 Department of Surgery, Yale University, PO Box 208062, New Haven, CT, USA. 2 Department of Ophthalmology, Yale University, 40 Temple Street, New Haven, CT, USA. 3 Aier School of Ophthalmology, Central South University, 198 Furong Middle Ave Section 2, Tianxin District, Changsha, China. 4Present address: Center for Advanced Vision Science, Department of Ophthalmology, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA.