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The G Protein-Coupled Receptor Subset of the Dog Genome Is More Similar
BMC Genomics BioMed Central Research article Open Access The G protein-coupled receptor subset of the dog genome is more similar to that in humans than rodents Tatjana Haitina1, Robert Fredriksson1, Steven M Foord2, Helgi B Schiöth*1 and David E Gloriam*2 Address: 1Department of Neuroscience, Functional Pharmacology, Uppsala University, BMC, Box 593, 751 24, Uppsala, Sweden and 2GlaxoSmithKline Pharmaceuticals, New Frontiers Science Park, 3rd Avenue, Harlow CM19 5AW, UK Email: Tatjana Haitina - [email protected]; Robert Fredriksson - [email protected]; Steven M Foord - [email protected]; Helgi B Schiöth* - [email protected]; David E Gloriam* - [email protected] * Corresponding authors Published: 15 January 2009 Received: 20 August 2008 Accepted: 15 January 2009 BMC Genomics 2009, 10:24 doi:10.1186/1471-2164-10-24 This article is available from: http://www.biomedcentral.com/1471-2164/10/24 © 2009 Haitina 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: The dog is an important model organism and it is considered to be closer to humans than rodents regarding metabolism and responses to drugs. The close relationship between humans and dogs over many centuries has lead to the diversity of the canine species, important genetic discoveries and an appreciation of the effects of old age in another species. The superfamily of G protein-coupled receptors (GPCRs) is one of the largest gene families in most mammals and the most exploited in terms of drug discovery. -
Table of Contents (PDF)
July 26, 2011 u vol. 108 u no. 30 u 12187–12560 Cover image: Pictured is a Tasmanian devil (Sarcophilus harrisii), a carnivorous marsupial whose numbers are dwindling due to an infectious facial cancer called Devil Facial Tumor Disease. Webb Miller et al. sequenced the genome of devils from northwest and south- east Tasmania, spanning the range of this threatened species on the Australian island. The authors report that the sequences reveal a worrisome dearth of genetic diversity among devils, suggesting the need for genetically characterized stocks to help breed hardier devils that might be better equipped to fight diseases. See the article by Miller et al. on pages 12348–12353. Image courtesy of Stephan C. Schuster. From the Cover 12348 Decoding the Tasmanian devil genome 12283 Illuminating chromosomal architecture 12295 Symmetry of cultured cells 12319 Caloric restriction and infertility 12366 Genetic diversity among ants Contents COMMENTARIES 12189 Methyl fingerprinting of the nucleosome reveals the molecular mechanism of high-mobility group THIS WEEK IN PNAS nucleosomal-2 (HMGN2) association Catherine A. Musselman and Tatiana G. Kutateladze See companion article on page 12283 12187 In This Issue 12191 Examining the establishment of cellular axes using intrinsic chirality LETTERS (ONLINE ONLY) Jason C. McSheene and Rebecca D. Burdine See companion article on page 12295 E341 Difference between restoring and predicting 3D 12193 Secrets of palm oil biosynthesis revealed structures of the loops in G-protein–coupled Toni Voelker receptors by molecular modeling See companion article on page 12527 Gregory V. Nikiforovich, Christina M. Taylor, Garland R. Marshall, and Thomas J. Baranski E342 Reply to Nikiforovich et al.: Restoration of the loop regions of G-protein–coupled receptors Dahlia A. -
Cellular Responses to Erbb-2 Overexpression in Human Mammary Luminal Epithelial Cells: Comparison of Mrna and Protein Expression
