Mouse Itih2 Knockout Project (CRISPR/Cas9)
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Frequent Expression Loss of Inter-Alpha-Trypsin Inhibitor Heavy Chain (ITIH) Genes in Multiple Human Solid Tumors: a Systematic Expression Analysis
Hamm, A; Veeck, J; Bektas, N; Wild, P J; Hartmann, A; Heindrichs, U; Kristiansen, G; Werbowetski-Ogilvie, T; Del Maestro, R; Knuechel, R; Dahl, E (2008). Frequent expression loss of Inter-alpha-trypsin inhibitor heavy chain (ITIH) genes in multiple human solid tumors: a systematic expression analysis. BMC Cancer, 8:25. Postprint available at: http://www.zora.uzh.ch University of Zurich Posted at the Zurich Open Repository and Archive, University of Zurich. Zurich Open Repository and Archive http://www.zora.uzh.ch Originally published at: BMC Cancer 2008, 8:25. Winterthurerstr. 190 CH-8057 Zurich http://www.zora.uzh.ch Year: 2008 Frequent expression loss of Inter-alpha-trypsin inhibitor heavy chain (ITIH) genes in multiple human solid tumors: a systematic expression analysis Hamm, A; Veeck, J; Bektas, N; Wild, P J; Hartmann, A; Heindrichs, U; Kristiansen, G; Werbowetski-Ogilvie, T; Del Maestro, R; Knuechel, R; Dahl, E Hamm, A; Veeck, J; Bektas, N; Wild, P J; Hartmann, A; Heindrichs, U; Kristiansen, G; Werbowetski-Ogilvie, T; Del Maestro, R; Knuechel, R; Dahl, E (2008). Frequent expression loss of Inter-alpha-trypsin inhibitor heavy chain (ITIH) genes in multiple human solid tumors: a systematic expression analysis. BMC Cancer, 8:25. Postprint available at: http://www.zora.uzh.ch Posted at the Zurich Open Repository and Archive, University of Zurich. http://www.zora.uzh.ch Originally published at: BMC Cancer 2008, 8:25. Frequent expression loss of Inter-alpha-trypsin inhibitor heavy chain (ITIH) genes in multiple human solid tumors: a systematic expression analysis Abstract BACKGROUND: The inter-alpha-trypsin inhibitors (ITI) are a family of plasma protease inhibitors, assembled from a light chain - bikunin, encoded by AMBP - and five homologous heavy chains (encoded by ITIH1, ITIH2, ITIH3, ITIH4, and ITIH5), contributing to extracellular matrix stability by covalent linkage to hyaluronan. -
Supplementary Information Changes in the Plasma Proteome At
Supplementary Information Changes in the plasma proteome at asymptomatic and symptomatic stages of autosomal dominant Alzheimer’s disease Julia Muenchhoff1, Anne Poljak1,2,3, Anbupalam Thalamuthu1, Veer B. Gupta4,5, Pratishtha Chatterjee4,5,6, Mark Raftery2, Colin L. Masters7, John C. Morris8,9,10, Randall J. Bateman8,9, Anne M. Fagan8,9, Ralph N. Martins4,5,6, Perminder S. Sachdev1,11,* Supplementary Figure S1. Ratios of proteins differentially abundant in asymptomatic carriers of PSEN1 and APP Dutch mutations. Mean ratios and standard deviations of plasma proteins from asymptomatic PSEN1 mutation carriers (PSEN1) and APP Dutch mutation carriers (APP) relative to reference masterpool as quantified by iTRAQ. Ratios that significantly differed are marked with asterisks (* p < 0.05; ** p < 0.01). C4A, complement C4-A; AZGP1, zinc-α-2-glycoprotein; HPX, hemopexin; PGLYPR2, N-acetylmuramoyl-L-alanine amidase isoform 2; α2AP, α-2-antiplasmin; APOL1, apolipoprotein L1; C1 inhibitor, plasma protease C1 inhibitor; ITIH2, inter-α-trypsin inhibitor heavy chain H2. 