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Reconstructability Analysis As a Tool for Identifying Gene-Gene Interactions in Studies of Human Diseases
Portland State University PDXScholar Systems Science Faculty Publications and Presentations Systems Science 3-2010 Reconstructability Analysis As A Tool For Identifying Gene-Gene Interactions In Studies Of Human Diseases Stephen Shervais Eastern Washington University Patricia L. Kramer Oregon Health & Science University Shawn K. Westaway Oregon Health & Science University Nancy J. Cox University of Chicago Martin Zwick Portland State University, [email protected] Follow this and additional works at: https://pdxscholar.library.pdx.edu/sysc_fac Part of the Bioinformatics Commons, Diseases Commons, and the Genomics Commons Let us know how access to this document benefits ou.y Citation Details Shervais, S., Kramer, P. L., Westaway, S. K., Cox, N. J., & Zwick, M. (2010). Reconstructability Analysis as a Tool for Identifying Gene-Gene Interactions in Studies of Human Diseases. Statistical Applications In Genetics & Molecular Biology, 9(1), 1-25. This Article is brought to you for free and open access. It has been accepted for inclusion in Systems Science Faculty Publications and Presentations by an authorized administrator of PDXScholar. Please contact us if we can make this document more accessible: [email protected]. Statistical Applications in Genetics and Molecular Biology Volume 9, Issue 1 2010 Article 18 Reconstructability Analysis as a Tool for Identifying Gene-Gene Interactions in Studies of Human Diseases Stephen Shervais∗ Patricia L. Kramery Shawn K. Westawayz Nancy J. Cox∗∗ Martin Zwickyy ∗Eastern Washington University, [email protected] yOregon Health & Science University, [email protected] zOregon Health & Science University, [email protected] ∗∗University of Chicago, [email protected] yyPortland State University, [email protected] Copyright c 2010 The Berkeley Electronic Press. -
Evaluation of the Genetic Susceptibility to the Metabolic Syndrome by the CAPN10 SNP19 Gene in the Population of South Benin
International Journal of Molecular Biology: Open Access Research Article Open Access Evaluation of the genetic susceptibility to the metabolic syndrome by the CAPN10 SNP19 gene in the population of South Benin Abstract Volume 4 Issue 6 - 2019 Metabolic syndrome is a multifactorial disorder whose etiology is resulting from the Nicodème Worou Chabi,1,2 Basile G interaction between genetic and environmental factors. Calpain 10 (CAPN10) is the first Sognigbé,1 Esther Duéguénon,1 Véronique BT gene associated with type 2 diabetes that has been identified by positional cloning with 1 1 sequencing method. This gene codes for cysteine protease; ubiquitously expressed in all Tinéponanti, Arnaud N Kohonou, Victorien 2 1 tissues, it is involved in the fundamental physiopathological aspects of insulin resistance T Dougnon, Lamine Baba Moussa and insulin secretion of type 2 diabetes. The goal of this study was to evaluate the genetic 1Department of Biochemistry and Cell Biology, University of susceptibility to the metabolic syndrome by the CAPN10 gene in the population of southern Abomey-Calavi, Benin 2 Benin. This study involved apparently healthy individuals’ aged 18 to 80 in four ethnic Laboratory of Research in Applied Biology, Polytechnic School of Abomey-Calavi, University of Abomey-Calavi, Benin groups in southern Benin. It included 74 subjects with metabolic syndrome and 323 non- metabolic syndrome patients who served as controls, with 222 women versus 175 men Correspondence: Nicodème Worou Chabi, Laboratory with an average age of 40.58 ± 14.03 years old. All subjects were genotyped for the SNP of Biochemistry and Molecular Biology, Department of 19 polymorphism of the CAPN10 gene with the PCR method in order to find associations Biochemistry and Cell Biology, Faculty of Science and between this polymorphism and the metabolic syndrome. -
Genome-Wide Screen of Cell-Cycle Regulators in Normal and Tumor Cells
