Genetic Algorithm to Detect Different Sizes' Communities from Protein
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Polyclonal Antibody to APC11 / ANAPC11 - Serum
OriGene Technologies, Inc. OriGene Technologies GmbH 9620 Medical Center Drive, Ste 200 Schillerstr. 5 Rockville, MD 20850 32052 Herford UNITED STATES GERMANY Phone: +1-888-267-4436 Phone: +49-5221-34606-0 Fax: +1-301-340-8606 Fax: +49-5221-34606-11 [email protected] [email protected] R1503 Polyclonal Antibody to APC11 / ANAPC11 - Serum Alternate names: Anaphase-promoting complex subunit 11, Cyclosome subunit 11, HSPC214, Hepatocellular carcinoma-associated RING finger protein Quantity: 0.1 ml Concentration: 85 mg/ml (by Refractometry) Background: APC11 is also known as Anaphase promoting complex subunit 11, APC11, Cyclosome subunit 11, Hepatocellular carcinoma associated RING finger protein, and HSPC214. APC11 is a component of the anaphase promoting complex/cyclosome (APC/C), a cell cycle-regulated E3 ubiquitin ligase that controls progression through mitosis and the G1 phase of the cell cycle. APC11 may function to recruit the E2 ubiquitin-conjugating enzymes to the complex. APC11 interacts with the cullin domain of ANAPC2 and also interacts with UBE2D2. APC11 shows both a cytoplasmic and nuclear localization. APC11 is expressed at high levels in skeletal muscle and heart; in moderate levels in brain, kidney, and liver; and at low levels in colon, thymus, spleen, small intestine, placenta, lung and peripheral blood leukocyte. APC11 is a member of the RING-type zinc finger family and is auto-ubiquitinylated. Uniprot ID: Q9NYG5 NCBI: NP_001002244.1 GeneID: 51529 Host: Rabbit Immunogen: This APC11 antibody was prepared from whole rabbit serum produced by repeated immunizations with a synthetic peptide corresponding to amino acids 76-84 of Human APC11 (C-terminal) coupled to KLH. -
A New Genetic Method for Isolating Functionally Interacting Genes
Copyright 2000 by the Genetics Society of America A New Genetic Method for Isolating Functionally Interacting Genes: High plo1؉-Dependent Mutants and Their Suppressors De®ne Genes in Mitotic and Septation Pathways in Fission Yeast C. Fiona Cullen,*,² Karen M. May,* Iain M. Hagan,³ David M. Glover²,§ and Hiroyuki Ohkura*,² *Institute of Cell and Molecular Biology, The University of Edinburgh, Edinburgh EH9 3JR, United Kingdom, ²Department of Anatomy and Physiology, Medical Sciences Institute, The University of Dundee, Dundee DD1 4HN, United Kingdom, ³School of Biological Sciences, The University of Manchester, Manchester M13 9PT, United Kingdom and §Department of Genetics, University of Cambridge, Cambridge CB2 3EH, United Kingdom Manuscript received February 2, 2000 Accepted for publication April 10, 2000 ABSTRACT We describe a general genetic method to identify genes encoding proteins that functionally interact with and/or are good candidates for downstream targets of a particular gene product. The screen identi®es mutants whose growth depends on high levels of expression of that gene. We apply this to the plo1ϩ gene that encodes a ®ssion yeast homologue of the polo-like kinases. plo1ϩ regulates both spindle formation and septation. We have isolated 17 high plo1ϩ-dependent (pld) mutants that show defects in mitosis or septation. Three mutants show a mitotic arrest phenotype. Among the 14 pld mutants with septation defects, 12 mapped to known loci: cdc7, cdc15, cdc11 spg1, and sid2. One of the pld mutants, cdc7-PD1, was selected for suppressor analysis. As multicopy suppressors, we isolated four known genes involved in septation in ®ssion yeast: spg1ϩ, sce3ϩ, cdc8ϩ, and rho1ϩ, and two previously uncharacterized genes, mpd1ϩ and mpd2ϩ. -