2 A) ADAD)CSF) ADAD)plasma) B) ADAD)CSF) ADAD)plasma) (Ringman)et)al)2015)) (current)study)) (Ringman)et)al)2015)) (current)study)) ATRN↓,%%AHSG↑% 32028% 49% %%%%%%%%HC2↑,%%ApoM↓% 24367% 31% 10083%% %%%%TBG↑,%%LUM↑% 24256% ApoC1↓↑% 16565% %%AMBP↑% 11738%%% SERPINA3↓↑% 24373% C6↓↑% ITIH2% 10574%% %%%%%%%CPN2↓%% ↓↑% %%%%%TTR↑% 11977% 10970% %SERPINF2↓↑% CFH↓% C5↑% CP↓↑% 16566% 11412%% 10127%% %%ITIH4↓↑% SerpinG1↓% 11967% %%ORM1↓↑% SerpinC1↓% 10612% %%%A1BG↑%%% %%%%FN1↓% 11461% %%%%ITIH1↑% C3↓↑% 11027% 19325% 10395%% %%%%%%HPR↓↑% HRG↓% %%% 13814%% 10338%% %%% %ApoA1 % %%%%%%%%%GSN↑% ↓↑ %%%%%%%%%%%%ApoD↓% 11385% C4BPA↓↑% 18976%% %%%%%%%%%%%%%%%%%ApoJ↓↑% 23266%%%% %%%%%%%%%%%%%%%%%%%%%%ApoA2↓↑% %%%%%%%%%%%%%%%%%%%%%%%%%%%%A2M↓↑% IGHM↑,%%GC↓↑,%%ApoB↓↑% 13769% % FGA↓↑,%%FGB↓↑,%%FGG↓↑% AFM↓↑,%%CFB↓↑,%% 19143%% ApoH↓↑,%%C4BPA↓↑% ApoA4↓↑%%% LOAD/MCI)plasma) LOAD/MCI)plasma) LOAD/MCI)plasma) LOAD/MCI)plasma) (Song)et)al)2014)) (Muenchhoff)et)al)2015)) (Song)et)al)2014)) (Muenchhoff)et)al)2015)) Supplementary Figure S2. -
The Oviductal Transcriptome Is Influenced by a Local Ovarian Effect in the Sow Rebeca López-Úbeda1,2, Marta Muñoz3, Luis Vieira1,2, Ronald H
López-Úbeda et al. Journal of Ovarian Research (2016) 9:44 DOI 10.1186/s13048-016-0252-9 RESEARCH Open Access The oviductal transcriptome is influenced by a local ovarian effect in the sow Rebeca López-Úbeda1,2, Marta Muñoz3, Luis Vieira1,2, Ronald H. F. Hunter4, Pilar Coy1,2,5* and Sebastian Canovas1,2,5* Abstract Background: Oviducts participate in fertilization and early embryo development, and they are influenced by systemic and local circulation. Local functional interplay between ovary, oviduct and uterus is important, as deduced from the previously observed differences in hormone concentrations, presence of sperm, or patterns of motility in the oviduct after unilateral ovariectomy (UO). However, the consequences of unilateral ovariectomy on the oviductal transcriptome remain unexplored. In this study, we have investigated the consequences of UO in a higher animal model as the pig. Methods: The influence of UO was analyzed on the number of ovulations on the contra ovary, which was increased, and on the ipsilateral oviductal transcriptome. Microarray analysis was performed and the results were validated by PCR. Differentially expressed genes (DEGs) with a fold change ≥ 2andafalsediscoveryrateof10%were analyzed by Ingenuity Pathway Analysis (IPA) to identify the main biofunctions affected by UO. Results: Data revealed two principal effects in the ipsilateral oviduct after UO: i) down-regulation of genes involved in the survival of sperm in the oviduct and early embryonic development, and ii) up-regulation of genes involved in others functions as protection against external agents and tumors. Conclusions: Results showed that unilateral ovariectomy results in an increased number of ovulation points on the contra ovary and changes in the transcriptome of the ipsilateral oviduct with consequences on key biological process that could affect fertility output. -
Supplementary Materials
Supplementary materials Supplementary Table S1: MGNC compound library Ingredien Molecule Caco- Mol ID MW AlogP OB (%) BBB DL FASA- HL t Name Name 2 shengdi MOL012254 campesterol 400.8 7.63 37.58 1.34 0.98 0.7 0.21 20.2 shengdi MOL000519 coniferin 314.4 3.16 31.11 0.42 -0.2 0.3 0.27 74.6 beta- shengdi MOL000359 414.8 8.08 36.91 1.32 0.99 0.8 0.23 20.2 sitosterol pachymic shengdi MOL000289 528.9 6.54 33.63 0.1 -0.6 0.8 0 9.27 acid Poricoic acid shengdi MOL000291 484.7 5.64 30.52 -0.08 -0.9 0.8 0 8.67 B Chrysanthem shengdi MOL004492 585 8.24 38.72 0.51 -1 0.6 0.3 17.5 axanthin 20- shengdi MOL011455 Hexadecano 418.6 1.91 32.7 -0.24 -0.4 0.7 0.29 104 ylingenol huanglian MOL001454 berberine 336.4 3.45 36.86 1.24 0.57 0.8 0.19 6.57 huanglian MOL013352 Obacunone 454.6 2.68 43.29 0.01 -0.4 0.8 0.31 -13 huanglian MOL002894 berberrubine 322.4 3.2 35.74 1.07 0.17 0.7 0.24 6.46 huanglian MOL002897 epiberberine 336.4 3.45 43.09 1.17 0.4 0.8 0.19 6.1 huanglian MOL002903 (R)-Canadine 339.4 3.4 55.37 1.04 0.57 0.8 0.2 6.41 huanglian MOL002904 Berlambine 351.4 2.49 36.68 0.97 0.17 0.8 0.28 7.33 Corchorosid huanglian MOL002907 404.6 1.34 105 -0.91 -1.3 0.8 0.29 6.68 e A_qt Magnogrand huanglian MOL000622 266.4 1.18 63.71 0.02 -0.2 0.2 0.3 3.17 iolide huanglian MOL000762 Palmidin A 510.5 4.52 35.36 -0.38 -1.5 0.7 0.39 33.2 huanglian MOL000785 palmatine 352.4 3.65 64.6 1.33 0.37 0.7 0.13 2.25 huanglian MOL000098 quercetin 302.3 1.5 46.43 0.05 -0.8 0.3 0.38 14.4 huanglian MOL001458 coptisine 320.3 3.25 30.67 1.21 0.32 0.9 0.26 9.33 huanglian MOL002668 Worenine -