British Journal of Cancer (2004) 90, 173 – 181 & 2004 Cancer Research UK All rights reserved 0007 – 0920/04 $25.00 www.bjcancer.com Cellular responses to ErbB-2 overexpression in human mammary luminal epithelial cells: comparison of mRNA and protein expression SL White1, S Gharbi1, MF Bertani1, H-L Chan1, MD Waterfield1 and JF Timms*,1 1 Ludwig Institute for Cancer Research, Wing 1.1, Cruciform Building, Gower Street, London WCIE 6BT, UK Microarray analysis offers a powerful tool for studying the mechanisms of cellular transformation, although the correlation between mRNA and protein expression is largely unknown. In this study, a microarray analysis was performed to compare transcription in response to overexpression of the ErbB-2 receptor tyrosine kinase in a model mammary luminal epithelial cell system, and in response to the ErbB-specific growth factor heregulin b1. We sought to validate mRNA changes by monitoring changes at the protein level using a parallel proteomics strategy, and report a surprisingly high correlation between transcription and translation for the subset of genes studied. We further characterised the identified targets and relate differential expression to changes in the biological properties of ErbB-2-overexpressing cells. We found differential regulation of several key cell cycle modulators, including cyclin D2, and downregulation of a large number of interferon-inducible genes, consistent with increased proliferation of the ErbB-2- overexpressing cells. Furthermore, differential expression of genes involved in extracellular matrix modelling and cellular adhesion was linked to altered adhesion of these cells. Finally, we provide evidence for enhanced autocrine activation of MAPK signalling and the AP-1 transcription complex. -
Multiple Facets of Jund Gene Expression Are Atypical Among AP-1 Family Members
Oncogene (2008) 27, 4757–4767 & 2008 Macmillan Publishers Limited All rights reserved 0950-9232/08 $30.00 www.nature.com/onc REVIEW Multiple facets of junD gene expression are atypical among AP-1 family members JM Hernandez1, DH Floyd2, KN Weilbaecher2, PL Green1,3 and K Boris-Lawrie1,3 1Department of Veterinary Biosciences and Center for Retrovirus Research, The Ohio State University, Columbus, OH, USA and 2Department of Medicine, Division of Molecular Oncology, Washington University School of Medicine, St Louis, MO, USA and 3Department of Medicine, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA JunD is a versatile AP-1 transcription factor that can 2003; Milde-Langosch, 2005). The AP-1 component activate or repress a diverse collection of target genes. proteins are characterized structurally by their leucine- Precise control of junD expression and JunD protein– zipper dimerization motif and basic DNA-binding protein interactions modulate tumor angiogenesis, cellular domain. They can either activate or repress transcription differentiation, proliferation and apoptosis. Molecular and this versatile functional activity is dependent on the and clinical knowledge of two decades has revealed specific components of the dimeric complex and the that precise JunD activity is elaborated by interrelated cellular environment (Eferl and Wagner, 2003; Hess layers of constitutive transcriptional control, complex et al., 2004). AP-1 figures prominently in transcriptional post-transcriptional regulation and a collection of regulation of early response genes (reviewed by Jochum post-translational modifications and protein–protein et al., 2001; Mechta-Grigoriou et al., 2001; Eferl and interactions. The stakes are high, as inappropriate JunD Wagner, 2003). -
Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model
Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 T + is online at: average * The Journal of Immunology , 34 of which you can access for free at: 2016; 197:1477-1488; Prepublished online 1 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600589 http://www.jimmunol.org/content/197/4/1477 Molecular Profile of Tumor-Specific CD8 Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. Waugh, Sonia M. Leach, Brandon L. Moore, Tullia C. Bruno, Jonathan D. Buhrman and Jill E. Slansky J Immunol cites 95 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2016/07/01/jimmunol.160058 9.DCSupplemental This article http://www.jimmunol.org/content/197/4/1477.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 25, 2021. The Journal of Immunology Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. -
Katalog 2015 Cover Paul Lin *Hinweis Förderung.Indd
Product List 2015 WE LIVE SERVICE Certificates quartett owns two productions sites that are certified according to EN ISO 9001:2008 Quality management systems - Requirements EN ISO 13485:2012 + AC:2012 Medical devices - Quality management systems - Requirements for regulatory purposes GMP Conformity Our quality management guarantees products of highest quality! 2 Foreword to the quartett product list 2015 quartett Immunodiagnostika, Biotechnologie + Kosmetik Vertriebs GmbH welcomes you as one of our new business partners as well as all of our previous loyal clients. You are now member of quartett´s worldwide customers. First of all we would like to introduce ourselves to you. Founded as a family-run company in 1986, quartett ensures for more than a quarter of a century consistent quality of products. Service and support of our valued customers are our daily businesses. And we will continue! In the end 80´s quartett offered radioimmunoassay and enzyme immunoassay kits from different manufacturers in the USA. In the beginning 90´s the company changed its strategy from offering products for routine diagnostic to the increasing field of research and development. Setting up a production plant in 1997 and a second one in 2011 supported this decision. The company specialized its product profile in the field of manufacturing synthetic peptides for antibody production, peptides such as protease inhibitors, biochemical reagents and products for histology, cytology and immunohistology. All products are exclusively manufactured in Germany without outsourcing any production step. Nowadays, we expand into all other diagnostic and research fields and supply our customers in universities, government institutes, pharmaceutical and biotechnological companies, hospitals, and private doctor offices. -
Table S1 the Four Gene Sets Derived from Gene Expression Profiles of Escs and Differentiated Cells
Table S1 The four gene sets derived from gene expression profiles of ESCs and differentiated cells Uniform High Uniform Low ES Up ES Down EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol 269261 Rpl12 11354 Abpa 68239 Krt42 15132 Hbb-bh1 67891 Rpl4 11537 Cfd 26380 Esrrb 15126 Hba-x 55949 Eef1b2 11698 Ambn 73703 Dppa2 15111 Hand2 18148 Npm1 11730 Ang3 67374 Jam2 65255 Asb4 67427 Rps20 11731 Ang2 22702 Zfp42 17292 Mesp1 15481 Hspa8 11807 Apoa2 58865 Tdh 19737 Rgs5 100041686 LOC100041686 11814 Apoc3 26388 Ifi202b 225518 Prdm6 11983 Atpif1 11945 Atp4b 11614 Nr0b1 20378 Frzb 19241 Tmsb4x 12007 Azgp1 76815 Calcoco2 12767 Cxcr4 20116 Rps8 12044 Bcl2a1a 219132 D14Ertd668e 103889 Hoxb2 20103 Rps5 12047 Bcl2a1d 381411 Gm1967 17701 Msx1 14694 Gnb2l1 12049 Bcl2l10 20899 Stra8 23796 Aplnr 19941 Rpl26 12096 Bglap1 78625 1700061G19Rik 12627 Cfc1 12070 Ngfrap1 12097 Bglap2 21816 Tgm1 12622 Cer1 19989 Rpl7 12267 C3ar1 67405 Nts 21385 Tbx2 19896 Rpl10a 12279 C9 435337 EG435337 56720 Tdo2 20044 Rps14 12391 Cav3 545913 Zscan4d 16869 Lhx1 19175 Psmb6 12409 Cbr2 244448 Triml1 22253 Unc5c 22627 Ywhae 12477 Ctla4 69134 2200001I15Rik 14174 Fgf3 19951 Rpl32 12523 Cd84 66065 Hsd17b14 16542 Kdr 66152 1110020P15Rik 12524 Cd86 81879 Tcfcp2l1 15122 Hba-a1 66489 Rpl35 12640 Cga 17907 Mylpf 15414 Hoxb6 15519 Hsp90aa1 12642 Ch25h 26424 Nr5a2 210530 Leprel1 66483 Rpl36al 12655 Chi3l3 83560 Tex14 12338 Capn6 27370 Rps26 12796 Camp 17450 Morc1 20671 Sox17 66576 Uqcrh 12869 Cox8b 79455 Pdcl2 20613 Snai1 22154 Tubb5 12959 Cryba4 231821 Centa1 17897 -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Developing Biomarkers for Livestock Science
