DOCSLIB.ORG

LRRN1 (S-17): Sc-103020

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
LRRN1 (S-17): Sc-103020 SAN TA C RUZ BI OTEC HNOL OG Y, INC . LRRN1 (S-17): sc-103020 BACKGROUND SOURCE Leucine-rich repeats (LRRs) are 20-30 amino acid motifs that mediate pro tein- LRRN1 (S-17) is an affinity purified goat polyclonal antibody raised against protein interactions. The primary function of these motifs is to provide a ver - a peptide mapping within an internal region of LRRN1 of human origin. satile structural framework for the formation of these protein-protein inter ac - tions. LRRs are present in a variety of proteins with diverse structure and func - PRODUCT tion, including innate immunity and nervous system development. Several Each vial contains 200 µg IgG in 1.0 ml of PBS with < 0.1% sodium azide human diseases are associated with mutations in the genes encoding LRR- and 0.1% gelatin. containing proteins. LRRN1 (leucine-rich repeat neuronal protein 1) is a 716 amino acid protein that contains 11 LRRs, one Ig-like C2-type (immuno- glob - Blocking peptide available for competition studies, sc-103020 P, (100 µg ulin-like) domain and one fibronectin type-III domain. The gene encoding this pep tide in 0.5 ml PBS containing < 0.1% sodium azide and 0.2% BSA). type I transmembrane protein is upregulated by N- and C-Myc and is found to be highly expressed in neuroblastomas that are associated with poor APPLICATIONS prognosis. Knockdown of the LRRN1 gene in cells exhibits reduced growth LRRN1 (S-17) is recommended for detection of LRRN1 of mouse, rat and rate and sensitizes cells to serum starvation. human origin by Western Blotting (starting dilution 1:200, dilution range 1:100-1:1000), immunofluorescence (starting dilution 1:50, dilution range REFERENCES 1:50-1:500) and solid phase ELISA (starting dilution 1:30, dilution range 1. Taguchi, A., et al. 1996. Molecular cloning of novel leucine-rich repeat 1:30- 1:3000); non cross-reactive with LRRN2 or LRRN3. proteins and their expression in the developing mouse nervous system. LRRN1 (S-17) is also recommended for detection of LRRN1 in additional Brain Res. Mol. Brain Res. 35: 31-40. species, including bovine. 2. Ohira, M., et al. 2003. Neuroblastoma oligo-capping cDNA project: toward Suitable for use as control antibody for LRRN1 siRNA (h): sc-78350, LRRN1 the understanding of the genesis and biology of neuroblastoma. Cancer siRNA (m): sc-149116, LRRN1 shRNA Plasmid (h): sc-78350-SH, LRRN1 shRNA Lett. 197: 63-68. Plasmid (m): sc-149116-SH, LRRN1 shRNA (h) Lentiviral Particles: sc-78350-V 3. Clark, H.F., et al. 2003. The secreted protein discovery initiative (SPDI), a and LRRN1 shRNA (m) Lentiviral Particles: sc-149116-V. large-scale effort to identify novel human secreted and transmembrane Molecular Weight of LRRN1: 81 kDa. proteins: a bioinformatics assessment. Genome Res. 13: 2265-2270. 4. Higgins, J.J., et al. 2004. Candidate genes for recessive non-syndromic RECOMMENDED SECONDARY REAGENTS mental retardation on chromosome 3p (MRT2A). Clin. Genet. 65: 496-500. To ensure optimal results, the following support (secondary) reagents are 5. Hamano, S., et al. 2004. Identification of novel human neuronal leucine- rich recommended: 1) Western Blotting: use donkey anti-goat IgG-HRP: sc-2020 repeat (hNLRR) family genes and inverse association of expression of (dilution range: 1:2000-1:100,000) or Cruz Marker™ compatible donkey Nbla10449/hNLRR-1 and Nbla10677/hNLRR-3 with the prognosis of pri mary anti- goat IgG-HRP: sc-2033 (dilution range: 1:2000-1:5000), Cruz Marker™ neuroblastomas. Int. J. Oncol. 24: 1457-1466. Molecular Weight Standards: sc-2035, TBS Blotto A Blocking Reagent: sc-2333 and Western Blotting Luminol Reagent: sc-2048. 