Analysis of Gene Expression Data for Gene Ontology
ANALYSIS OF GENE EXPRESSION DATA FOR GENE ONTOLOGY BASED PROTEIN FUNCTION PREDICTION A Thesis Presented to The Graduate Faculty of The University of Akron In Partial Fulfillment of the Requirements for the Degree Master of Science Robert Daniel Macholan May 2011 ANALYSIS OF GENE EXPRESSION DATA FOR GENE ONTOLOGY BASED PROTEIN FUNCTION PREDICTION Robert Daniel Macholan Thesis Approved: Accepted: _______________________________ _______________________________ Advisor Department Chair Dr. Zhong-Hui Duan Dr. Chien-Chung Chan _______________________________ _______________________________ Committee Member Dean of the College Dr. Chien-Chung Chan Dr. Chand K. Midha _______________________________ _______________________________ Committee Member Dean of the Graduate School Dr. Yingcai Xiao Dr. George R. Newkome _______________________________ Date ii ABSTRACT A tremendous increase in genomic data has encouraged biologists to turn to bioinformatics in order to assist in its interpretation and processing. One of the present challenges that need to be overcome in order to understand this data more completely is the development of a reliable method to accurately predict the function of a protein from its genomic information. This study focuses on developing an effective algorithm for protein function prediction. The algorithm is based on proteins that have similar expression patterns. The similarity of the expression data is determined using a novel measure, the slope matrix. The slope matrix introduces a normalized method for the comparison of expression levels throughout a proteome. The algorithm is tested using real microarray gene expression data. Their functions are characterized using gene ontology annotations. The results of the case study indicate the protein function prediction algorithm developed is comparable to the prediction algorithms that are based on the annotations of homologous proteins. -
New Approaches to Functional Process Discovery in HPV 16-Associated Cervical Cancer Cells by Gene Ontology
Cancer Research and Treatment 2003;35(4):304-313 New Approaches to Functional Process Discovery in HPV 16-Associated Cervical Cancer Cells by Gene Ontology Yong-Wan Kim, Ph.D.1, Min-Je Suh, M.S.1, Jin-Sik Bae, M.S.1, Su Mi Bae, M.S.1, Joo Hee Yoon, M.D.2, Soo Young Hur, M.D.2, Jae Hoon Kim, M.D.2, Duck Young Ro, M.D.2, Joon Mo Lee, M.D.2, Sung Eun Namkoong, M.D.2, Chong Kook Kim, Ph.D.3 and Woong Shick Ahn, M.D.2 1Catholic Research Institutes of Medical Science, 2Department of Obstetrics and Gynecology, College of Medicine, The Catholic University of Korea, Seoul; 3College of Pharmacy, Seoul National University, Seoul, Korea Purpose: This study utilized both mRNA differential significant genes of unknown function affected by the display and the Gene Ontology (GO) analysis to char- HPV-16-derived pathway. The GO analysis suggested that acterize the multiple interactions of a number of genes the cervical cancer cells underwent repression of the with gene expression profiles involved in the HPV-16- cancer-specific cell adhesive properties. Also, genes induced cervical carcinogenesis. belonging to DNA metabolism, such as DNA repair and Materials and Methods: mRNA differential displays, replication, were strongly down-regulated, whereas sig- with HPV-16 positive cervical cancer cell line (SiHa), and nificant increases were shown in the protein degradation normal human keratinocyte cell line (HaCaT) as a con- and synthesis. trol, were used. Each human gene has several biological Conclusion: The GO analysis can overcome the com- functions in the Gene Ontology; therefore, several func- plexity of the gene expression profile of the HPV-16- tions of each gene were chosen to establish a powerful associated pathway, identify several cancer-specific cel- cervical carcinogenesis pathway. -