bioRxiv preprint doi: https://doi.org/10.1101/060350; this version posted June 23, 2016. 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. Genome-wide screen of cell-cycle regulators in normal and tumor cells identifies a differential response to nucleosome depletion Maria Sokolova1, Mikko Turunen1, Oliver Mortusewicz3, Teemu Kivioja1, Patrick Herr3, Anna Vähärautio1, Mikael Björklund1, Minna Taipale2, Thomas Helleday3 and Jussi Taipale1,2,* 1Genome-Scale Biology Program, P.O. Box 63, FI-00014 University of Helsinki, Finland. 2Science for Life laboratory, Department of Biosciences and Nutrition, Karolinska Institutet, SE- 141 83 Stockholm, Sweden. 3Science for Life laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, S-171 21 Stockholm, Sweden To identify cell cycle regulators that enable cancer cells to replicate DNA and divide in an unrestricted manner, we performed a parallel genome-wide RNAi screen in normal and cancer cell lines. In addition to many shared regulators, we found that tumor and normal cells are differentially sensitive to loss of the histone genes transcriptional regulator CASP8AP2. In cancer cells, loss of CASP8AP2 leads to a failure to synthesize sufficient amount of histones in the S-phase of the cell cycle, resulting in slowing of individual replication forks. Despite this, DNA replication fails to arrest, and tumor cells progress in an elongated S-phase that lasts several days, finally resulting in death of most of the affected cells. -
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 -
Calpain-10 Regulates Actin Dynamics by Proteolysis of Microtubule-Associated Protein 1B
www.nature.com/scientificreports OPEN Calpain-10 regulates actin dynamics by proteolysis of microtubule-associated protein 1B Received: 15 September 2015 Tomohisa Hatta1, Shun-ichiro Iemura1,6, Tomokazu Ohishi2, Hiroshi Nakayama3, Accepted: 1 November 2018 Hiroyuki Seimiya 2, Takao Yasuda4, Katsumi Iizuka5, Mitsunori Fukuda4, Jun Takeda5, Published: xx xx xxxx Tohru Natsume1 & Yukio Horikawa5 Calpain-10 (CAPN10) is the calpain family protease identifed as the frst candidate susceptibility gene for type 2 diabetes mellitus (T2DM). However, the detailed molecular mechanism has not yet been elucidated. Here we report that CAPN10 processes microtubule associated protein 1 (MAP1) family proteins into heavy and light chains and regulates their binding activities to microtubules and actin flaments. Immunofuorescent analysis of Capn10−/− mouse embryonic fbroblasts shows that MAP1B, a member of the MAP1 family of proteins, is localized at actin flaments rather than at microtubules. Furthermore, fuorescence recovery after photo-bleaching analysis shows that calpain-10 regulates actin dynamics via MAP1B cleavage. Moreover, in pancreatic islets from CAPN10 knockout mice, insulin secretion was signifcantly increased both at the high and low glucose levels. These fndings indicate that defciency of calpain-10 expression may afect insulin secretion by abnormal actin reorganization, coordination and dynamics through MAP1 family processing. Calpains are a family of intracellular non-lysosomal calcium-activated neutral cysteine proteases known to cleave various substrate proteins and modulate their activities. Tere are 16 calpains, some of which are ubiquitously expressed and others displaying tissue-specifc distribution. Some calpains contain a penta-EF-hand domain (typical or classical calpains), and others do not (atypical calpains). Several calpain family members are impli- cated in the development of various diseases including Alzheimer’s disease, cataracts, ischemic stroke, traumatic brain injury, limb-girdle muscular dystrophy 2A and type 2 diabetes mellitus (T2DM)1. -
Product Datasheet HIST1H2BO Overexpression