2) Immunofluo- 6. Haines, B.P., et al. 2005. The NLRR gene family and mouse development: rescence: use donkey anti-goat IgG-FITC: sc-2024 (dilution range: 1:100- Modified differential display PCR identifies NLRR-1 as a gene expressed 1:400) or donkey anti-goat IgG-TR: sc-2783 (dilution range: 1:100-1:400) in early somitic myoblasts. Dev. Biol. 281: 145-159. with UltraCruz™ Mounting Medium: sc-24941. 7. García-Calero, E., et al. 2006. Expression of Lrrn1 marks the prospective site of the zona limitans thalami in the early embryonic chicken dien cephalon. STORAGE Gene Expr. Patterns 6: 879-885. Store at 4° C, **DO NOT FREEZE**. Stable for one year from the date of 8. Andreae, L.C., et al. 2007. Analysis of Lrrn1 expression and its relationship shipment. Non-hazardous. No MSDS required. to neuromeric boundaries during chick neural development. Neural Dev. 2: 22. RESEARCH USE For research use only, not for use in diagnostic procedures. 9. Hossain, M.S., et al. 2008. N-MYC promotes cell proliferation through a direct transactivation of neuronal leucine-rich repeat protein-1 (NLRR1) gene in neuroblastoma. Oncogene 27: 6075-6082. PROTOCOLS See our web site at www.scbt.com or our catalog for detailed protocols and CHROMOSOMAL LOCATION support products. Genetic locus: LRRN1 (human) mapping to 3p26.2; Lrrn1 (mouse) mapping to 6 E1. Santa Cruz Biotechnology, Inc. 1.800.457.3801 831.457.3800 fax 831.457.3801 Europe +00800 4573 8000 49 6221 4503 0 www.scbt.com.
Load more

Recommended publications
  • Table 2. Functional Classification of Genes Differentially Regulated After HOXB4 Inactivation in HSC/Hpcs
    Table 2. Functional classification of genes differentially regulated after HOXB4 inactivation in HSC/HPCs Symbol Gene description Fold-change (mean ± SD) Signal transduction Adam8 A disintegrin and metalloprotease domain 8 1.91 ± 0.51 Arl4 ADP-ribosylation factor-like 4 - 1.80 ± 0.40 Dusp6 Dual specificity phosphatase 6 (Mkp3) - 2.30 ± 0.46 Ksr1 Kinase suppressor of ras 1 1.92 ± 0.42 Lyst Lysosomal trafficking regulator 1.89 ± 0.34 Mapk1ip1 Mitogen activated protein kinase 1 interacting protein 1 1.84 ± 0.22 Narf* Nuclear prelamin A recognition factor 2.12 ± 0.04 Plekha2 Pleckstrin homology domain-containing. family A. (phosphoinosite 2.15 ± 0.22 binding specific) member 2 Ptp4a2 Protein tyrosine phosphatase 4a2 - 2.04 ± 0.94 Rasa2* RAS p21 activator protein 2 - 2.80 ± 0.13 Rassf4 RAS association (RalGDS/AF-6) domain family 4 3.44 ± 2.56 Rgs18 Regulator of G-protein signaling - 1.93 ± 0.57 Rrad Ras-related associated with diabetes 1.81 ± 0.73 Sh3kbp1 SH3 domain kinase bindings protein 1 - 2.19 ± 0.53 Senp2 SUMO/sentrin specific protease 2 - 1.97 ± 0.49 Socs2 Suppressor of cytokine signaling 2 - 2.82 ± 0.85 Socs5 Suppressor of cytokine signaling 5 2.13 ± 0.08 Socs6 Suppressor of cytokine signaling 6 - 2.18 ± 0.38 Spry1 Sprouty 1 - 2.69 ± 0.19 Sos1 Son of sevenless homolog 1 (Drosophila) 2.16 ± 0.71 Ywhag 3-monooxygenase/tryptophan 5- monooxygenase activation protein. - 2.37 ± 1.42 gamma polypeptide Zfyve21 Zinc finger. FYVE domain containing 21 1.93 ± 0.57 Ligands and receptors Bambi BMP and activin membrane-bound inhibitor - 2.94 ± 0.62
    [Show full text]
  • Genomic Correlates of Relationship QTL Involved in Fore- Versus Hind Limb Divergence in Mice
