Product Name: CCDC70 Polyclonal Antibody, ALEXA FLUOR® 594 Conjugated Catalog No

Total Page：16

File Type：pdf, Size：1020Kb

Product Name: CCDC70 Polyclonal Antibody, ALEXA FLUOR® 594 Conjugated Catalog No. : TAP01-93077R-A594 Intended Use: For Research Use Only. Not for used in diagnostic procedures. Size 100ul Concentration 1ug/ul Gene ID 83446 ISO Type Rabbit IgG Clone N/A Immunogen Range Conjugation ALEXA FLUOR® 594 Subcellular Locations Applications IF(IHC-P) Cross Reactive Species Human, Mouse, Rat Source KLH conjugated synthetic peptide derived from human CCDC70 Applications with IF(IHC-P)(1:50-200) Dilutions Purification Purified by Protein A. Background Comprising nearly 4% of human DNA, chromosome 13 contains around 114 million base pairs and 400 genes. Key tumor suppressor genes on chromosome 13 include the breast cancer susceptibility gene, BRCA2, and the RB1 (retinoblastoma) gene. RB1 encodes a crucial tumor suppressor protein which, when defective, leads to malignant growth in the retina and has been implicated in a variety of other cancers. The gene SLITRK1, which is associated with Tourette syndrome, is on chromosome 13. As with most chromosomes,polysomy of part or all of chromosome 13 is deleterious to development and decreases the odds of survival. Trisomy 13, also known as Patau syndrome, is quite deadly and the few who survive past one year suffer from permanent neurologic defects, difficultyeating and vulnerability to serious respiratory infections. The gene encoding CCDC70 (Coiled-coil domain-containing protein 70), a 233 amino acid secreted protein, exists on human chromosome 13. Synonyms CCDC 70; Coiled coil domain containing 70; Coiled coil domain containing protein 70; FLJ25853; CCD70_HUMAN. Storage Aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Store at 4°C for 12 months. If unexpected results are observed which cannot be explained by variations in laboratory procedures and a problem with the reagent is suspected, contact Technical Support at [email protected] or your distributor service. .

Copy Link

Recommended publications

Manual Annotation and Analysis of the Defensin Gene Cluster in the C57BL
BMC Genomics BioMed Central Research article Open Access Manual annotation and analysis of the defensin gene cluster in the C57BL/6J mouse reference genome Clara Amid*†1, Linda M Rehaume*†2, Kelly L Brown2,3, James GR Gilbert1, Gordon Dougan1, Robert EW Hancock2 and Jennifer L Harrow1 Address: 1Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire CB10 1SA, UK, 2University of British Columbia, Centre for Microbial Disease & Immunity Research, 2259 Lower Mall, Vancouver, BC, V6T 1Z4, Canada and 3Department of Rheumatology and Inflammation Research, Göteborg University, Guldhedsgatan 10, S-413 46 Göteborg, Sweden Email: Clara Amid* - [email protected]; Linda M Rehaume* - [email protected]; Kelly L Brown - [email protected]; James GR Gilbert - [email protected]; Gordon Dougan - [email protected]; Robert EW Hancock - [email protected]; Jennifer L Harrow - [email protected] * Corresponding authors †Equal contributors Published: 15 December 2009 Received: 15 May 2009 Accepted: 15 December 2009 BMC Genomics 2009, 10:606 doi:10.1186/1471-2164-10-606 This article is available from: http://www.biomedcentral.com/1471-2164/10/606 © 2009 Amid et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: Host defense peptides are a critical component of the innate immune system. Human alpha- and beta-defensin genes are subject to copy number variation (CNV) and historically the organization of mouse alpha-defensin genes has been poorly defined.
