Differential Expression of Genes Encoding Proteins of the HGF/MET
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The Genetical Society of Great Britain
Heredity 59 (1987) 151—160 The Genetical Society of Great Britain THEGENETICAL SOCIETY (Abstracts of papers presented at the TVVO HUNDRED AND FIFTH MEETING of the Society held on Friday, 14th and Saturday, 15th November 1986 at UNIVERSITY COLLEGE, LONDON) 1. Selection of somatic cell D. J. Porteous, P. A. Boyd, N. D. Hastie and hybrids with specific chromosome V. van Heyningen content for mapping the WAGR MAC Clinical and Population Cytogenetics Unit, Western General Hospital, Crewe Road, syndrome Edinburgh EH4 2XU. J. M. Fletcher, H. Morrison, J. A. Fantes, Clonedprobes for a number of available chromo- A. Seawright, S. Christie, D. J. Porteous, some ii assigned genes were used to define the N. D. Hastie and V. van Heyningen extent of deletions associated with the Wilms' MAC Clinical and Population Cytogenetics Unit, tumour, aniridia, genitourinary abnormalities and Western General Hospital, Crewe Road, mental retardation (WAGR) syndrome. Establish- Edinburgh EH4 2XU. ing reliable dosage studies for a number of different probes has proved difficult. We have therefore WAGR(Wilms tumour, aniridia, genitourinary abnormalities and mental retardation) syndrome concentrated on segregating the deleted chromo- is frequently associated with deletions on the short some 11 from a number of patients in somatic cell arm of chromosome 11. The deletions vary in size hybrids and analysing DNA from these to produce but always include part of band lipl3. To home a consistent map of chromosome lip. At the same in on the Wilms tumour and aniridia loci the end time we have determined the deletion breakpoints points of the different deletion breakpoints need at a molecular level and shown that the results are to be defined at the DNA level. -
Screening and Identification of Key Biomarkers in Clear Cell Renal Cell Carcinoma Based on Bioinformatics Analysis
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.21.423889; this version posted December 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder.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. Screening and identification of key biomarkers in clear cell renal cell carcinoma based on bioinformatics analysis Basavaraj Vastrad1, Chanabasayya Vastrad*2 , Iranna Kotturshetti 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. 3. Department of Ayurveda, Rajiv Gandhi Education Society`s Ayurvedic Medical College, Ron, Karnataka 562209, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2020.12.21.423889; this version posted December 23, 2020. 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. Abstract Clear cell renal cell carcinoma (ccRCC) is one of the most common types of malignancy of the urinary system. The pathogenesis and effective diagnosis of ccRCC have become popular topics for research in the previous decade. In the current study, an integrated bioinformatics analysis was performed to identify core genes associated in ccRCC. An expression dataset (GSE105261) was downloaded from the Gene Expression Omnibus database, and included 26 ccRCC and 9 normal kideny samples. Assessment of the microarray dataset led to the recognition of differentially expressed genes (DEGs), which was subsequently used for pathway and gene ontology (GO) enrichment analysis. -
Cytogenomic SNP Microarray - Fetal ARUP Test Code 2002366 Maternal Contamination Study Fetal Spec Fetal Cells
