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Adherent Intestinal Cells from Atlantic Salmon Show Phagocytic Ability and Express Macrophage-Specific Genes
fcell-08-580848 October 11, 2020 Time: 9:56 # 1 ORIGINAL RESEARCH published: 15 October 2020 doi: 10.3389/fcell.2020.580848 Adherent Intestinal Cells From Atlantic Salmon Show Phagocytic Ability and Express Macrophage-Specific Genes Youngjin Park1, Qirui Zhang2, Geert F. Wiegertjes3, Jorge M.O. Fernandes1 and Viswanath Kiron1* 1 Faculty of Biosciences and Aquaculture, Nord University, Bodø, Norway, 2 Division of Clinical Genetics, Lund University, Lund, Sweden, 3 Aquaculture and Fisheries Group, Wageningen University & Research, Wageningen, Netherlands Our knowledge of the intestinal immune system of fish is rather limited compared to mammals. Very little is known about the immune cells including the phagocytic cells Edited by: Yi Feng, in fish intestine. Hence, employing imaging flow cytometry and RNA sequencing, we The University of Edinburgh, studied adherent cells isolated from healthy Atlantic salmon. Phagocytic activity and United Kingdom selected gene expression of adherent cells from the distal intestine (adherent intestinal Reviewed by: cells, or AIC) were compared with those from head kidney (adherent kidney cells, or Dimitar Borisov Iliev, Institute of Molecular Biology (BAS), AKC). Phagocytic activity of the two cell types was assessed based on the uptake Bulgaria of Escherichia coli BioParticlesTM. AIC showed phagocytic ability but the phagocytes Sherri L. Christian, Memorial University of Newfoundland, were of different morphology compared to AKC. Transcriptomic analysis revealed that Canada AIC expressed genes associated with macrophages, T cells, and endothelial cells. *Correspondence: Heatmap analysis of selected genes indicated that the adherent cells from the two Viswanath Kiron organs had apparently higher expression of macrophage-related genes. We believe [email protected] that the adherent intestinal cells have phagocytic characteristics and high expression Specialty section: of genes commonly associated with macrophages. -
Hyaluronidase PH20 (SPAM1) Rabbit Polyclonal Antibody – TA337855
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 TA337855 Hyaluronidase PH20 (SPAM1) Rabbit Polyclonal Antibody Product data: Product Type: Primary Antibodies Applications: WB Recommended Dilution: WB Reactivity: Human Host: Rabbit Isotype: IgG Clonality: Polyclonal Immunogen: The immunogen for anti-SPAM1 antibody is: synthetic peptide directed towards the C- terminal region of Human SPAM1. Synthetic peptide located within the following region: CYSTLSCKEKADVKDTDAVDVCIADGVCIDAFLKPPMETEEPQIFYNASP Formulation: Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose. Note that this product is shipped as lyophilized powder to China customers. Purification: Affinity Purified Conjugation: Unconjugated Storage: Store at -20°C as received. Stability: Stable for 12 months from date of receipt. Predicted Protein Size: 58 kDa Gene Name: sperm adhesion molecule 1 Database Link: NP_694859 Entrez Gene 6677 Human P38567 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 Hyaluronidase PH20 (SPAM1) Rabbit Polyclonal Antibody – TA337855 Background: Hyaluronidase degrades hyaluronic acid, a major structural proteoglycan found in extracellular matrices and basement membranes. Six members of the hyaluronidase family are clustered into two tightly linked groups on chromosome 3p21.3 and 7q31.3. This gene was previously referred to as HYAL1 and HYA1 and has since been assigned the official symbol SPAM1; another family member on chromosome 3p21.3 has been assigned HYAL1. -
Evaluation of the Prognostic Potential of Hyaluronic Acid and Hyaluronidase (HYAL1) for Prostate Cancer1