[Show full text]
High Density Mapping to Identify Genes Associated to Gastrointestinal Nematode Infections Resistance in Spanish Churra Sheep
Facultad de Veterinaria Departamento de Producción Animal HIGH DENSITY MAPPING TO IDENTIFY GENES ASSOCIATED TO GASTROINTESTINAL NEMATODE INFECTIONS RESISTANCE IN SPANISH CHURRA SHEEP (MAPEO DE ALTA DENSIDAD PARA LA IDENTIFICACIÓN DE GENES RELACIONADOS CON LA RESISTENCIA A LAS INFECCIONES GASTROINTESTINALES POR NEMATODOS EN EL GANADO OVINO DE RAZA CHURRA) Marina Atlija León, Mayo de 2016 Supervisors: Beatriz Gutiérrez-Gil1 María Martínez-Valladares2, 3 1 Departamento de Producción Animal, Facultad de Veterinaria, Universidad de León, Campus de Vegazana s/n, León 24071, Spain. 2 Instituto de Ganadería de Montaña. CSIC-ULE. 24346. Grulleros. León. 3 Departamento de Sanidad Animal. Universidad de León. 24071. León. The research work included in this PhD Thesis memory has been supported by the European funded Initial Training Network (ITN) project NematodeSystemHealth ITN (FP7-PEOPLE-2010-ITN Ref. 264639), a competitive grant from the Castilla and León regional government (Junta de Castilla y León) (Ref. LE245A12-2) and a national project from the Spanish Ministry of Economy and Competitiveness (AGL2012-34437). Marina Atlija is a grateful grantee of a Marie Curie fellowship funded in the framework of the NematodeSystemHealth ITN (FP7-PEOPLE-2010-ITN Ref. 264639). “If all the matter in the universe except the nematodes were swept away, our world would still be dimly recognizable, and if, as disembodied spirits, we could then investigate it, we should find its mountains, hills, vales, rivers, lakes, and oceans represented by a film of nematodes. The location of towns would be decipherable, since for every massing of human beings there would be a corresponding massing of certain nematodes. Trees would still stand in ghostly rows representing our streets and highways.
[Show full text]
Family-Based Investigation of the Genetics and Epigenetics of Obesity in Qatar
Family-Based Investigation of the Genetics and Epigenetics of Obesity in Qatar Mashael Nedham A J Alshafai A Thesis Submitted for the Degree of Doctor of Philosophy Department of Genomics of Common Disease School of Public Health Imperial College London July 2015 1 Abstract Abstract Single nucleotide polymorphisms (SNPs), copy number variations (CNVs) and DNA methylation patterns play a role in the susceptibility to obesity. Despite the alarming figures of obesity in the Arab world, the genetics of obesity remain understudied in Arabs. Here, I recruited ten multigenerational Qatari families segregating obesity, and generated genome-wide SNP genotyping, whole genome sequencing and genome-wide methylation profiling data using Illumina platforms to investigate the role of rare mutations, CNVs, and DNA methylation patterns in the susceptibility to obesity. For the identification of obesity mutations, I first identified candidate obesity regions through linkage and run of homozygosity analyses, and then investigated these regions to detect potential deleterious mutations. These analyses highlighted putative rare variants for obesity risk at PCSK1, NMUR2, CLOCK and RETSAT. The functional impact of the PCSK1 mutation on obesity was previously demonstrated while for the other candidates further work is needed to confirm their impact. For the identification of common obesity CNVs, I performed a genome-wide CNV association analysis with BMI and identified a common duplication of ~5.6kb on 19p13.3 that associates with higher BMI. Moreover, I investigated large (≥500kb) rare CNVs and identified a ~618kb deletion on 16p11.2 in the most extremely obese subject in my samples, which confirms the contribution of the previously reported 16p11.2 deletions to severe obesity beyond European populations.
[Show full text]
Systems Physiology and Nutrition In
SYSTEMS PHYSIOLOGY AND NUTRITION IN DAIRY CATTLE: APPLICATIONS OF OMICS AND BIOINFORMATICS TO BETTER UNDERSTAND THE HEPATIC METABOLOMICS AND TRANSCRIPTOMICS ADAPTATIONS IN TRANSITION DAIRY COWS BY KHURAM SHAHZAD DISSERTATION Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Informatics in the Graduate College of the University of Illinois at Urbana-Champaign, 2017 Urbana, Illinois Doctoral Committee: Associate Professor, Juan J. Loor, Chair Professor Gustavo Caetano-Anolles Associate Professor, Juan Steibel, Michigan State University Assistant Professor Phil Cardoso ABSTRACT Application of systems concepts to better understand physiological and metabolic changes in dairy cows during the transition into lactation could enhance our understanding about the role of nutrients in helping to meet the animal’s requirements for optimal production and health. Four different analyses focused on the liver were conducted to analyze metabolic disorder or thermal stress. The first three analyses dealt with supplementation of methionine to prevent clinical ketosis development in high-genetic merit dairy cows. Four groups of cows were formed retrospectively based on clinical health evaluated at 1 week postpartum: cows that remained healthy (OVE), cows that developed ketosis (K), and healthy cows supplemented with one of two commercial methionine products [Smartamine M (SM), and MetaSmart (MS)]. The liver tissue samples (n = 6/group) were harvested at -10 d before calving, and were used for metabolomics (GC-MS, LC-MS; Metabolon Inc.) and transcriptomics (44K-whole-transcriptome microarray; Agilent) analyses. Therefore, the main goals of the analyses were to 1) uncover metabolome and transcriptome patterns in the prepartum liver that were unique to those cows that became ketotic postpartum, and to 2) uncover unique patterns affected by supplemental methionine.