    Loyola University Chicago Loyola eCommons Biology: Faculty Publications and Other Works Faculty Publications 2013 Genomic Correlates of Relationship QTL Involved in Fore- Versus Hind Limb Divergence in Mice Mihaela Palicev Gunter P. Wagner James P. Noonan Benedikt Hallgrimsson James M. Cheverud Loyola University Chicago, [email protected] Follow this and additional works at: https://ecommons.luc.edu/biology_facpubs Part of the Biology Commons Recommended Citation Palicev, M, GP Wagner, JP Noonan, B Hallgrimsson, and JM Cheverud. "Genomic Correlates of Relationship QTL Involved in Fore- Versus Hind Limb Divergence in Mice." Genome Biology and Evolution 5(10), 2013. This Article is brought to you for free and open access by the Faculty Publications at Loyola eCommons. It has been accepted for inclusion in Biology: Faculty Publications and Other Works by an authorized administrator of Loyola eCommons. For more information, please contact [email protected]. This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License. © Palicev et al., 2013. GBE Genomic Correlates of Relationship QTL Involved in Fore- versus Hind Limb Divergence in Mice Mihaela Pavlicev1,2,*, Gu¨ nter P. Wagner3, James P. Noonan4, Benedikt Hallgrı´msson5,and James M. Cheverud6 1Konrad Lorenz Institute for Evolution and Cognition Research, Altenberg, Austria 2Department of Pediatrics, Cincinnati Children‘s Hospital Medical Center, Cincinnati, Ohio 3Yale Systems Biology Institute and Department of Ecology and Evolutionary Biology, Yale University 4Department of Genetics, Yale University School of Medicine 5Department of Cell Biology and Anatomy, The McCaig Institute for Bone and Joint Health and the Alberta Children’s Hospital Research Institute for Child and Maternal Health, University of Calgary, Calgary, Canada 6Department of Anatomy and Neurobiology, Washington University *Corresponding author: E-mail: [email protected].
    [Show full text]
  • Whole-Genome Microarray Detects Deletions and Loss of Heterozygosity of Chromosome 3 Occurring Exclusively in Metastasizing Uveal Melanoma
    Anatomy and Pathology Whole-Genome Microarray Detects Deletions and Loss of Heterozygosity of Chromosome 3 Occurring Exclusively in Metastasizing Uveal Melanoma Sarah L. Lake,1 Sarah E. Coupland,1 Azzam F. G. Taktak,2 and Bertil E. Damato3 PURPOSE. To detect deletions and loss of heterozygosity of disease is fatal in 92% of patients within 2 years of diagnosis. chromosome 3 in a rare subset of fatal, disomy 3 uveal mela- Clinical and histopathologic risk factors for UM metastasis noma (UM), undetectable by fluorescence in situ hybridization include large basal tumor diameter (LBD), ciliary body involve- (FISH). ment, epithelioid cytomorphology, extracellular matrix peri- ϩ ETHODS odic acid-Schiff-positive (PAS ) loops, and high mitotic M . Multiplex ligation-dependent probe amplification 3,4 5 (MLPA) with the P027 UM assay was performed on formalin- count. Prescher et al. showed that a nonrandom genetic fixed, paraffin-embedded (FFPE) whole tumor sections from 19 change, monosomy 3, correlates strongly with metastatic death, and the correlation has since been confirmed by several disomy 3 metastasizing UMs. Whole-genome microarray analy- 3,6–10 ses using a single-nucleotide polymorphism microarray (aSNP) groups. Consequently, fluorescence in situ hybridization were performed on frozen tissue samples from four fatal dis- (FISH) detection of chromosome 3 using a centromeric probe omy 3 metastasizing UMs and three disomy 3 tumors with Ͼ5 became routine practice for UM prognostication; however, 5% years’ metastasis-free survival. to 20% of disomy 3 UM patients unexpectedly develop metas- tases.11 Attempts have therefore been made to identify the RESULTS. Two metastasizing UMs that had been classified as minimal region(s) of deletion on chromosome 3.12–15 Despite disomy 3 by FISH analysis of a small tumor sample were found these studies, little progress has been made in defining the key on MLPA analysis to show monosomy 3.