[CANCER RESEARCH 63, 2638–2644, May 15, 2003] Evaluation of the Prognostic Potential of Hyaluronic Acid and Hyaluronidase (HYAL1) for Prostate Cancer1 J. Timothy Posey, Mark S. Soloway, Sinan Ekici, Mario Sofer, Francisco Civantos, Robert C. Duncan, and Vinata B. Lokeshwar2 Departments of Urology [J. T. P., M. S. S., S. E., M. S., F. C., V. B. L.], Department of Epidemiology [R. C. D.], and Cell Biology and Anatomy [V. B. L.], University of Miami School of Medicine, Miami, Florida 33101 ABSTRACT lapse), local/systemic recurrence] in ϳ10–50% of cases, depending on a variety of prognostic factors (5–7). Treatment failure may be Despite the development of nomograms designed to evaluate the prog- attributable to a local recurrence or distant metastasis. Existing pre- nosis of a patient with prostate cancer (CaP), the information has been operative indicators (i.e., PSA levels, clinical stage, biopsy Gleason limited to prostate-specific antigen (PSA), clinical stage, Gleason score, and tumor volume estimates. To improve our ability to predict prognosis, sum) or their combination in nomograms, as well as surgical and ϩ Ϫ information regarding the molecular properties of CaP is needed. Hyalu- pathologic parameters (i.e., prostatectomy Gleason sum, margin / , ronic acid (HA) is a glycosaminoglycan that promotes tumor metastasis. node status, seminal vesicle, and EPE), provide a limited estimate of Hyaluronidase (HAase) is an enzyme that degrades HA into angiogenic the prognosis for CaP (8, 9). Identifying molecules that are expressed fragments. We recently showed that in CaP tissues, whereas HA is local- in clinically localized CaP but associate with CaP invasion and ized mostly in the tumor-associated stroma, HYAL1 type HAase is exclu- metastasis might significantly improve the prognostic capabilities and sively localized in CaP cells (Lokeshwar et al. -
Transcriptional Regulation of RKIP in Prostate Cancer Progression
Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Sciences Transcriptional Regulation of RKIP in Prostate Cancer Progression Submitted by: Sandra Marie Beach In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences Examination Committee Major Advisor: Kam Yeung, Ph.D. Academic William Maltese, Ph.D. Advisory Committee: Sonia Najjar, Ph.D. Han-Fei Ding, M.D., Ph.D. Manohar Ratnam, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: May 16, 2007 Transcriptional Regulation of RKIP in Prostate Cancer Progression Sandra Beach University of Toledo ACKNOWLDEGMENTS I thank my major advisor, Dr. Kam Yeung, for the opportunity to pursue my degree in his laboratory. I am also indebted to my advisory committee members past and present, Drs. Sonia Najjar, Han-Fei Ding, Manohar Ratnam, James Trempe, and Douglas Pittman for generously and judiciously guiding my studies and sharing reagents and equipment. I owe extended thanks to Dr. William Maltese as a committee member and chairman of my department for supporting my degree progress. The entire Department of Biochemistry and Cancer Biology has been most kind and helpful to me. Drs. Roy Collaco and Hong-Juan Cui have shared their excellent technical and practical advice with me throughout my studies. I thank members of the Yeung laboratory, Dr. Sungdae Park, Hui Hui Tang, Miranda Yeung for their support and collegiality. The data mining studies herein would not have been possible without the helpful advice of Dr. Robert Trumbly. I am also grateful for the exceptional assistance and shared microarray data of Dr. -
Pathway-Based Genome-Wide Association Analysis of Coronary Heart Disease Identifies Biologically Important Gene Sets
European Journal of Human Genetics (2012) 20, 1168–1173 & 2012 Macmillan Publishers Limited All rights reserved 1018-4813/12 www.nature.com/ejhg ARTICLE Pathway-based genome-wide association analysis of coronary heart disease identifies biologically important gene sets Lisa de las Fuentes1,4, Wei Yang2,4, Victor G Da´vila-Roma´n1 and C Charles Gu*,2,3 Genome-wide association (GWA) studies of complex diseases including coronary heart disease (CHD) challenge investigators attempting to identify relevant genetic variants among hundreds of thousands of markers being tested. A selection strategy based purely on statistical significance will result in many false negative findings after adjustment for multiple testing. Thus, an integrated analysis using information from the learned genetic pathways, molecular functions, and biological processes is desirable. In this study, we applied a customized method, variable set enrichment analysis (VSEA), to the Framingham Heart Study data (404 467 variants, n ¼ 6421) to evaluate enrichment of genetic association in 1395 gene sets for their contribution to CHD. We identified 25 gene sets with nominal Po0.01; at least four sets are previously known for their roles in CHD: vascular genesis (GO:0001570), fatty-acid biosynthetic process (GO:0006633), fatty-acid metabolic process (GO:0006631), and glycerolipid metabolic process (GO:0046486). Although the four gene sets include 170 genes, only three of the genes contain a variant ranked among the top 100 in single-variant association tests of the 404 467 variants tested. Significant enrichment for novel gene sets less known for their importance to CHD were also identified: Rac 1 cell-motility signaling pathway (h_rac1 Pathway, Po0.001) and sulfur amino-acid metabolic process (GO:0000096, Po0.001). -