[Show full text]
The Potential Genetic Network of Human Brain SARS-Cov-2 Infection
bioRxiv preprint doi: https://doi.org/10.1101/2020.04.06.027318; this version posted April 6, 2020. 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 4.0 International license. The potential genetic network of human brain SARS-CoV-2 infection. Colline Lapina 1,2,3, Mathieu Rodic 1, Denis Peschanski 4,5, and Salma Mesmoudi 1, 3, 4, 5 1 Prematuration Program: linkAllBrains. CNRS. Paris. France 2 Graduate School in Cognitive Engineering (ENSC). Talence. France 3 Complex Systems Institute Paris île-de-France. Paris. France 4 CNRS, Paris-1-Panthéon-Sorbonne University. CESSP-UMR8209. Paris. France 5 MATRICE Equipex. Paris. France Abstract The literature reports several symptoms of SARS-CoV-2 in humans such as fever, cough, fatigue, pneumonia, and headache. Furthermore, patients infected with similar strains (SARS-CoV and MERS-CoV) suffered testis, liver, or thyroid damage. Angiotensin-converting enzyme 2 (ACE2) serves as an entry point into cells for some strains of coronavirus (SARS-CoV, MERS-CoV, SARS-CoV-2). Our hypothesis was that as ACE2 is essential to the SARS-CoV-2 virus invasion, then brain regions where ACE2 is the most expressed are more likely to be disturbed by the infection. Thus, the expression of other genes which are also over-expressed in those damaged areas could be affected. We used mRNA expression levels data of genes provided by the Allen Human Brain Atlas (ABA), and computed spatial correlations with the LinkRbrain platform.
[Show full text]
Mouse Ccdc70 Knockout Project (CRISPR/Cas9)
https://www.alphaknockout.com Mouse Ccdc70 Knockout Project (CRISPR/Cas9) Objective: To create a Ccdc70 knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Ccdc70 gene (NCBI Reference Sequence: NM_026459 ; Ensembl: ENSMUSG00000017049 ) is located on Mouse chromosome 8. 2 exons are identified, with the ATG start codon in exon 2 and the TAG stop codon in exon 2 (Transcript: ENSMUST00000017193). Exon 2 will be selected as target site. Cas9 and gRNA will be co-injected into fertilized eggs for KO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Exon 2 starts from about 0.15% of the coding region. Exon 2 covers 100.0% of the coding region. The size of effective KO region: ~669 bp. The KO region does not have any other known gene. Page 1 of 8 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele 5' gRNA region gRNA region 3' 1 2 Legends Exon of mouse Ccdc70 Knockout region Page 2 of 8 https://www.alphaknockout.com Overview of the Dot Plot (up) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 2000 bp section upstream of start codon is aligned with itself to determine if there are tandem repeats. Tandem repeats are found in the dot plot matrix. The gRNA site is selected outside of these tandem repeats. Overview of the Dot Plot (down) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 2000 bp section downstream of stop codon is aligned with itself to determine if there are tandem repeats.
[Show full text]
Epigenetic Trajectories to Childhood Asthma
Epigenetic Trajectories to Childhood Asthma Item Type text; Electronic Dissertation Authors DeVries, Avery Publisher The University of Arizona. Rights Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction, presentation (such as public display or performance) of protected items is prohibited except with permission of the author. Download date 04/10/2021 09:24:24 Link to Item http://hdl.handle.net/10150/630233 1 EPIGENETIC TRAJECTORIES TO CHILDHOOD ASTHMA by Avery DeVries __________________________ Copyright © Avery DeVries 2018 A Dissertation Submitted to the Faculty of the DEPARTMENT OF CELLULAR AND MOLECULAR MEDICINE In Partial Fulfillment of the Requirements For the Degree of DOCTOR OF PHILOSOPHY In the Graduate College THE UNIVERSITY OF ARIZONA 2018 2 3 STATEMENT BY AUTHOR This dissertation has been submitted in partial fulfillment of the requirements for an advanced degree at the University of Arizona and is deposited in the University Library to be made available to borrowers under rules of the Library. Brief quotations from this dissertation are allowable without special permission, provided that an accurate acknowledgement of the source is made. Requests for permission for extended quotation from or reproduction of this manuscript in whole or in part may be granted by the head of the major department or the Dean of the Graduate College when in his or her judgment the proposed use of the material is in the interests of scholarship. In all other instances, however, permission must be obtained from the author. SIGNED: Avery DeVries 4 ACKNOWLEDGEMENTS I would like to thank my dissertation mentor, Donata Vercelli, for endless support throughout this journey and for always encouraging and challenging me to be a better scientist.