    [Show full text]
  • A Conserved Gene Family Encodes Transmembrane Proteins with Fibronectin, Immunoglobulin and Leucine-Rich Repeat Domains (FIGLER) Delicia L
    A conserved gene family encodes transmembrane proteins with fibronectin, immunoglobulin and leucine-rich repeat domains (FIGLER) Delicia L. Munfus, University of Alabama at Birmingham Christopher L. Haga, University of Alabama at Birmingham Peter D. Burrows, University of Alabama at Birmingham Max Cooper, Emory University Journal Title: BMC Biology Volume: Volume 5, Number 1 Publisher: BioMed Central | 2007-09-13, Pages 36-36 Type of Work: Article | Final Publisher PDF Publisher DOI: 10.1186/1741-7007-5-36 Permanent URL: https://pid.emory.edu/ark:/25593/rqdhh Final published version: http://dx.doi.org/10.1186/1741-7007-5-36 Copyright information: © 2007 Munfus et al; licensee BioMed Central Ltd. This is an Open Access work distributed under the terms of the Creative Commons Attribution 2.0 Generic License (http://creativecommons.org/licenses/by/2.0/). Accessed October 6, 2021 6:19 AM EDT BMC Biology BioMed Central Research article Open Access A conserved gene family encodes transmembrane proteins with fibronectin, immunoglobulin and leucine-rich repeat domains (FIGLER) Delicia L Munfus†1,2, Christopher L Haga†1,2, Peter D Burrows1,2,3 and Max D Cooper*1,2,4,5 Address: 1Division of Developmental and Clinical Immunology, University of Alabama at Birmingham, Birmingham, AL 35294-3300, USA, 2Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294-3300, USA, 3Department of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294-3300,, 4Department of Medicine, University of Alabama at Birmingham, Birmingham,
    [Show full text]
  • Supplemental Table 1. Complete Gene Lists and GO Terms from Figure 3C
    Supplemental Table 1. Complete gene lists and GO terms from Figure 3C. Path 1 Genes: RP11-34P13.15, RP4-758J18.10, VWA1, CHD5, AZIN2, FOXO6, RP11-403I13.8, ARHGAP30, RGS4, LRRN2, RASSF5, SERTAD4, GJC2, RHOU, REEP1, FOXI3, SH3RF3, COL4A4, ZDHHC23, FGFR3, PPP2R2C, CTD-2031P19.4, RNF182, GRM4, PRR15, DGKI, CHMP4C, CALB1, SPAG1, KLF4, ENG, RET, GDF10, ADAMTS14, SPOCK2, MBL1P, ADAM8, LRP4-AS1, CARNS1, DGAT2, CRYAB, AP000783.1, OPCML, PLEKHG6, GDF3, EMP1, RASSF9, FAM101A, STON2, GREM1, ACTC1, CORO2B, FURIN, WFIKKN1, BAIAP3, TMC5, HS3ST4, ZFHX3, NLRP1, RASD1, CACNG4, EMILIN2, L3MBTL4, KLHL14, HMSD, RP11-849I19.1, SALL3, GADD45B, KANK3, CTC- 526N19.1, ZNF888, MMP9, BMP7, PIK3IP1, MCHR1, SYTL5, CAMK2N1, PINK1, ID3, PTPRU, MANEAL, MCOLN3, LRRC8C, NTNG1, KCNC4, RP11, 430C7.5, C1orf95, ID2-AS1, ID2, GDF7, KCNG3, RGPD8, PSD4, CCDC74B, BMPR2, KAT2B, LINC00693, ZNF654, FILIP1L, SH3TC1, CPEB2, NPFFR2, TRPC3, RP11-752L20.3, FAM198B, TLL1, CDH9, PDZD2, CHSY3, GALNT10, FOXQ1, ATXN1, ID4, COL11A2, CNR1, GTF2IP4, FZD1, PAX5, RP11-35N6.1, UNC5B, NKX1-2, FAM196A, EBF3, PRRG4, LRP4, SYT7, PLBD1, GRASP, ALX1, HIP1R, LPAR6, SLITRK6, C16orf89, RP11-491F9.1, MMP2, B3GNT9, NXPH3, TNRC6C-AS1, LDLRAD4, NOL4, SMAD7, HCN2, PDE4A, KANK2, SAMD1, EXOC3L2, IL11, EMILIN3, KCNB1, DOK5, EEF1A2, A4GALT, ADGRG2, ELF4, ABCD1 Term Count % PValue Genes regulation of pathway-restricted GDF3, SMAD7, GDF7, BMPR2, GDF10, GREM1, BMP7, LDLRAD4, SMAD protein phosphorylation 9 6.34 1.31E-08 ENG pathway-restricted SMAD protein GDF3, SMAD7, GDF7, BMPR2, GDF10, GREM1, BMP7, LDLRAD4, phosphorylation
    [Show full text]
  • Genetic Drivers of Pancreatic Islet Function