Product Datasheet HIST1H2BO Overexpression Lysate NBP2-07991 Unit Size: 0.1 mg Store at -80C. Avoid freeze-thaw cycles. Protocols, Publications, Related Products, Reviews, Research Tools and Images at: www.novusbio.com/NBP2-07991 Updated 3/17/2020 v.20.1 Earn rewards for product reviews and publications. Submit a publication at www.novusbio.com/publications Submit a review at www.novusbio.com/reviews/destination/NBP2-07991 Page 1 of 2 v.20.1 Updated 3/17/2020 NBP2-07991 HIST1H2BO Overexpression Lysate Product Information Unit Size 0.1 mg Concentration The exact concentration of the protein of interest cannot be determined for overexpression lysates. Please contact technical support for more information. Storage Store at -80C. Avoid freeze-thaw cycles. Buffer RIPA buffer Target Molecular Weight 13.7 kDa Product Description Description Transient overexpression lysate of histone cluster 1, H2bo (HIST1H2BO) The lysate was created in HEK293T cells, using Plasmid ID RC219561 and based on accession number NM_003527. The protein contains a C-MYC/DDK Tag. Gene ID 8348 Gene Symbol HIST1H2BO Species Human Notes HEK293T cells in 10-cm dishes were transiently transfected with a non-lipid polymer transfection reagent specially designed and manufactured for large volume DNA transfection. Transfected cells were cultured for 48hrs before collection. The cells were lysed in modified RIPA buffer (25mM Tris-HCl pH7.6, 150mM NaCl, 1% NP-40, 1mM EDTA, 1xProteinase inhibitor cocktail mix, 1mM PMSF and 1mM Na3VO4, and then centrifuged to clarify the lysate. Protein concentration was measured by BCA protein assay kit.This product is manufactured by and sold under license from OriGene Technologies and its use is limited solely for research purposes. -
Calpain-10 and Adiponectin Gene Polymorphisms in Korean Type 2 Diabetes Patients
Original Endocrinol Metab 2018;33:364-371 https://doi.org/10.3803/EnM.2018.33.3.364 Article pISSN 2093-596X · eISSN 2093-5978 Calpain-10 and Adiponectin Gene Polymorphisms in Korean Type 2 Diabetes Patients Ji Sun Nam1,2, Jung Woo Han1, Sang Bae Lee1, Ji Hong You1, Min Jin Kim1, Shinae Kang1,2, Jong Suk Park1,2, Chul Woo Ahn1,2 1Department of Internal Medicine, 2Severance Institute for Vascular and Metabolic Research, Yonsei University College of Medicine, Seoul, Korea Background: Genetic variations in calpain-10 and adiponectin gene are known to influence insulin secretion and resistance in type 2 diabetes mellitus. Recently, several single nucleotide polymorphisms (SNPs) in calpain-10 and adiponectin gene have been report- ed to be associated with type 2 diabetes and various metabolic derangements. We investigated the associations between specific cal- pain-10 and adiponectin gene polymorphisms and Korean type 2 diabetes patients. Methods: Overall, 249 type 2 diabetes patients and 131 non-diabetic control subjects were enrolled in this study. All the subjects were genotyped for SNP-43 and -63 of calpain-10 gene and G276T and T45G frequencies of the adiponectin gene. The clinical char- acteristics and measure of glucose metabolism were compared within these genotypes. Results: Among calpain-10 polymorphisms, SNP-63 T/T were more frequent in diabetes patients, and single SNP-63 increases the susceptibility to type 2 diabetes. However, SNP-43 in calpain-10 and T45G and intron G276T in adiponectin gene were not signifi- cantly associated with diabetes, insulin resistance, nor insulin secretion. Conclusion: Variations in calpain-10, SNP-63 seems to increase the susceptibility to type 2 diabetes in Koreans while SNP-43 and adiponectin SNP-45, -276 are not associated with impaired glucose metabolism. -
Original Article Whole Exome Sequencing for Mutation Screening
Original Article Iran J Ped Hematol Oncol. 2020, Vol 10, No 1, 38-48 Whole Exome Sequencing for Mutation Screening in Hemophagocytic Lymphohistiocytosis Edris Sharif Rahmani MSc1, Majid Fathi MSc1, Mohammad Foad Abazari MSc2, Hojat Shahraki MSc3, Vahid Ziaee Fellow4,5, Hamzeh Rahimi PhD6, Arshad Hosseini PhD1,* 1. Department of Medical Biotechnology, School of Allied Medicine, Iran University of Medical Science. Tehran- Iran. 2. Department of Genetics, Tehran Medical Sciences Branch, Islamic Azad University, Tehran- Iran. 3. Department of Laboratory Sciences, School of Allied Medical Sciences, Zahedan University of Medical Sciences, Zahedan- Iran. 4. Pediatric Rheumatology Research Group, Rheumatology Research Center, Tehran University of Medical Sciences. Tehran- Iran. 5. Department of