[Show full text]
STAT3 Targets Suggest Mechanisms of Aggressive Tumorigenesis in Diffuse Large B Cell Lymphoma
STAT3 Targets Suggest Mechanisms of Aggressive Tumorigenesis in Diffuse Large B Cell Lymphoma Jennifer Hardee*,§, Zhengqing Ouyang*,1,2,3, Yuping Zhang*,4 , Anshul Kundaje*,†, Philippe Lacroute*, Michael Snyder*,5 *Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305; §Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, CT 06520; and †Department of Computer Science, Stanford University School of Engineering, Stanford, CA 94305 1The Jackson Laboratory for Genomic Medicine, Farmington, CT 06030 2Department of Biomedical Engineering, University of Connecticut, Storrs, CT 06269 3Department of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, CT 06030 4Department of Biostatistics, Yale School of Public Health, Yale University, New Haven, CT 06520 5Corresponding author: Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305. Email: [email protected] DOI: 10.1534/g3.113.007674 Figure S1 STAT3 immunoblotting and immunoprecipitation with sc-482. Western blot and IPs show a band consistent with expected size (88 kDa) of STAT3. (A) Western blot using antibody sc-482 versus nuclear lysates. Lanes contain (from left to right) lysate from K562 cells, GM12878 cells, HeLa S3 cells, and HepG2 cells. (B) IP of STAT3 using sc-482 in HeLa S3 cells. Lane 1: input nuclear lysate; lane 2: unbound material from IP with sc-482; lane 3: material IP’d with sc-482; lane 4: material IP’d using control rabbit IgG. Arrow indicates the band of interest. (C) IP of STAT3 using sc-482 in K562 cells. Lane 1: input nuclear lysate; lane 2: material IP’d using control rabbit IgG; lane 3: material IP’d with sc-482.
[Show full text]
WO 2016/004387 Al 7 January 2016 (07.01.2016) P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2016/004387 Al 7 January 2016 (07.01.2016) P O P C T (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61P 35/00 (2006.01) kind of national protection available): AE, AG, AL, AM, AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, (21) International Application Number: BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, PCT/US20 15/039 108 DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (22) International Filing Date: HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, 2 July 2015 (02.07.2015) KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, (25) Filing Language: English PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, SC, (26) Publication Language: English SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (30) Priority Data: 62/020,3 10 2 July 2014 (02.07.2014) US (84) Designated States (unless otherwise indicated, for every kind of regional protection available): ARIPO (BW, GH, (71) Applicant: H. LEE MOFFITT CANCER CENTER GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, ST, SZ, AND RESEARCH INSTITUTE, INC. [US/US]; 12902 TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, Magnolia Dr., Tampa, FL 336 12-9497 (US).
[Show full text]
Investigating the Roles of Neurogenin 3 in Human Pancreas and Intestine
University of Cincinnati March 2, 2016 Investigating the roles of Neurogenin 3 in human pancreas and intestine development and disease. A dissertation submitted to the Graduate School of the University of Cincinnati in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Graduate Program in Molecular and Developmental Biology of the College of Medicine by Patrick Sean McGrath Bachelor of Science, Colorado State University, May 2009 Committee Chair: James M. Wells, Ph.D. Brian Gebelein, Ph.D. Michael A. Helmrath, MD, MS Stacey S. Huppert, Ph.D. Aaron M. Zorn, Ph.D. Summary The incidence of diabetes mellitus, a disease defined by the inability to properly regulate glucose, is increasing at an alarming rate and affects an estimated 26 million people in the U.S. creating an economic cost of $245 billion per year (American Diabetes, 2013). Glucose homeostasis is regulated through a complex interplay of hormones produced by both the pancreatic and intestinal endocrine systems. Neurogenin 3 is a basic helix-loop-helix (bHLH) transcription factor which acts as a “master regulator” of endocrine cell specification. Mouse studies have shown Neurog3 to be necessary and sufficient for the formation of all endocrine lineages in both the pancreas and intestine. Human patients harboring NEUROG3 mutations have a complete loss of intestinal endocrine cells, but surprisingly retain at least some endocrine pancreas function, calling into question whether NEUROG3 is required for human endocrine pancreas development. To test this directly, we generated human embryonic stem cell (hESC) lines where both alleles of NEUROG3 were disrupted using CRISPR/Cas9-mediated gene targeting.