    | INVESTIGATION Genetic Drivers of Pancreatic Islet Function Mark P. Keller,*,1 Daniel M. Gatti,†,1 Kathryn L. Schueler,* Mary E. Rabaglia,* Donnie S. Stapleton,* Petr Simecek,† Matthew Vincent,† Sadie Allen,‡ Aimee Teo Broman,§ Rhonda Bacher,§ Christina Kendziorski,§ Karl W. Broman,§ Brian S. Yandell,** Gary A. Churchill,†,2 and Alan D. Attie*,2 *Department of Biochemistry, §Department of Biostatistics and Medical Informatics, and **Department of Horticulture, University of Wisconsin–Madison, Wisconsin 53706-1544, †The Jackson Laboratory, Bar Harbor, Maine 06409, and ‡Maine School of Science and Mathematics, Limestone, Maine 06409, ORCID IDs: 0000-0002-7405-5552 (M.P.K.); 0000-0002-4914-6671 (K.W.B.); 0000-0001-9190-9284 (G.A.C.); 0000-0002-0568-2261 (A.D.A.) ABSTRACT The majority of gene loci that have been associated with type 2 diabetes play a role in pancreatic islet function. To evaluate the role of islet gene expression in the etiology of diabetes, we sensitized a genetically diverse mouse population with a Western diet high in fat (45% kcal) and sucrose (34%) and carried out genome-wide association mapping of diabetes-related phenotypes. We quantified mRNA abundance in the islets and identified 18,820 expression QTL. We applied mediation analysis to identify candidate causal driver genes at loci that affect the abundance of numerous transcripts. These include two genes previously associated with monogenic diabetes (PDX1 and HNF4A), as well as three genes with nominal association with diabetes-related traits in humans (FAM83E, IL6ST, and SAT2). We grouped transcripts into gene modules and mapped regulatory loci for modules enriched with transcripts specific for a-cells, and another specific for d-cells.
    [Show full text]
  • Epigenetic Alterations of Chromosome 3 Revealed by Noti-Microarrays in Clear Cell Renal Cell Carcinoma
    Hindawi Publishing Corporation BioMed Research International Volume 2014, Article ID 735292, 9 pages http://dx.doi.org/10.1155/2014/735292 Research Article Epigenetic Alterations of Chromosome 3 Revealed by NotI-Microarrays in Clear Cell Renal Cell Carcinoma Alexey A. Dmitriev,1,2 Evgeniya E. Rudenko,3 Anna V. Kudryavtseva,1,2 George S. Krasnov,1,4 Vasily V. Gordiyuk,3 Nataliya V. Melnikova,1 Eduard O. Stakhovsky,5 Oleksii A. Kononenko,5 Larissa S. Pavlova,6 Tatiana T. Kondratieva,6 Boris Y. Alekseev,2 Eleonora A. Braga,7,8 Vera N. Senchenko,1 and Vladimir I. Kashuba3,9 1 Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow 119991, Russia 2 P.A. Herzen Moscow Oncology Research Institute, Ministry of Healthcare of the Russian Federation, Moscow 125284, Russia 3 Institute of Molecular Biology and Genetics, Ukrainian Academy of Sciences, Kiev 03680, Ukraine 4 Mechnikov Research Institute for Vaccines and Sera, Russian Academy of Medical Sciences, Moscow 105064, Russia 5 National Cancer Institute, Kiev 03022, Ukraine 6 N.N. Blokhin Russian Cancer Research Center, Russian Academy of Medical Sciences, Moscow 115478, Russia 7 Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow 125315, Russia 8 Research Center of Medical Genetics, Russian Academy of Medical Sciences, Moscow 115478, Russia 9 DepartmentofMicrobiology,TumorandCellBiology,KarolinskaInstitute,17177Stockholm,Sweden Correspondence should be addressed to Alexey A. Dmitriev; alex [email protected] Received 19 February 2014; Revised 10 April 2014; Accepted 17 April 2014; Published 22 May 2014 Academic Editor: Carole Sourbier Copyright © 2014 Alexey A. Dmitriev et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
    [Show full text]
  • Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
    Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Science (Cancer Biology) Aneuploidy: Using genetic instability to preserve a haploid genome? Submitted by: Ramona Ramdath In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Science Examination Committee Signature/Date Major Advisor: David Allison, M.D., Ph.D. Academic James Trempe, Ph.D. Advisory Committee: David Giovanucci, Ph.D. Randall Ruch, Ph.D. Ronald Mellgren, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: April 10, 2009 Aneuploidy: Using genetic instability to preserve a haploid genome? Ramona Ramdath University of Toledo, Health Science Campus 2009 Dedication I dedicate this dissertation to my grandfather who died of lung cancer two years ago, but who always