Pediatrics, Children’s Medical Center, Pediatrics Center of Excellence, Tehran University of Medical Sciences. Tehran- Iran. 6. Department of Molecular Medicine, Biotechnology Research Center, Pasteur Institute of Iran. Tehran-Iran. *Corresponding author: Dr Arshad Hosseini, Department of Medical Biotechnology, School of Allied Medicine, Iran University of Medical Sciences, Tehran, IR Iran. E-mail: [email protected]. ORCID: 0000-0002-2077-0817. Received: 18 July 2019 Accepted: 19 November 2019 Abstract Background: Hemophagocytic lymphohistiocytosis (HLH) is an immune system disorder characterized by uncontrolled hyper-inflammation owing to hypercytokinemia from the activated but ineffective cytotoxic cells. Establishing a correct diagnosis for HLH patients due to the similarity of this disease with other conditions like malignant lymphoma and leukemia and similarity among its two forms is difficult and not always a successful procedure. Besides, the molecular characterization of HLH due to the locus and allelic heterogeneity is a challenging issue. -
Functional Annotation of Human Long Noncoding Rnas Using Chromatin
bioRxiv preprint doi: https://doi.org/10.1101/2021.01.13.426305; this version posted January 14, 2021. 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. 1 Funconal annotaon of human long noncoding RNAs using chroman conformaon data Saumya Agrawal1, Tanvir Alam2, Masaru Koido1,3, Ivan V. Kulakovskiy4,5, Jessica Severin1, Imad ABugessaisa1, Andrey Buyan5,6, Josee Dos&e7, Masayoshi Itoh1,8, Naoto Kondo9, Yunjing Li10, Mickaël Mendez11, Jordan A. Ramilowski1,12, Ken Yagi1, Kayoko Yasuzawa1, CHi Wai Yip1, Yasushi Okazaki1, MicHael M. Ho9man11,13,14,15, Lisa Strug10, CHung CHau Hon1, CHikashi Terao1, Takeya Kasukawa1, Vsevolod J. Makeev4,16, Jay W. SHin1, Piero Carninci1, MicHiel JL de Hoon1 1RIKEN Center for Integra&ve Medical Sciences, YokoHama, Japan. 2College of Science and Engineering, Hamad Bin KHalifa University, DoHa, Qatar. 3Ins&tute of Medical Science, THe University of Tokyo, Tokyo, Japan. 4Vavilov Ins&tute of General Gene&cs, Russian Academy of Sciences, Moscow, Russia. 5Ins&tute of Protein ResearcH, Russian Academy of Sciences, PusHcHino, Russia. 6Faculty of Bioengineering and Bioinforma&cs, Lomonosov Moscow State University, Moscow, Russia. 7Department of BiocHemistry, Rosalind and Morris Goodman Cancer ResearcH Center, McGill University, Montréal, QuéBec, Canada. 8RIKEN Preven&ve Medicine and Diagnosis Innova&on Program, Wako, Japan. 9RIKEN Center for Life Science TecHnologies, YokoHama, Japan. 10Division of Biosta&s&cs, Dalla Lana ScHool of PuBlic HealtH, University of Toronto, Toronto, Ontario, Canada. 11Department of Computer Science, University of Toronto, Toronto, Ontario, Canada. 12Advanced Medical ResearcH Center, YokoHama City University, YokoHama, Japan. -
Functional Assays for the Diagnosis of Primary Defects in Lymphocyte Cytotoxicity
From the Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden FUNCTIONAL ASSAYS FOR THE DIAGNOSIS OF PRIMARY DEFECTS IN LYMPHOCYTE CYTOTOXICITY Samuel CC Chiang Stockholm 2015 All previously published papers were reproduced with permission from the publisher. Published by Karolinska Institutet. Printed by E-print AB © Samuel CC Chiang, 2015 ISBN 978-91-7676-123-6 Back cover: 7-year collection of patient data. Image of files #1-24 holding patient information, consent forms, shipping invoices, and assay results from patient samples processed between 2008 and 2015. The open unfilled file #25 represents our anticipation of future cases. The first person to notice this gets a free lunch from Sam. Contact me! Functional Assays for the Diagnosis of Primary Defects in Lymphocyte Cytotoxicity THESIS FOR DOCTORAL DEGREE (Ph.D.) By Samuel Cern Cher, Chiang Principal Supervisor: Opponent: Assistant Professor Yenan T Bryceson Associate Professor Mirjam van der Burg Karolinska Institutet University Medical Center Rotterdam Department of Medicine, Huddinge Department of Immunology Center for Infectious Medicine Examination Board: Co-supervisors: Professor Qiang Pan Hammarström Professor Hans-Gustaf