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Supplementary Figure S1. Results of flow cytometry analysis, performed to estimate CD34 positivity, after immunomagnetic separation in two different experiments. As monoclonal antibody for labeling the sample, the fluorescein isothiocyanate (FITC)- conjugated mouse anti-human CD34 MoAb (Mylteni) was used. Briefly, cell samples were incubated in the presence of the indicated MoAbs, at the proper dilution, in PBS containing 5% FCS and 1% Fc receptor (FcR) blocking reagent (Miltenyi) for 30 min at 4 C. Cells were then washed twice, resuspended with PBS and analyzed by a Coulter Epics XL (Coulter Electronics Inc., Hialeah, FL, USA) flow cytometer. only use Non-commercial 1 Supplementary Table S1. Complete list of the datasets used in this study and their sources. GEO Total samples Geo selected GEO accession of used Platform Reference series in series samples samples GSM142565 GSM142566 GSM142567 GSM142568 GSE6146 HG-U133A 14 8 - GSM142569 GSM142571 GSM142572 GSM142574 GSM51391 GSM51392 GSE2666 HG-U133A 36 4 1 GSM51393 GSM51394 only GSM321583 GSE12803 HG-U133A 20 3 GSM321584 2 GSM321585 use Promyelocytes_1 Promyelocytes_2 Promyelocytes_3 Promyelocytes_4 HG-U133A 8 8 3 GSE64282 Promyelocytes_5 Promyelocytes_6 Promyelocytes_7 Promyelocytes_8 Non-commercial 2 Supplementary Table S2. Chromosomal regions up-regulated in CD34+ samples as identified by the LAP procedure with the two-class statistics coded in the PREDA R package and an FDR threshold of 0.5. Functional enrichment analysis has been performed using DAVID (http://david.abcc.ncifcrf.gov/) -
Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Science (Cancer Biology) Aneuploidy: Using genetic instability to preserve a haploid genome? Submitted by: Ramona Ramdath In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Science Examination Committee Signature/Date Major Advisor: David Allison, M.D., Ph.D. Academic James Trempe, Ph.D. Advisory Committee: David Giovanucci, Ph.D. Randall Ruch, Ph.D. Ronald Mellgren, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: April 10, 2009 Aneuploidy: Using genetic instability to preserve a haploid genome? Ramona Ramdath University of Toledo, Health Science Campus 2009 Dedication I dedicate this dissertation to my grandfather who died of lung cancer two years ago, but who always instilled in us the value and importance of education. And to my mom and sister, both of whom have been pillars of support and stimulating conversations. To my sister, Rehanna, especially- I hope this inspires you to achieve all that you want to in life, academically and otherwise. ii Acknowledgements As we go through these academic journeys, there are so many along the way that make an impact not only on our work, but on our lives as well, and I would like to say a heartfelt thank you to all of those people: My Committee members- Dr. James Trempe, Dr. David Giovanucchi, Dr. Ronald Mellgren and Dr. Randall Ruch for their guidance, suggestions, support and confidence in me. My major advisor- Dr. David Allison, for his constructive criticism and positive reinforcement. -
APC/C Is Essential for Hematopoiesis and Impaired in Aplastic Anemia