instilled in us the value and importance of education. And to my mom and sister, both of whom have been pillars of support and stimulating conversations. To my sister, Rehanna, especially- I hope this inspires you to achieve all that you want to in life, academically and otherwise. ii Acknowledgements As we go through these academic journeys, there are so many along the way that make an impact not only on our work, but on our lives as well, and I would like to say a heartfelt thank you to all of those people: My Committee members- Dr. James Trempe, Dr. David Giovanucchi, Dr. Ronald Mellgren and Dr. Randall Ruch for their guidance, suggestions, support and confidence in me. My major advisor- Dr. David Allison, for his constructive criticism and positive reinforcement.
    [Show full text]
  • Single-Cell RNA-Seq of Dopaminergic Neurons Informs Candidate Gene Selection for Sporadic
    bioRxiv preprint doi: https://doi.org/10.1101/148049; this version posted August 31, 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 Single-cell RNA-seq of dopaminergic neurons informs candidate gene selection for sporadic 2 Parkinson's disease 3 4 Paul W. Hook1, Sarah A. McClymont1, Gabrielle H. Cannon1, William D. Law1, A. Jennifer 5 Morton2, Loyal A. Goff1,3*, Andrew S. McCallion1,4,5* 6 7 1McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of 8 Medicine, Baltimore, Maryland, United States of America 9 2Department of Physiology Development and Neuroscience, University of Cambridge, 10 Cambridge, United Kingdom 11 3Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, 12 Maryland, United States of America 13 4Department of Comparative and Molecular Pathobiology, Johns Hopkins University School of 14 Medicine, Baltimore, Maryland, United States of America 15 5Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, 16 United States of America 17 *, To whom correspondence should be addressed: [email protected] and [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/148049; this version posted August 31, 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.
    [Show full text]
  • RKIP Regulates Differentiation- Related Features in Melanocytic Cells
    Cancers 2020. 12 S1 of S14 Supplementary Materials: RKIP Regulates Differentiation- Related Features in Melanocytic Cells Cristina Penas, Aintzane Apraiz, Iraia Muñoa, Yoana Arroyo-Berdugo, Javier Rasero, Pilar A. Ezkurra, Veronica Velasco, Nerea Subiran, Anja K. Bosserhoff, Santos Alonso, Aintzane Asumendi and Maria D. Boyano Figure S1. Representative images of manually scored RKIP staining categories in FFPE biopsies from patients. At the feft: Hematoxylin-Eosin staining (H-E). At the right: Immunohistochemistry (IHC) of RKIP for increasing Breslow Index. (a-b) Strong staining for intradermal nevus and in situ melanoma, respectively; (c) weak staining for a melanoma with Breslow Index between 1 and 2 mm; (d-e) negative staining for melanomas thicker than 2 mm. Cancers 2020. 12 S2 of S14 Figure S2. RNA Sequencing data analysis. Each row of the figure represents an over-represented gene signature generated by analyzing the up-regulated and down-regulated genes from a differential expression analysis of RKIP Knockdown melanocytes HEMn-LP. Results from the EnrichR Website with a p-value > 0.05. Figure S3. RNA Sequencing data quality. (a) Read counts normalization per sample; (b) Spearman correlation coefficient between replicates; (c) Principal component analysis for replicates. Cancers 2020. 12 S3 of S14 Figure S4. Details of Western Blot from Figure 2 related with RKIP expression in several cell lines. (a) Blots for RKIP and Tubulin in primary and metastatic melanoma and in three primary melanocytes HEMn-DP (dark pigmented), HEMn-LP (light pigmented) and HEM2710. On the right, original blot for each analyzed protein. Highlighted with a red square the information included in the Figure 3 (horizontal rotation).