Mass Spectrometry Discovery-Based Proteomics to Examine Anti-Aging Effects of the Nutraceutical NT-020 in Rat Serum" (2020)
University of South Florida Scholar Commons Graduate Theses and Dissertations Graduate School March 2020 Mass Spectrometry Discovery-Based Proteomics to Examine Anti- Aging Effects of the Nutraceutical NT-020 in Rat Serum Samantha M. Portis University of South Florida Follow this and additional works at: https://scholarcommons.usf.edu/etd Part of the Bioinformatics Commons, and the Neurosciences Commons Scholar Commons Citation Portis, Samantha M., "Mass Spectrometry Discovery-Based Proteomics to Examine Anti-Aging Effects of the Nutraceutical NT-020 in Rat Serum" (2020). Graduate Theses and Dissertations. https://scholarcommons.usf.edu/etd/8279 This Dissertation is brought to you for free and open access by the Graduate School at Scholar Commons. It has been accepted for inclusion in Graduate Theses and Dissertations by an authorized administrator of Scholar Commons. For more information, please contact [email protected]. Mass Spectrometry Discovery-Based Proteomics to Examine Anti-Aging Effects of the Nutraceutical NT-020 in Rat Serum by Samantha M. Portis A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy Medical Sciences with a concentration in Neuroscience Department of Molecular Pharmacology and Physiology College of Medicine University of South Florida Major Professor: Paul R. Sanberg, Ph.D., D.Sc Co-Major Professor: Paula C. Bickford, Ph.D. Kevin Nash, Ph.D. Dominic D’Agostino, Ph.D. Brent Small, Ph.D. Date of Approval: March 28, 2020 Keywords: aging, proteome, serum, inflammation, bioinformatics Copyright © 2020, Samantha M. Portis Dedication I dedicate this work to my family, Alan, Candace, Carolyn, and Jimmy, my brother, Patrick, and my partner, Will. -
Single Cell Analysis of Human Foetal Liver Captures the Transcriptional Profile of Hepatobiliary Hybrid Progenitors
ARTICLE https://doi.org/10.1038/s41467-019-11266-x OPEN Single cell analysis of human foetal liver captures the transcriptional profile of hepatobiliary hybrid progenitors Joe M. Segal 1,8, Deniz Kent1,8, Daniel J. Wesche2,3, Soon Seng Ng 1, Maria Serra1, Bénédicte Oulès 1, Gozde Kar4, Guy Emerton4, Samuel J.I. Blackford 1, Spyros Darmanis5, Rosa Miquel1, Tu Vinh Luong1, Ryo Yamamoto2, Andrew Bonham2, Wayel Jassem6, Nigel Heaton6, Alessandra Vigilante1, Aileen King7, Rocio Sancho 1, Sarah Teichmann 4, Stephen R. Quake5,9, Hiromitsu Nakauchi2,9 & S. Tamir Rashid1,2,9 1234567890():,; The liver parenchyma is composed of hepatocytes and bile duct epithelial cells (BECs). Controversy exists regarding the cellular origin of human liver parenchymal tissue generation during embryonic development, homeostasis or repair. Here we report the existence of a hepatobiliary hybrid progenitor (HHyP) population in human foetal liver using single-cell RNA sequencing. HHyPs are anatomically restricted to the ductal plate of foetal liver and maintain a transcriptional profile distinct from foetal hepatocytes, mature hepatocytes and mature BECs. In addition, molecular heterogeneity within the EpCAM+ population of freshly isolated foetal and adult human liver identifies diverse gene expression signatures of hepatic and biliary lineage potential. Finally, we FACS isolate foetal HHyPs and confirm their hybrid progenitor phenotype in vivo. Our study suggests that hepatobiliary progenitor cells pre- viously identified in mice also exist in humans, and can be distinguished from other par- enchymal populations, including mature BECs, by distinct gene expression profiles. 1 Centre for Stem Cells and Regenerative Medicine & Institute for Liver Studies, King’s College London, London WC2R 2LS, UK. -