Developing biomarkers for livestock Science Ongoing research and future developments Marinus te Pas Outline . Introduction ● What are biomarkers ● Why do we need them . Examples ● omics levels . The future ● Big data ● Systems biology / Synthetic biology 2 Introduction: What are biomarkers? . Biological processes underlie all livestock (production) traits ● Measure the status of a biological process = know the trait! . Can be any molecule in a cell ● No need to know the causal factor for a trait . Well known example: blood glucose level for diabetes Introduction: Why do we need biomarkers? . The mission of WageningenUR: Sustainably produce enough high quality food for all people on the planet with an ecological footprint as low as possible 4 What can the industry do with biomarkers? . Diagnostic tool ● What is the biological mechanism underlying a trait? . Prediction tool ● What outcome can I expect from an intervention? . Monitoring tool ● What is the actual status of a process? . Speed up your process, improve your traits Some examples * Transcriptomics * Proteomics * Metabolomics Why Biomarkers for meat quality? . Meat quality has low heritability (h2=0.1-0.2) ● Predictive capacity of genetic markers low . High environmental influence ● Feed, animal handling (stress), management (housing), ... Meat quality can only be measured after 1-several days post slaughter . Need to differentiate between retail, processing industry, restaurants, .... Biomarkers can do all that and more faster, predictive, .. Example Transcriptomics biomarkers for meat quality . Pork production chain . Biomarkers for traits . High quality fresh pork . Meat colour N production chain ● A* 14 . German Pietrain ● L* 4 (microarray) ● Reflection 10 . Verification: Danish . Drip loss 2 Yorkshire (PCR) . Ultimate pH 6 . -
Primary Driver Mutations in GTF2I Specific to the Development Of
cancers Article Primary Driver Mutations in GTF2I Specific to the Development of Thymomas Rumi Higuchi 1, Taichiro Goto 1,* , Yosuke Hirotsu 2 , Yujiro Yokoyama 1, Takahiro Nakagomi 1, Sotaro Otake 1, Kenji Amemiya 2,3, Toshio Oyama 3, Hitoshi Mochizuki 2 and Masao Omata 2,4 1 Lung Cancer and Respiratory Disease Center, Yamanashi Central Hospital, Yamanashi 400-8506, Japan; [email protected] (R.H.); [email protected] (Y.Y.); [email protected] (T.N.); [email protected] (S.O.) 2 Genome Analysis Center, Yamanashi Central Hospital, Yamanashi 400-8506, Japan; [email protected] (Y.H.); [email protected] (K.A.); [email protected] (H.M.); [email protected] (M.O.) 3 Department of Pathology, Yamanashi Central Hospital, Yamanashi 400-8506, Japan; [email protected] 4 Department of Gastroenterology, The University of Tokyo Hospital, Tokyo 113-8655, Japan * Correspondence: [email protected]; Tel.: +81-55-253-7111 Received: 16 June 2020; Accepted: 22 July 2020; Published: 24 July 2020 Abstract: Thymomas are rare mediastinal tumors that are difficult to treat and pose a major public health concern. Identifying mutations in target genes is vital for the development of novel therapeutic strategies. Type A thymomas possess a missense mutation in GTF2I (chromosome 7 c.74146970T>A) with high frequency. However, the molecular pathways underlying the tumorigenesis of other thymomas remain to be elucidated. We aimed to detect this missense mutation in GTF2I in other thymoma subtypes (types B). This study involved 22 patients who underwent surgery for thymomas between January 2014 and August 2019. -