    [Show full text]
  • Identifying Lineage Relationships in Human T Cell Populations
    Identifying lineage relationships in human T cell populations by Celia Lara Menckeberg A thesis submitted to The University of Birmingham for the degree of DOCTOR OF PHILOSOPHY School of Immunity and Infection College of Medical and Dental Sciences The University of Birmingham December 2010 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. ii ABSTRACT CD4+ and CD8+ T cell populations can be divided into subpopulations based on expression of surface markers CCR7 and CD45RA. The resulting populations are referred to as naive, central memory, effector memory and effector memory RA+ (EMRA). The aim of this study was to identify potential lineage relationships between these subpopulations for both CD4+ and CD8+ T cells through microarray analysis. The genes found to distinguish between these subpopulations include many molecules with known functions in T cell differentiation, including CCR7, CD45RA, granzymes, L-selectin and TNF receptors. Several genes from the tetraspanin family of proteins were found to be differentially expressed at mRNA and protein level; suggesting a possible role for these genes in CD4+ and CD8+ T cell activation, migration and lysosomal function.
    [Show full text]
  • Age-Related DNA Hydroxymethylation Is Enriched for Gene Expression and Immune System Processes in Human Peripheral Blood
    Epigenetics ISSN: 1559-2294 (Print) 1559-2308 (Online) Journal homepage: https://www.tandfonline.com/loi/kepi20 Age-related DNA hydroxymethylation is enriched for gene expression and immune system processes in human peripheral blood Nicholas D. Johnson, Luoxiu Huang, Ronghua Li, Yun Li, Yuchen Yang, Hye Rim Kim, Crystal Grant, Hao Wu, Eric A. Whitsel, Douglas P. Kiel, Andrea A. Baccarelli, Peng Jin, Joanne M. Murabito & Karen N. Conneely To cite this article: Nicholas D. Johnson, Luoxiu Huang, Ronghua Li, Yun Li, Yuchen Yang, Hye Rim Kim, Crystal Grant, Hao Wu, Eric A. Whitsel, Douglas P. Kiel, Andrea A. Baccarelli, Peng Jin, Joanne M. Murabito & Karen N. Conneely (2019): Age-related DNA hydroxymethylation is enriched for gene expression and immune system processes in human peripheral blood, Epigenetics, DOI: 10.1080/15592294.2019.1666651 To link to this article: https://doi.org/10.1080/15592294.2019.1666651 View supplementary material Accepted author version posted online: 11 Sep 2019. Published online: 26 Sep 2019. Submit your article to this journal Article views: 179 View related articles View Crossmark data Full Terms & Conditions of access and use can be found at https://www.tandfonline.com/action/journalInformation?journalCode=kepi20 EPIGENETICS https://doi.org/10.1080/15592294.2019.1666651 RESEARCH PAPER Age-related DNA hydroxymethylation is enriched for gene expression and immune system processes in human peripheral blood Nicholas D. Johnsona,b, Luoxiu Huanga, Ronghua Lia, Yun Li c,d, Yuchen Yangc, Hye Rim Kim a,e, Crystal Grant a,f, Hao Wug, Eric A. Whitsel h,i, Douglas P. Kiel j, Andrea A. Baccarellik, Peng Jin a, Joanne M.
    [Show full text]