Synonymous Variants Associated with Alzheimer Disease in Multiplex Families
ARTICLE OPEN ACCESS Synonymous variants associated with Alzheimer disease in multiplex families Min Tang, PhD, Maria Eugenia Alaniz, PhD, Daniel Felsky, PhD, Badri Vardarajan, PhD, Correspondence Dolly Reyes-Dumeyer, BA, Rafael Lantigua, MD, Martin Medrano, MD, David A. Bennett, MD, Dr. Reitz [email protected] Philip L. de Jager, MD, PhD, Richard Mayeux, MD, MSc, Ismael Santa-Maria, PhD, and Christiane Reitz, MD, PhD Neurol Genet 2020;6:e450. doi:10.1212/NXG.0000000000000450 Abstract Objective Synonymous variants can lead to disease; nevertheless, the majority of sequencing studies conducted in Alzheimer disease (AD) only assessed coding variation. Methods To detect synonymous variants modulating AD risk, we conducted a whole-genome sequencing study on 67 Caribbean Hispanic (CH) families multiply affected by AD. Identified disease- associated variants were further assessed in an independent cohort of CHs, expression quanti- tative trait locus (eQTL) data, brain autopsy data, and functional experiments. Results Rare synonymous variants in 4 genes (CDH23, SLC9A3R1, RHBDD2, and ITIH2) segregated with AD status in multiplex families and had a significantly higher frequency in these families compared with reference populations of similar ancestry. In comparison to subjects without dementia, expression of CDH23 (β =0.53,p =0.006)andSLC9A3R1 (β =0.50,p = 0.02) was increased,andexpressionofRHBDD2 (β = −0.70, p = 0.02) decreased in individuals with AD at death. In line with this finding, increased expression of CDH23 (β = 0.26 ± 0.08, p = 4.9E-4) and decreased expression of RHBDD2 (β = −0.60 ± 0.12, p = 5.5E-7) were related to brain amyloid load (p = 0.0025). -
A Serum Proteome Signature to Predict Mortality in Severe COVID-19 Patients
Research Article A serum proteome signature to predict mortality in severe COVID-19 patients Franziska Vollmy¨ 1,2, Henk van den Toorn1,2, Riccardo Zenezini Chiozzi1,2, Ottavio Zucchetti3, Alberto Papi4, Carlo Alberto Volta5, Luisa Marracino6, Francesco Vieceli Dalla Sega7, Francesca Fortini7, Vadim Demichev8,9,10, Pinkus Tober-Lau11 , Gianluca Campo3,7, Marco Contoli4, Markus Ralser8,9, Florian Kurth11,12, Savino Spadaro5 , Paola Rizzo6,7, Albert JR Heck1,2 Here, we recorded serum proteome profiles of 33 severe Introduction COVID-19 patients admitted to respiratory and intensive care units because of respiratory failure. We received, for most pa- The coronavirus disease 2019 (COVID-19) pandemic caused by tients, blood samples just after admission and at two more later severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has time points. With the aim to predict treatment outcome, we fo- affected many people with a worrying fatality rate up to 60% for cused on serum proteins different in abundance between the critical cases. Not all people infected by the virus are affected group of survivors and non-survivors. We observed that a small equally. Several parameters have been defined that may influence panel of about a dozen proteins were significantly different in and/or predict disease severity and mortality, with age, gender, abundance between these two groups. The four structurally and body mass, and underlying comorbidities being some of the most functionally related type-3 cystatins AHSG, FETUB, histidine-rich well established. To -