Protein Identities in Evs Isolated from U87-MG GBM Cells As Determined by NG LC-MS/MS
Protein identities in EVs isolated from U87-MG GBM cells as determined by NG LC-MS/MS. No. Accession Description Σ Coverage Σ# Proteins Σ# Unique Peptides Σ# Peptides Σ# PSMs # AAs MW [kDa] calc. pI 1 A8MS94 Putative golgin subfamily A member 2-like protein 5 OS=Homo sapiens PE=5 SV=2 - [GG2L5_HUMAN] 100 1 1 7 88 110 12,03704523 5,681152344 2 P60660 Myosin light polypeptide 6 OS=Homo sapiens GN=MYL6 PE=1 SV=2 - [MYL6_HUMAN] 100 3 5 17 173 151 16,91913397 4,652832031 3 Q6ZYL4 General transcription factor IIH subunit 5 OS=Homo sapiens GN=GTF2H5 PE=1 SV=1 - [TF2H5_HUMAN] 98,59 1 1 4 13 71 8,048185945 4,652832031 4 P60709 Actin, cytoplasmic 1 OS=Homo sapiens GN=ACTB PE=1 SV=1 - [ACTB_HUMAN] 97,6 5 5 35 917 375 41,70973209 5,478027344 5 P13489 Ribonuclease inhibitor OS=Homo sapiens GN=RNH1 PE=1 SV=2 - [RINI_HUMAN] 96,75 1 12 37 173 461 49,94108966 4,817871094 6 P09382 Galectin-1 OS=Homo sapiens GN=LGALS1 PE=1 SV=2 - [LEG1_HUMAN] 96,3 1 7 14 283 135 14,70620005 5,503417969 7 P60174 Triosephosphate isomerase OS=Homo sapiens GN=TPI1 PE=1 SV=3 - [TPIS_HUMAN] 95,1 3 16 25 375 286 30,77169764 5,922363281 8 P04406 Glyceraldehyde-3-phosphate dehydrogenase OS=Homo sapiens GN=GAPDH PE=1 SV=3 - [G3P_HUMAN] 94,63 2 13 31 509 335 36,03039959 8,455566406 9 Q15185 Prostaglandin E synthase 3 OS=Homo sapiens GN=PTGES3 PE=1 SV=1 - [TEBP_HUMAN] 93,13 1 5 12 74 160 18,68541938 4,538574219 10 P09417 Dihydropteridine reductase OS=Homo sapiens GN=QDPR PE=1 SV=2 - [DHPR_HUMAN] 93,03 1 1 17 69 244 25,77302971 7,371582031 11 P01911 HLA class II histocompatibility antigen, -
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Patterns of DNA methylation on the human X chromosome and use in analyzing X-chromosome inactivation by Allison Marie Cotton B.Sc., The University of Guelph, 2005 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY in The Faculty of Graduate Studies (Medical Genetics) THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver) January 2012 © Allison Marie Cotton, 2012 Abstract The process of X-chromosome inactivation achieves dosage compensation between mammalian males and females. In females one X chromosome is transcriptionally silenced through a variety of epigenetic modifications including DNA methylation. Most X-linked genes are subject to X-chromosome inactivation and only expressed from the active X chromosome. On the inactive X chromosome, the CpG island promoters of genes subject to X-chromosome inactivation are methylated in their promoter regions, while genes which escape from X- chromosome inactivation have unmethylated CpG island promoters on both the active and inactive X chromosomes. The first objective of this thesis was to determine if the DNA methylation of CpG island promoters could be used to accurately predict X chromosome inactivation status. The second objective was to use DNA methylation to predict X-chromosome inactivation status in a variety of tissues. A comparison of blood, muscle, kidney and neural tissues revealed tissue-specific X-chromosome inactivation, in which 12% of genes escaped from X-chromosome inactivation in some, but not all, tissues. X-linked DNA methylation analysis of placental tissues predicted four times higher escape from X-chromosome inactivation than in any other tissue. Despite the hypomethylation of repetitive elements on both the X chromosome and the autosomes, no changes were detected in the frequency or intensity of placental Cot-1 holes. -
Identifying Host Genetic Factors Controlling Susceptibility to Blood-Stage Malaria in Mice