Patient Report |FINAL Client: Example Client ABC123 Patient: Patient, Example 123 Test Drive Salt Lake City, UT 84108 DOB 2/13/1987 UNITED STATES Gender: Female Patient Identifiers: 01234567890ABCD, 012345 Physician: Doctor, Example Visit Number (FIN): 01234567890ABCD Collection Date: 00/00/0000 00:00 Cytogenomic SNP Microarray - Fetal ARUP test code 2002366 Maternal Contamination Study Fetal Spec Fetal Cells Single fetal genotype present; no maternal cells present. Fetal and maternal samples were tested using STR markers to rule out maternal cell contamination. This result has been reviewed and approved by Maternal Specimen Yes Cytogenomic SNP Microarray - Fetal Abnormal * (Ref Interval: Normal) Test Performed: Cytogenomic SNP Microarray- Fetal (ARRAY FE) Specimen Type: Direct (uncultured) villi Indication for Testing: Patient with 46,XX,t(4;13)(p16.3;q12) (Quest: EN935475D) ----------------------------------------------------------------- ----- RESULT SUMMARY Abnormal Microarray Result (Male) Unbalanced Translocation Involving Chromosomes 4 and 13 Classification: Pathogenic 4p Terminal Deletion (Wolf-Hirschhorn syndrome) Copy number change: 4p16.3p16.2 loss Size: 5.1 Mb 13q Proximal Region Deletion Copy number change: 13q11q12.12 loss Size: 6.1 Mb ----------------------------------------------------------------- ----- RESULT DESCRIPTION This analysis showed a terminal deletion (1 copy present) involving chromosome 4 within 4p16.3p16.2 and a proximal interstitial deletion (1 copy present) involving chromosome 13 within 13q11q12.12. This -
PARSANA-DISSERTATION-2020.Pdf
DECIPHERING TRANSCRIPTIONAL PATTERNS OF GENE REGULATION: A COMPUTATIONAL APPROACH by Princy Parsana A dissertation submitted to The Johns Hopkins University in conformity with the requirements for the degree of Doctor of Philosophy Baltimore, Maryland July, 2020 © 2020 Princy Parsana All rights reserved Abstract With rapid advancements in sequencing technology, we now have the ability to sequence the entire human genome, and to quantify expression of tens of thousands of genes from hundreds of individuals. This provides an extraordinary opportunity to learn phenotype relevant genomic patterns that can improve our understanding of molecular and cellular processes underlying a trait. The high dimensional nature of genomic data presents a range of computational and statistical challenges. This dissertation presents a compilation of projects that were driven by the motivation to efficiently capture gene regulatory patterns in the human transcriptome, while addressing statistical and computational challenges that accompany this data. We attempt to address two major difficulties in this domain: a) artifacts and noise in transcriptomic data, andb) limited statistical power. First, we present our work on investigating the effect of artifactual variation in gene expression data and its impact on trans-eQTL discovery. Here we performed an in-depth analysis of diverse pre-recorded covariates and latent confounders to understand their contribution to heterogeneity in gene expression measurements. Next, we discovered 673 trans-eQTLs across 16 human tissues using v6 data from the Genotype Tissue Expression (GTEx) project. Finally, we characterized two trait-associated trans-eQTLs; one in Skeletal Muscle and another in Thyroid. Second, we present a principal component based residualization method to correct gene expression measurements prior to reconstruction of co-expression networks. -
Hepatocyte Growth Factor Activator Inhibitor Type 1 (Hai-1/Spint1) Is a Suppressor of Intestinal Tumorigenesis
Author Manuscript Published OnlineFirst on February 27, 2013; DOI: 10.1158/0008-5472.CAN-12-3337 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Hepatocyte growth factor activator inhibitor type 1 (Hai-1/Spint1) is a suppressor of intestinal tumorigenesis Shinri Hoshiko,*,# Makiko Kawaguchi,* Tsuyoshi Fukushima,* Yukihiro Haruyama,* Kenji Yorita,* Hiroyuki Tanaka,* Motoharu Seiki,‡ Haruhiko Inatsu,# Kazuo Kitamura# and Hiroaki Kataoka* *Section of Oncopathology and Regenerative Biology, Department of Pathology and #Section of Circulatory and Body Fluid Regulation, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan; ‡Division of Cancer Cell Research, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. S.H. and M.K. contributed equally to this study Running title: HAI-1 suppresses intestinal tumorigenesis Key words: HAI-1, carcinogenesis, colon cancer, hepatocyte growth factor, epithelial integrity Financial support: This work was supported by Grant-in-Aid for Scientific Research no. 24390099 (H.K.) and no. 23790250 (M.K.) from the Ministry of Education, Science, Sports and Culture, Japan. Corresponding author: Hiroaki Kataoka, Section of Oncopathology and Regenerative Biology, Department of Pathology, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan. Phone, +81-985-852809; Fax, +81-985-856003; E-mail, [email protected] 1 Downloaded from cancerres.aacrjournals.org on September 28, 2021. © 2013 American Association for Cancer Research. Author Manuscript Published OnlineFirst on February 27, 2013; DOI: 10.1158/0008-5472.CAN-12-3337 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. -