Identification of Novel Regulatory Genes in Acetaminophen
IDENTIFICATION OF NOVEL REGULATORY GENES IN ACETAMINOPHEN INDUCED HEPATOCYTE TOXICITY BY A GENOME-WIDE CRISPR/CAS9 SCREEN A THESIS IN Cell Biology and Biophysics and Bioinformatics Presented to the Faculty of the University of Missouri-Kansas City in partial fulfillment of the requirements for the degree DOCTOR OF PHILOSOPHY By KATHERINE ANNE SHORTT B.S, Indiana University, Bloomington, 2011 M.S, University of Missouri, Kansas City, 2014 Kansas City, Missouri 2018 © 2018 Katherine Shortt All Rights Reserved IDENTIFICATION OF NOVEL REGULATORY GENES IN ACETAMINOPHEN INDUCED HEPATOCYTE TOXICITY BY A GENOME-WIDE CRISPR/CAS9 SCREEN Katherine Anne Shortt, Candidate for the Doctor of Philosophy degree, University of Missouri-Kansas City, 2018 ABSTRACT Acetaminophen (APAP) is a commonly used analgesic responsible for over 56,000 overdose-related emergency room visits annually. A long asymptomatic period and limited treatment options result in a high rate of liver failure, generally resulting in either organ transplant or mortality. The underlying molecular mechanisms of injury are not well understood and effective therapy is limited. Identification of previously unknown genetic risk factors would provide new mechanistic insights and new therapeutic targets for APAP induced hepatocyte toxicity or liver injury. This study used a genome-wide CRISPR/Cas9 screen to evaluate genes that are protective against or cause susceptibility to APAP-induced liver injury. HuH7 human hepatocellular carcinoma cells containing CRISPR/Cas9 gene knockouts were treated with 15mM APAP for 30 minutes to 4 days. A gene expression profile was developed based on the 1) top screening hits, 2) overlap with gene expression data of APAP overdosed human patients, and 3) biological interpretation including assessment of known and suspected iii APAP-associated genes and their therapeutic potential, predicted affected biological pathways, and functionally validated candidate genes. -
T-, B-And NK-Lymphoid, but Not Myeloid Cells Arise from Human
Leukemia (2007) 21, 311–319 & 2007 Nature Publishing Group All rights reserved 0887-6924/07 $30.00 www.nature.com/leu ORIGINAL ARTICLE T-, B- and NK-lymphoid, but not myeloid cells arise from human CD34 þ CD38ÀCD7 þ common lymphoid progenitors expressing lymphoid-specific genes I Hoebeke1,3, M De Smedt1, F Stolz1,4, K Pike-Overzet2, FJT Staal2, J Plum1 and G Leclercq1 1Department of Clinical Chemistry, Microbiology and Immunology, Ghent University Hospital, Ghent, Belgium and 2Department of Immunology, Erasmus University Medical Center, Rotterdam, The Netherlands Hematopoietic stem cells in the bone marrow (BM) give rise to share a direct common progenitor either, as CLPs were not all blood cells. According to the classic model of hematopoi- found in the fetal liver.5 Instead, fetal B and T cells would esis, the differentiation paths leading to the myeloid and develop through B/myeloid and T/myeloid intermediates. lymphoid lineages segregate early. A candidate ‘common 6 lymphoid progenitor’ (CLP) has been isolated from The first report of a human CLP came from Galy et al. who À þ CD34 þ CD38À human cord blood cells based on CD7 expres- showed that a subpopulation of adult and fetal BM Lin CD34 sion. Here, we confirm the B- and NK-differentiation potential of cells expressing the early B- and T-cell marker CD10 is not þ À þ CD34 CD38 CD7 cells and show in addition that this capable of generating monocytic, granulocytic, erythroid or population has strong capacity to differentiate into T cells. As megakaryocytic cells, but can differentiate into dendritic cells, CD34 þ CD38ÀCD7 þ cells are virtually devoid of myeloid B, T and NK cells. -