Ljunggren Karolinska Institutet Karolinska Institutet Department of Laboratory Medicine Department of Medicine, Huddinge Division of Clinical Immunology Center for Infectious Medicine Professor Ola Winqvist Professor Jan-Inge Henter Karolinska Institutet Karolinska Institutet Department of Medicine, Solna Department of Women's and Children's Health Childhood Cancer Research Unit Dr. Med. Hans Christian Erichsen Oslo University Hospital Department of Pediatric Research For the life of the body is in its blood Leviticus 17:11 ABSTRACT Cytotoxic lymphocytes encompass natural killer (NK) cells and cytotoxic T lymphocytes (CTL). -
Rap1-Mediated Chromatin and Gene Expression Changes at Senescence
University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2019 Rap1-Mediated Chromatin And Gene Expression Changes At Senescence Shufei Song University of Pennsylvania Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Biochemistry Commons, and the Cell Biology Commons Recommended Citation Song, Shufei, "Rap1-Mediated Chromatin And Gene Expression Changes At Senescence" (2019). Publicly Accessible Penn Dissertations. 3557. https://repository.upenn.edu/edissertations/3557 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/3557 For more information, please contact [email protected]. Rap1-Mediated Chromatin And Gene Expression Changes At Senescence Abstract ABSTRACT RAP1-MEDIATED CHROMATIN AND GENE EXPRESSION CHANGES AT SENESCENCE The telomeric protein Rap1 has been extensively studied for its roles as a transcriptional activator and repressor. Indeed, in both yeast and mammals, Rap1 is known to bind throughout the genome to reorganize chromatin and regulate gene transcription. Previously, our lab published evidence that Rap1 plays important roles in cellular senescence. In telomerase-deficient S. cerevisiae, Rap1 relocalizes from telomeres and subtelomeres to new Rap1 target at senescence (NRTS). This leads to two types of histone loss: Rap1 lowers global histone levels by repressing histone gene transcription and it also results in local nucleosome displacement at the promoters of the activated NRTS. Here, I examine mechanisms of site-specific histone loss by presenting evidence that Rap1 can directly interact with histone tetramers H3/H4, and map this interaction to a three-amino-acid-patch within the DNA binding domain. Functional studies are performed in vivo using a mutant form of Rap1 with weakened histone interactions, and deficient promoter clearance as well as blunted gene activation is observed, indicating that direct Rap1-H3/H4 interactions are involved in nucleosome displacement. -
Discovery and Systematic Characterization of Risk Variants and Genes For
medRxiv preprint doi: https://doi.org/10.1101/2021.05.24.21257377; this version posted June 2, 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 4.0 International license . 1 Discovery and systematic characterization of risk variants and genes for 2 coronary artery disease in over a million participants 3 4 Krishna G Aragam1,2,3,4*, Tao Jiang5*, Anuj Goel6,7*, Stavroula Kanoni8*, Brooke N Wolford9*, 5 Elle M Weeks4, Minxian Wang3,4, George Hindy10, Wei Zhou4,11,12,9, Christopher Grace6,7, 6 Carolina Roselli3, Nicholas A Marston13, Frederick K Kamanu13, Ida Surakka14, Loreto Muñoz 7 Venegas15,16, Paul Sherliker17, Satoshi Koyama18, Kazuyoshi Ishigaki19, Bjørn O Åsvold20,21,22, 8 Michael R Brown23, Ben Brumpton20,21, Paul S de Vries23, Olga Giannakopoulou8, Panagiota 9 Giardoglou24, Daniel F Gudbjartsson25,26, Ulrich Güldener27, Syed M. Ijlal Haider15, Anna 10 Helgadottir25, Maysson Ibrahim28, Adnan Kastrati27,29, Thorsten Kessler27,29, Ling Li27, Lijiang 11 Ma30,31, Thomas Meitinger32,33,29, Sören Mucha15, Matthias Munz15, Federico Murgia28, Jonas B 12 Nielsen34,20, Markus M Nöthen35, Shichao Pang27, Tobias Reinberger15, Gudmar Thorleifsson25, 13 Moritz von Scheidt27,29, Jacob K Ulirsch4,11,36, EPIC-CVD Consortium, Biobank Japan, David O 14 Arnar25,37,38, Deepak S Atri39,3, Noël P Burtt4, Maria C Costanzo4, Jason Flannick40, Rajat M 15 Gupta39,3,4, Kaoru Ito18, Dong-Keun Jang4,