SPINT1) by Transcription Published: Xx Xx Xxxx Factor CDX2 E
www.nature.com/scientificreports OPEN Intestinal regulation of suppression of tumorigenicity 14 (ST14) and serine peptidase inhibitor, Kunitz Received: 5 April 2018 Accepted: 23 July 2018 type -1 (SPINT1) by transcription Published: xx xx xxxx factor CDX2 E. Thomas Danielsen 1,2, Anders Krüger Olsen2, Mehmet Coskun3, Annika W. Nonboe2, Sylvester Larsen 1,4, Katja Dahlgaard1, Eric Paul Bennett5, Cathy Mitchelmore1, Lotte Katrine Vogel2 & Jesper Thorvald Troelsen 1 The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1). The balance of the protease/inhibitor gene expression ratio is vital in preventing the oncogenic potential of matriptase. The intestinal cell lineage is regulated by a transcriptional regulatory network where the tumor suppressor, Caudal homeobox 2 (CDX2) is considered to be an intestinal master transcription factor. In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. We fnd that CDX2 is not required for the basal ST14 and SPINT1 gene expression; however changes in CDX2 expression afects the ST14/SPINT1 mRNA ratio. Exploring CDX2 ChIP-seq data from intestinal cell lines, we identifed genomic CDX2-enriched enhancer elements for both ST14 and SPINT1, which regulate their corresponding gene promoter activity. We show that CDX2 displays both repressive and enhancing regulatory abilities in a cell specifc manner. Together, these data reveal new insight into transcriptional mechanisms controlling the intestinal matriptase/inhibitor balance. -
Oncogenomics of C-Myc Transgenic Mice Reveal Novel Regulators of Extracellular Signaling, Angiogenesis and Invasion with Clinica
www.impactjournals.com/oncotarget/ Oncotarget, 2017, Vol. 8, (No. 60), pp: 101808-101831 Research Paper Oncogenomics of c-Myc transgenic mice reveal novel regulators of extracellular signaling, angiogenesis and invasion with clinical significance for human lung adenocarcinoma Yari Ciribilli1,2 and Jürgen Borlak2 1Centre for Integrative Biology (CIBIO), University of Trento, 38123 Povo (TN), Italy 2Centre for Pharmacology and Toxicology, Hannover Medical School, 30625 Hannover, Germany Correspondence to: Jürgen Borlak, email: [email protected] Keywords: c-Myc transgenic mouse model of lung cancer, papillary adenocarcinomas, whole genome scans, c-Myc regulatory gene networks, c-Myc targeted regulators of extracellular signaling Received: June 26, 2017 Accepted: September 21, 2017 Published: October 23, 2017 Copyright: Ciribilli et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT The c-Myc transcription factor is frequently deregulated in cancers. To search for disease diagnostic and druggable targets a transgenic lung cancer disease model was investigated. Oncogenomics identified c-Myc target genes in lung tumors. These were validated by RT-PCR, Western Blotting, EMSA assays and ChIP-seq data retrieved from public sources. Gene reporter and ChIP assays verified functional importance of c-Myc binding sites. The clinical significance was established by RT-qPCR in tumor and matched healthy control tissues, by RNA-seq data retrieved from the TCGA Consortium and by immunohistochemistry recovered from the Human Protein Atlas repository. In transgenic lung tumors 25 novel candidate genes were identified. -
SARS-Cov-2 Entry Protein TMPRSS2 and Its Homologue, TMPRSS4