[Show full text]
Microrna-15A and -16-1 Act Via MYB to Elevate Fetal Hemoglobin Expression in Human Trisomy 13
MicroRNA-15a and -16-1 act via MYB to elevate fetal hemoglobin expression in human trisomy 13 Vijay G. Sankarana,b,c,d, Tobias F. Mennee,f, Danilo Šcepanovicg, Jo-Anne Vergilioh, Peng Jia, Jinkuk Kima,g,i, Prathapan Thirua, Stuart H. Orkind,e,f,j, Eric S. Landera,b,k,l, and Harvey F. Lodisha,b,l,1 aWhitehead Institute for Biomedical Research, Cambridge, MA 02142; bBroad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142; Departments of cMedicine and hPathology and eDivision of Hematology/Oncology, Children’s Hospital Boston, Boston, MA 02115; Departments of dPediatrics and kSystems Biology, Harvard Medical School, Boston, MA 02115; lDepartment of Biology and iHoward Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02142; gHarvard–Massachusetts Institute of Technology Division of Health Sciences and Technology, Cambridge, MA 02142; fDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA 02115; and jThe Howard Hughes Medical Institute, Boston, MA 02115 Contributed by Harvey F. Lodish, December 13, 2010 (sent for review November 8, 2010) Many human aneuploidy syndromes have unique phenotypic other hematopoietic cells shifts to the bone marrow, the pre- consequences, but in most instances it is unclear whether these dominant postnatal site for hematopoiesis, another switch phenotypes are attributable to alterations in the dosage of speciﬁc occurs, resulting in down-regulation of γ-globin and concomitant genes. In human trisomy 13, there is delayed switching and up-regulation of the adult β-globin gene (6, 8, 10). There is persistence of fetal hemoglobin (HbF) and elevation of embryonic a limited understanding of the molecular control of these globin hemoglobin in newborns.
[Show full text]
Microrna-15A and -16-1 Act Via MYB to Elevate Fetal Hemoglobin Expression in Human Trisomy 13
MicroRNA-15a and -16-1 act via MYB to elevate fetal hemoglobin expression in human trisomy 13 Vijay G. Sankarana,b,c,d, Tobias F. Mennee,f, Danilo Šcepanovicg, Jo-Anne Vergilioh, Peng Jia, Jinkuk Kima,g,i, Prathapan Thirua, Stuart H. Orkind,e,f,j, Eric S. Landera,b,k,l, and Harvey F. Lodisha,b,l,1 aWhitehead Institute for Biomedical Research, Cambridge, MA 02142; bBroad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142; Departments of cMedicine and hPathology and eDivision of Hematology/Oncology, Children’s Hospital Boston, Boston, MA 02115; Departments of dPediatrics and kSystems Biology, Harvard Medical School, Boston, MA 02115; lDepartment of Biology and iHoward Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02142; gHarvard–Massachusetts Institute of Technology Division of Health Sciences and Technology, Cambridge, MA 02142; fDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA 02115; and jThe Howard Hughes Medical Institute, Boston, MA 02115 Contributed by Harvey F. Lodish, December 13, 2010 (sent for review November 8, 2010) Many human aneuploidy syndromes have unique phenotypic other hematopoietic cells shifts to the bone marrow, the pre- consequences, but in most instances it is unclear whether these dominant postnatal site for hematopoiesis, another switch phenotypes are attributable to alterations in the dosage of speciﬁc occurs, resulting in down-regulation of γ-globin and concomitant genes. In human trisomy 13, there is delayed switching and up-regulation of the adult β-globin gene (6, 8, 10). There is persistence of fetal hemoglobin (HbF) and elevation of embryonic a limited understanding of the molecular control of these globin hemoglobin in newborns.
[Show full text]