Datasheet BA3564-2 Anti-FES Antibody
Product datasheet Anti-FES Antibody Catalog Number: BA3564-2 BOSTER BIOLOGICAL TECHNOLOGY Special NO.1, International Enterprise Center, 2nd Guanshan Road, Wuhan, China Web: www.boster.com.cn Phone: +86 27 67845390 Fax: +86 27 67845390 Email: [email protected] Basic Information Product Name Anti-FES Antibody Gene Name FES Source Rabbit IgG Species Reactivity human,mouse,rat Tested Application WB Contents 500ug/ml antibody with PBS ,0.02% NaN3 , 1mg BSA and 50% glycerol. Immunogen A synthetic peptide corresponding to a sequence at the C-terminus of human FES(808-822aa STIYQELQSIRKRHR). Purification Immunogen affinity purified. Observed MW Dilution Ratios Western blot: 1:500-2000 Storage 12 months from date of receipt,-20℃ as supplied.6 months 2 to 8℃ after reconstitution. Avoid repeated freezing and thawing Background Information FES(feline sarcoma oncogene) is an enzyme that in humans is encoded by the FES gene, also known as Proto-oncogene tyrosine-protein kinase Fes/Fps, Feline sarcoma/Fujinami avian sarcoma oncogene homolog, Proto-oncogene c-Fes, Proto-oncogene c-Fps, p93c-fes c-fes/fps protein, FPS, Oncogene FES, feline sarcoma virus, FPS. This gene encodes the human cellular counterpart of a feline sarcoma retrovirus protein with transforming capabilities. Non-onc intervening sequences were present in the human counterpart. The gene product has tyrosine-specific protein kinase activity and that activity is required for maintenance of°Cellular transformation. Its chromosomal location has linked it to a specific translocation event identified in patients with acute promyelocytic leukemia, but it is also involved in normal hematopoiesis. A truncated transcript has been identified that is generated utilizing a start site in one of the far downstream exons but a protein product associated with this transcript has not been identified. -
Supplementary Table 1
SI Table S1. Broad protein kinase selectivity for PF-2771. Kinase, PF-2771 % Inhibition at 10 μM Service Kinase, PF-2771 % Inhibition at 1 μM Service rat RPS6KA1 (RSK1) 39 Dundee AURKA (AURA) 24 Invitrogen IKBKB (IKKb) 26 Dundee CDK2 /CyclinA 21 Invitrogen mouse LCK 25 Dundee rabbit MAP2K1 (MEK1) 19 Dundee AKT1 (AKT) 21 Dundee IKBKB (IKKb) 16 Dundee CAMK1 (CaMK1a) 19 Dundee PKN2 (PRK2) 14 Dundee RPS6KA5 (MSK1) 18 Dundee MAPKAPK5 14 Dundee PRKD1 (PKD1) 13 Dundee PIM3 12 Dundee MKNK2 (MNK2) 12 Dundee PRKD1 (PKD1) 12 Dundee MARK3 10 Dundee NTRK1 (TRKA) 12 Invitrogen SRPK1 9 Dundee MAPK12 (p38g) 11 Dundee MAPKAPK5 9 Dundee MAPK8 (JNK1a) 11 Dundee MAPK13 (p38d) 8 Dundee rat PRKAA2 (AMPKa2) 11 Dundee AURKB (AURB) 5 Dundee NEK2 11 Invitrogen CSK 5 Dundee CHEK2 (CHK2) 11 Invitrogen EEF2K (EEF-2 kinase) 4 Dundee MAPK9 (JNK2) 9 Dundee PRKCA (PKCa) 4 Dundee rat RPS6KA1 (RSK1) 8 Dundee rat PRKAA2 (AMPKa2) 4 Dundee DYRK2 7 Dundee rat CSNK1D (CKId) 3 Dundee AKT1 (AKT) 7 Dundee LYN 3 BioPrint PIM2 7 Invitrogen CSNK2A1 (CKIIa) 3 Dundee MAPK15 (ERK7) 6 Dundee CAMKK2 (CAMKKB) 1 Dundee mouse LCK 5 Dundee PIM3 1 Dundee PDPK1 (PDK1) (directed 5 Invitrogen rat DYRK1A (MNB) 1 Dundee RPS6KB1 (p70S6K) 5 Dundee PBK 0 Dundee CSNK2A1 (CKIIa) 4 Dundee PIM1 -1 Dundee CAMKK2 (CAMKKB) 4 Dundee DYRK2 -2 Dundee SRC 4 Invitrogen MAPK12 (p38g) -2 Dundee MYLK2 (MLCK_sk) 3 Invitrogen NEK6 -3 Dundee MKNK2 (MNK2) 2 Dundee RPS6KB1 (p70S6K) -3 Dundee SRPK1 2 Dundee AKT2 -3 Dundee MKNK1 (MNK1) 2 Dundee RPS6KA3 (RSK2) -3 Dundee CHEK1 (CHK1) 2 Invitrogen rabbit MAP2K1 (MEK1) -4 Dundee