bioRxiv preprint doi: https://doi.org/10.1101/2021.04.26.441280; this version posted April 26, 2021. 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 SARS-CoV-2 Entry Protein TMPRSS2 and Its 2 Homologue, TMPRSS4 Adopts Structural Fold Similar 3 to Blood Coagulation and Complement Pathway 4 Related Proteins ∗,a ∗∗,b b 5 Vijaykumar Yogesh Muley , Amit Singh , Karl Gruber , Alfredo ∗,a 6 Varela-Echavarría a 7 Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, México b 8 Institute of Molecular Biosciences, University of Graz, Graz, Austria 9 Abstract The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) utilizes TMPRSS2 receptor to enter target human cells and subsequently causes coron- avirus disease 19 (COVID-19). TMPRSS2 belongs to the type II serine proteases of subfamily TMPRSS, which is characterized by the presence of the serine- protease domain. TMPRSS4 is another TMPRSS member, which has a domain architecture similar to TMPRSS2. TMPRSS2 and TMPRSS4 have been shown to be involved in SARS-CoV-2 infection. However, their normal physiological roles have not been explored in detail. In this study, we analyzed the amino acid sequences and predicted 3D structures of TMPRSS2 and TMPRSS4 to under- stand their functional aspects at the protein domain level. Our results suggest that these proteins are likely to have common functions based on their conserved domain organization. -
Microrna-1182 and Let-7A Exert Synergistic Inhibition on Invasion
Pan et al. Cancer Cell Int (2021) 21:161 https://doi.org/10.1186/s12935-021-01797-z Cancer Cell International PRIMARY RESEARCH Open Access MicroRNA-1182 and let-7a exert synergistic inhibition on invasion, migration and autophagy of cholangiocarcinoma cells through down-regulation of NUAK1 Xin Pan*, Gang Wang and Baoming Wang Abstract Background: Cholangiocarcinoma (CCA) is the second most common primary liver malignancy worldwide. Several microRNAs (miRNAs) have been implicated as potential tumor suppressors in CCA. This study aims to explore the potential efects of miR-1182 and let-7a on CCA development. Methods: Bioinformatics analysis was conducted to screen diferentially expressed genes in CCA, Western blot analysis detected NUAK1 protein expression and RT-qPCR detected miR-1182, let-7a and NUAK1 expression in CCA tissues and cell lines. Dual luciferase reporter gene assay and RIP were applied to validate the relationship between miR-1182 and NUAK1 as well as between let-7a and NUAK1. Functional experiment was conducted to investigate the role of miR-1182, let-7a and NUAK1 in cell migration, proliferation and autophagy. Then, the CCA cells that received various treatments were implanted to mice to establish animal model, followed by tumor observation and HE staining to evaluate lung metastasis. Results: CCA tissues and cells were observed to have a high expression of NUAK1 and poor expression of miR-1182 and let-7a. NUAK1 was indicated as a target gene of miR-1182 and let-7a. Importantly, upregulation of either miR-1182 or let-7a induced autophagy, and inhibited cell progression and in vivo tumor growth and lung metastasis; moreover, combined treatment of miR-1182 and let-7a overexpression presented with enhanced inhibitory efect on NUAK1 expression and CCA progression, but such synergistic efect could be reversed by overexpression of NUAK1. -
ST14 (NM 021978) Human 3' UTR Clone – SC207486 | Origene
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 SC207486 ST14 (NM_021978) Human 3' UTR Clone Product data: Product Type: 3' UTR Clones Product Name: ST14 (NM_021978) Human 3' UTR Clone Vector: pMirTarget (PS100062) Symbol: ST14 Synonyms: ARCI11; CAP3; HAI; MT-SP1; MTSP1; PRSS14; SNC19; TADG15; TMPRSS14 ACCN: NM_021978 Insert Size: 569 bp Insert Sequence: >SC207486 3’UTR clone of NM_021978 The sequence shown below is from the reference sequence of NM_021978. The complete sequence of this clone may contain minor differences, such as SNPs. Blue=Stop Codon Red=Cloning site GGCAAGTTGGACGCCCGCAAGATCCGCGAGATTCTCATTAAGGCCAAGAAGGGCGGAAAGATCGCCGTG TAACAATTGGCAGAGCTCAGAATTCAAGCGATCGCC GACTGGATCAAAGAGAACACTGGGGTATAGGGGCCGGGGCCACCCAAATGTGTACACCTGCGGGGCCAC CCATCGTCCACCCCAGTGTGCACGCCTGCAGGCTGGAGACTGGACCGCTGACTGCACCAGCGCCCCCAG