www.impactjournals.com/oncotarget/ Oncotarget, 2017, Vol. 8, (No. 38), pp: 63360-63369 Research Paper APC/C is essential for hematopoiesis and impaired in aplastic anemia Jia Wang1,*, Min-Zhi Yin2,*, Ke-Wen Zhao1,*, Fang Ke1,*, Wen-Jie Jin3, Xiao-Lin Guo1, Tian-Hui Liu1, Xiao-Ye Liu1, Hao Gu1, Xiao-Min Yu1, Zhen Li1, Li-Li Mu1, Deng-Li Hong1, Jing Chen4 and Guo-Qiang Chen1 1Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, 200025, China 2Department of Pathology, Shanghai Children’s Medical Center, SJTU-SM, Shanghai, 200025, China 3Department of Orthopaedics, Shanghai Ninth People's Hospital, SJTU-SM, Shanghai, 200025, China 4Key Laboratory of Pediatric Hematology and Oncology Ministry of Health, Department of Hematology and Oncology, Shanghai Children’s Medical Center, SJTU-SM, Shanghai, 200127, China *These authors have contributed equally to this work Correspondence to: Guo-Qiang Chen, email: [email protected] Jing Chen, email: [email protected] Deng-Li Hong, email: [email protected] Keywords: anaphase promoting complex/cyclosome (APC/C), Anapc2, hematopoietic stem and progenitor cells (HSPCs), dormant HPSCs, aplastic anemia Received: November 22, 2016 Accepted: June 02, 2017 Published: June 28, 2017 Copyright: Wang 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 Anaphase promoting complex/cyclosome (APC/C) is essential for cell cycle progression. -
A 20S Complex Containing CDC27 and CDC16 Catalyzes the Mitosis-Specific Conjugation of Ubiquitin to Cyclin B
Cell, Vol. 81,279-288, April 21, 1995, Copyright© 1995 by Cell Press A 20S Complex Containing CDC27 and CDC16 Catalyzes the Mitosis-Specific Conjugation of Ubiquitin to Cyclin B Randall W. King,*t Jan-Michael Peters,*t cyclin degradation is required to exit mitosis (Surana et Stuart Tugendreich,$ Mark Rolfe,§ Philip Hieter,$ al., 1993; Holloway et al., 1993). Treatments that interfere and Marc W. Kirschnert with the proteolysis of endogenous cyclin B, however, ar- tDepartment of Cell Biology rest cell division earlier, at anaphase (Holloway et al., Harvard Medical School 1993). This discrepancy can be explained by hypothesiz- Boston, Massachusetts 02115 ing that chromosome segregation and cyclin proteolysis $Department of Molecular Biology and Genetics depend upon common components. Support for this idea Johns Hopkins School of Medicine has emerged recently from studies in budding yeast, in Baltimore, Maryland 21205 which CDC16 and CDC23, genes required for progression §Mitotix, Incorporated through anaphase, have been shown to be required for One Kendall Square the proteolysis of B-type cyclins (Irniger et al., 1995 [this Cambridge, Massachusetts 02139 issue of Cell]). The proteins encoded by these genes form a complex with the CDC27 protein (Lamb et al., 1994), a homolog of which is also required for anaphase progres- Summary sion in mammalian cells (Tugendreich et al., 1995 [this issue of Cell]). Cyclin B is degraded at the onset of anaphase by a Biochemical evidence suggests that cyclin proteolysis ubiquitin-dependent proteolytic system. We have frac- is mediated by the ubiquitin pathway: cyclin B-ubiquitin tionated mitotic Xenopus egg extracts to identify com- conjugates can be observed in mitotic, but not interphase, ponents required for this process. -
The Genome of Schmidtea Mediterranea and the Evolution Of
OPEN ArtICLE doi:10.1038/nature25473 The genome of Schmidtea mediterranea and the evolution of core cellular mechanisms Markus Alexander Grohme1*, Siegfried Schloissnig2*, Andrei Rozanski1, Martin Pippel2, George Robert Young3, Sylke Winkler1, Holger Brandl1, Ian Henry1, Andreas Dahl4, Sean Powell2, Michael Hiller1,5, Eugene Myers1 & Jochen Christian Rink1 The planarian Schmidtea mediterranea is an important model for stem cell research and regeneration, but adequate genome resources for this species have been lacking. Here we report a highly contiguous genome assembly of S. mediterranea, using long-read sequencing and a de novo assembler (MARVEL) enhanced for low-complexity reads. The S. mediterranea genome is highly