Evaluation of Proteomic and Transcriptomic Biomarker Discovery
EVALUATION OF PROTEOMIC AND TRANSCRIPTOMIC BIOMARKER DISCOVERY TECHNOLOGIES IN OVARIAN CANCER. CLARE RITA ELIZABETH COVENEY A thesis submitted in partial fulfilment of the requirements of the Nottingham Trent University for the degree of Doctor of Philosophy October 2016 Copyright Statement “This work is the intellectual property of the author. You may copy up to 5% of this work for private study, or personal, non-commercial research. Any re-use of the information contained within this document should be fully referenced, quoting the author, title, university, degree level and pagination. Queries or requests for any other use, or if a more substantial copy is required, should be directed in the owner(s) of the Intellectual Property Rights.” Acknowledgments This work was funded by The John Lucille van Geest Foundation and undertaken at the John van Geest Cancer Research Centre, at Nottingham Trent University. I would like to extend my foremost gratitude to my supervisory team Professor Graham Ball, Dr David Boocock, Professor Robert Rees for their guidance, knowledge and advice throughout the course of this project. I would also like to show my appreciation of the hard work of Mr Ian Scott, Professor Bob Shaw and Dr Matharoo-Ball, Dr Suman Malhi and later Mr Viren Asher who alongside colleagues at The Nottingham University Medical School and Derby City General Hospital initiated the ovarian serum collection project that lead to this work. I also would like to acknowledge the work of Dr Suha Deen at Queen’s Medical Centre and Professor Andrew Green and Christopher Nolan of the Cancer & Stem Cells Division of the School of Medicine, University of Nottingham for support with the immunohistochemistry. -
The Juvenile Alopecia Mutation (Jal) Maps to Mouse Chromosome 2, and Is an Allele of GATA Binding Protein 3 (Gata3) Ramirez Et Al
The juvenile alopecia mutation (jal) maps to mouse Chromosome 2, and is an allele of GATA binding protein 3 (Gata3) Ramirez et al. Ramirez et al. BMC Genetics 2013, 14:40 http://www.biomedcentral.com/1471-2156/14/40 Ramirez et al. BMC Genetics 2013, 14:40 http://www.biomedcentral.com/1471-2156/14/40 RESEARCH ARTICLE Open Access The juvenile alopecia mutation (jal) maps to mouse Chromosome 2, and is an allele of GATA binding protein 3 (Gata3) Francisco Ramirez†, Aaron M Feliciano†, Elisabeth B Adkins, Kevin M Child, Legairre A Radden II, Alexis Salas, Nelson Vila-Santana, José M Horák, Samantha R Hughes, Damek V Spacek and Thomas R King* Abstract Background: Mice homozygous for the juvenile alopecia mutation (jal) display patches of hair loss that appear as soon as hair develops in the neonatal period and persist throughout life. Although a report initially describing this mouse variant suggested that jal maps to mouse Chromosome 13, our preliminary mapping analysis did not support that claim. Results: To map jal to a particular mouse chromosome, we produced a 103-member intraspecific backcross panel that segregated for jal, and typed it for 93 PCR-scorable, microsatellite markers that are located throughout the mouse genome. Only markers from the centromeric tip of Chromosome 2 failed to segregate independently from jal, suggesting that jal resides in that region. To more precisely define jal’s location, we characterized a second, 374-member backcross panel for the inheritance of five microsatellite markers from proximal Chromosome 2. This analysis restricted jal’s position between D2Mit359 and D2Mit80, an interval that includes Il2ra (for interleukin 2 receptor, alpha chain), a gene that is known to be associated with alopecia areata in humans.