AACATACACTGTGAACTCAATCTCCAGGGCTCCAAATCTGCCTAGAAAACCTCTCGCTTCCTCAGCCTC CAAAGTGGAGCTGGGAGGTAGAAGGGGAGGACACTGGTGGTTCTACTGACCCAACTGGGGGCAAAGGTT TGAAGACACAGCCTCCCCCGCCAGCCCCAAGCTGGGCCGAGGCGCGTTTGTGCATATCTGCCTCCCCTG TCTCTAAGGAGCAGCGGGAACGGAGCTTCGGGGCCTCCTCAGTGAAGGTGGTGGGGCTGCCGGATCTGG GCTGTGGGGCCCTTGGGCCACGCTCTTGAGGAAGCCCAGGCTCGGAGGACCCTGGAAAACAGACGGGTC TGAGACTGAAATTGTTTTACCAGCTCCCAGGGTGGACTTCAGTGTGTGTATTTGTGTAAATGAGTAAAA CATTTTATTTCTTTTTA ACGCGTAAGCGGCCGCGGCATCTAGATTCGAAGAAAATGACCGACCAAGCGACGCCCAACCTGCCATCA CGAGATTTCGATTCCACCGCCGCCTTCTATGAAAGG Restriction Sites: SgfI-MluI OTI Disclaimer: -
SPINT2 Suppresses Hippo Effector YAP and Limits Cellular Tolerance for Aneuploidy
SPINT2 Suppresses Hippo Effector YAP and Limits Cellular Tolerance for Aneuploidy The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Zhang, Huadi. 2017. SPINT2 Suppresses Hippo Effector YAP and Limits Cellular Tolerance for Aneuploidy. Doctoral dissertation, Harvard University, Graduate School of Arts & Sciences. Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:42061511 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA SPINT2 Suppresses Hippo Effector YAP and Limits Cellular Tolerance for Aneuploidy A dissertation presented by Huadi Zhang to The Division of Medical Sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the subject of Biological and Biomedical Sciences Harvard University Cambridge, Massachusetts August 2017 © 2017 Huadi Zhang All rights reserved. Dissertation Advisor: Professor David Pellman Huadi Zhang SPINT2 Suppresses Hippo Effector YAP and Limits Cellular Tolerance for Aneuploidy Abstract Oncogenic transformation is often accompanied by chromosome instability, an increased rate of chromosome missegregation. The consequent gain or loss of chromosomes—termed aneuploidy—hinders the growth of most non-cancerous tissues, but is prevalent in tumors. During tumorigenesis, aneuploidy contributes to cellular heterogeneity and may promote downstream mutations, including chromosome rearrangements and oncogene amplification. Cellular mechanisms that safeguard against aneuploidy remain unclear. The Hippo pathway is a tumor-suppressor mechanism with essential roles in regulating tissue homeostasis. -
High-Throughput Characterization of Blood Serum Proteomics of IBD Patients with Respect to Aging and Genetic Factors
RESEARCH ARTICLE High-Throughput Characterization of Blood Serum Proteomics of IBD Patients with Respect to Aging and Genetic Factors Antonio F. Di Narzo1,2, Shannon E. Telesco3, Carrie Brodmerkel3, Carmen Argmann1,2, Lauren A. Peters2,4, Katherine Li3, Brian Kidd1,2, Joel Dudley1,2, Judy Cho1,2, Eric E. Schadt1,2, Andrew Kasarskis1,2, Radu Dobrin3*, Ke Hao1,2* 1 Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America, 2 Icahn Institute of Genomics and Multiscale Biology, Icahn School of a1111111111 Medicine at Mount Sinai, New York, New York, United States of America, 3 Janssen R&D, LLC, Spring a1111111111 House, Pennsylvania, United States of America, 4 Graduate School of Biomedical Sciences, Icahn School of a1111111111 Medicine at Mount Sinai, New York, New York, United States of America a1111111111 a1111111111 * [email protected] (RD); [email protected] (KH) Abstract OPEN ACCESS To date, no large scale, systematic description of the blood serum proteome has been per- Citation: Di Narzo AF, Telesco SE, Brodmerkel C, formed in inflammatory bowel disease (IBD) patients. By using microarray technology, a Argmann C, Peters LA, Li K, et al. (2017) High- more complete description of the blood proteome of IBD patients is feasible. It may help to Throughput Characterization of Blood Serum achieve a better understanding of the disease. We analyzed blood serum profiles of 1128 Proteomics of IBD Patients with Respect to Aging and Genetic Factors. PLoS Genet 13(1): e1006565. proteins in IBD patients of European descent (84 Crohn's Disease (CD) subjects and 88 doi:10.1371/journal.pgen.1006565 Ulcerative Colitis (UC) subjects) as well as 15 healthy control subjects, and linked protein Editor: Gregory S.