Identifying host genetic factors controlling susceptibility to blood-stage malaria in mice Aurélie Laroque Department of Biochemistry McGill University Montreal, Quebec, Canada December 2016 A thesis submitted to McGill University in partial fulfilment of the requirements of the degree of Doctor of Philosophy. © Aurélie Laroque, 2016 ABSTRACT This thesis examines genetic factors controlling host response to blood stage malaria in mice. We first phenotyped 25 inbred strains for resistance/susceptibility to Plasmodium chabaudi chabaudi AS infection. A broad spectrum of responses was observed, which suggests rich genetic diversity among different mouse strains in response to malaria. A F2 intercross was generated between susceptible SM/J and resistant C57BL/6 mice and the progeny was phenotyped for susceptibility to P. chabaudi chabaudi AS infection. A whole genome scan revealed the Char1 locus as a key regulator of parasite density. Using a haplotype mapping approach, we reduced the locus to a 0.4Mb conserved interval that segregates with resistance/susceptibility to infection for the search of positional candidate genes. In addition, I pursued the work on the Char10 locus that was previously identified in [AcB62xCBA/PK]F2 animals (LOD=10.8, 95% Bayesian CI=50.7-75Mb). Pyruvate kinase deficiency was found to protect mice and humans against malaria. However, AcB62 mice are susceptible to P. chabaudi infection despite carrying the protective PklrI90N mutation. We characterized the Char10 locus and showed that it modulates the severity of the pyruvate deficiency phenotype by regulating erythroid responses. We created 4 congenic lines carrying different portions of the Char10 interval and demonstrated that Char10 is found within a maximal 4Mb interval. -
De Novo, Systemic, Deleterious Amino Acid Substitutions Are Common in Large Cytoskeleton‑Related Protein Coding Regions
BIOMEDICAL REPORTS 6: 211-216, 2017 De novo, systemic, deleterious amino acid substitutions are common in large cytoskeleton‑related protein coding regions REBECCA J. STOLL1, GRACE R. THOMPSON1, MOHAMMAD D. SAMY1 and GEORGE BLANCK1,2 1Department of Molecular Medicine, Morsani College of Medicine, University of South Florida; 2Immunology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA Received June 13, 2016; Accepted October 31, 2016 DOI: 10.3892/br.2016.826 Abstract. Human mutagenesis is largely random, thus large Introduction coding regions, simply on the basis of probability, represent relatively large mutagenesis targets. Thus, we considered Genetic damage is largely random and therefore tends to the possibility that large cytoskeletal-protein related coding affect the larger, functional regions of the human genome regions (CPCRs), including extra-cellular matrix (ECM) more frequently than the smaller regions (1). For example, coding regions, would have systemic nucleotide variants that a systematic study has revealed that cancer fusion genes, on are not present in common SNP databases. Presumably, such average, are statistically, significantly larger than other human variants arose recently in development or in recent, preceding genes (2,3). The large introns of potential cancer fusion genes generations. Using matched breast cancer and blood-derived presumably allow for many different productive recombina- normal datasets from the cancer genome atlas, CPCR single tion opportunities, i.e., many recombinations that would allow nucleotide variants (SNVs) not present in the All SNPs(142) for exon juxtaposition and the generation of hybrid proteins. or 1000 Genomes databases were identified. Using the Protein Smaller cancer fusion genes tend to be associated with the rare Variation Effect Analyzer internet-based tool, it was discov- types of cancer, for example EWS RNA binding protein 1 in ered that apparent, systemic mutations (not shared among Ewing's sarcoma. -
MAML1 Antibody A
Revision 1 C 0 2 - t MAML1 Antibody a e r o t S Orders: 877-616-CELL (2355) [email protected] Support: 877-678-TECH (8324) 8 0 Web: [email protected] 6 www.cellsignal.com 4 # 3 Trask Lane Danvers Massachusetts 01923 USA For Research Use Only. Not For Use In Diagnostic Procedures. Applications: Reactivity: Sensitivity: MW (kDa): Source: UniProt ID: Entrez-Gene Id: WB, IP H Endogenous 130 Rabbit Q92585 9794 Product Usage Information Application Dilution Western Blotting 1:1000 Immunoprecipitation 1:50 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody. Specificity / Sensitivity MAML1 Antibody detects endogenous levels of total MAML1 protein. It does not cross- react with MAML2 and MAML3. Species Reactivity: Human Source / Purification Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding His811 of human MAML1. Antibodies are purified by protein A and peptide affinity chromatography. Background Mastermind-like (MAML) family of proteins are homologs of Drosophila Mastermind. The family is composed of three members in mammals: MAML1, MAML2, and MAML3 (1,2). MAML proteins form complexes with the intracellular domain of Notch (ICN) and the transcription factor CSL (RBP-Jκ) to regulate Notch target gene expression (3-5). MAML1 also interacts with myocyte enhancer factor 2C (MEF2C) to regulate myogenesis (6). MAML2 is frequently found to be fused with Mucoepidermoid carcinoma translocated gene 1 (MECT1, also know as WAMTP1 or TORC1) in patients with mucoepidermoid carcinomas and Warthin's tumors (7). -
A Systems Genomics Approach to Uncover Patient-Specific Pathogenic Pathways and Proteins in a Complex Disease
bioRxiv preprint doi: https://doi.org/10.1101/692269; this version posted July 4, 2019. 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. A systems genomics approach to uncover patient-specific pathogenic pathways and proteins in a complex disease 1,2,3,4,§ 5,§ 1,4,6,§ 4,7 Johanne Brooks , Dezso Modos , Padhmanand Sudhakar , David Fazekas , Azedine 5 8 4 1,4 6,9 Zoufir , Orsolya Kapuy , Mate Szalay-Beko , Matthew Madgwick , Bram Verstockt , Lindsay 1,2 1,2,3 3 10 6,9 Hall Alastair Watson , Mark Tremelling , Miles Parkes , Severine Vermeire , Andreas 5 1,2,* 1,4,* Bender , Simon R. Carding , Tamas Korcsmaros 1 Gut Health and Microbes Programme, The Quadram Institute Bioscience, Norwich Research Park, Norwich, UK 2 Norwich Medical School, University of East Anglia, Norwich, UK 3 Department of Gastroenterology, Norfolk and Norwich University Hospitals, Norwich, UK 4 Earlham Institute, Norwich Research Park, Norwich, UK 5 Centre for Molecular Science Informatics, Department of Chemistry, University of Cambridge, Cambridge, UK 6 KU Leuven, Department of Chronic diseases, Metabolism and Ageing, Leuven, Belgium 7 Department of Genetics, Eötvös Loránd University, Budapest, Hungary 8 Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest, Hungary 9 University Hospitals Leuven, Department of Gastroenterology and Hepatology, KU Leuven, Leuven, Belgium 10 Inflammatory Bowel Disease Research Group, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK. § equal contribution * joint corresponding authors bioRxiv preprint doi: https://doi.org/10.1101/692269; this version posted July 4, 2019. -
Supporting Information
Supporting Information Pouryahya et al. SI Text Table S1 presents genes with the highest absolute value of Ricci curvature. We expect these genes to have significant contribution to the network’s robustness. Notably, the top two genes are TP53 (tumor protein 53) and YWHAG gene. TP53, also known as p53, it is a well known tumor suppressor gene known as the "guardian of the genome“ given the essential role it plays in genetic stability and prevention of cancer formation (1, 2). Mutations in this gene play a role in all stages of malignant transformation including tumor initiation, promotion, aggressiveness, and metastasis (3). Mutations of this gene are present in more than 50% of human cancers, making it the most common genetic event in human cancer (4, 5). Namely, p53 mutations play roles in leukemia, breast cancer, CNS cancers, and lung cancers, among many others (6–9). The YWHAG gene encodes the 14-3-3 protein gamma, a member of the 14-3-3 family proteins which are involved in many biological processes including signal transduction regulation, cell cycle pro- gression, apoptosis, cell adhesion and migration (10, 11). Notably, increased expression of 14-3-3 family proteins, including protein gamma, have been observed in a number of human cancers including lung and colorectal cancers, among others, suggesting a potential role as tumor oncogenes (12, 13). Furthermore, there is evidence that loss Fig. S1. The histogram of scalar Ricci curvature of 8240 genes. Most of the genes have negative scalar Ricci curvature (75%). TP53 and YWHAG have notably low of p53 function may result in upregulation of 14-3-3γ in lung cancer Ricci curvatures.