polymorphic and repetitive, and harbours a novel class of giant retroelements. Furthermore, the genome assembly lacks a number of highly conserved genes, including critical components of the mitotic spindle assembly checkpoint, but planarians maintain checkpoint function. Our genome assembly provides a key model system resource that will be useful for studying regeneration and the evolutionary plasticity of core cell biological mechanisms. Rapid regeneration from tiny pieces of tissue makes planarians a prime De novo long read assembly of the planarian genome model system for regeneration. Abundant adult pluripotent stem cells, In preparation for genome sequencing, we inbred the sexual strain termed neoblasts, power regeneration and the continuous turnover of S. mediterranea (Fig. 1a) for more than 17 successive sib- mating of all cell types1–3, and transplantation of a single neoblast can rescue generations in the hope of decreasing heterozygosity. We also developed a lethally irradiated animal4. Planarians therefore also constitute a a new DNA isolation protocol that meets the purity and high molecular prime model system for stem cell pluripotency and its evolutionary weight requirements of PacBio long-read sequencing12 (Extended Data underpinnings5. -
Table S2.Up Or Down Regulated Genes in Tcof1 Knockdown Neuroblastoma N1E-115 Cells Involved in Differentbiological Process Anal
Table S2.Up or down regulated genes in Tcof1 knockdown neuroblastoma N1E-115 cells involved in differentbiological process analysed by DAVID database Pop Pop Fold Term PValue Genes Bonferroni Benjamini FDR Hits Total Enrichment GO:0044257~cellular protein catabolic 2.77E-10 MKRN1, PPP2R5C, VPRBP, MYLIP, CDC16, ERLEC1, MKRN2, CUL3, 537 13588 1.944851 8.64E-07 8.64E-07 5.02E-07 process ISG15, ATG7, PSENEN, LOC100046898, CDCA3, ANAPC1, ANAPC2, ANAPC5, SOCS3, ENC1, SOCS4, ASB8, DCUN1D1, PSMA6, SIAH1A, TRIM32, RNF138, GM12396, RNF20, USP17L5, FBXO11, RAD23B, NEDD8, UBE2V2, RFFL, CDC GO:0051603~proteolysis involved in 4.52E-10 MKRN1, PPP2R5C, VPRBP, MYLIP, CDC16, ERLEC1, MKRN2, CUL3, 534 13588 1.93519 1.41E-06 7.04E-07 8.18E-07 cellular protein catabolic process ISG15, ATG7, PSENEN, LOC100046898, CDCA3, ANAPC1, ANAPC2, ANAPC5, SOCS3, ENC1, SOCS4, ASB8, DCUN1D1, PSMA6, SIAH1A, TRIM32, RNF138, GM12396, RNF20, USP17L5, FBXO11, RAD23B, NEDD8, UBE2V2, RFFL, CDC GO:0044265~cellular macromolecule 6.09E-10 MKRN1, PPP2R5C, VPRBP, MYLIP, CDC16, ERLEC1, MKRN2, CUL3, 609 13588 1.859332 1.90E-06 6.32E-07 1.10E-06 catabolic process ISG15, RBM8A, ATG7, LOC100046898, PSENEN, CDCA3, ANAPC1, ANAPC2, ANAPC5, SOCS3, ENC1, SOCS4, ASB8, DCUN1D1, PSMA6, SIAH1A, TRIM32, RNF138, GM12396, RNF20, XRN2, USP17L5, FBXO11, RAD23B, UBE2V2, NED GO:0030163~protein catabolic process 1.81E-09 MKRN1, PPP2R5C, VPRBP, MYLIP, CDC16, ERLEC1, MKRN2, CUL3, 556 13588 1.87839 5.64E-06 1.41E-06 3.27E-06 ISG15, ATG7, PSENEN, LOC100046898, CDCA3, ANAPC1, ANAPC2, ANAPC5, SOCS3, ENC1, SOCS4, -
The Genetics of Bipolar Disorder
Molecular Psychiatry (2008) 13, 742–771 & 2008 Nature Publishing Group All rights reserved 1359-4184/08 $30.00 www.nature.com/mp FEATURE REVIEW The genetics of bipolar disorder: genome ‘hot regions,’ genes, new potential candidates and future directions A Serretti and L Mandelli Institute of Psychiatry, University of Bologna, Bologna, Italy Bipolar disorder (BP) is a complex disorder caused by a number of liability genes interacting with the environment. In recent years, a large number of linkage and association studies have been conducted producing an extremely large number of findings often not replicated or partially replicated. Further, results from linkage and association studies are not always easily comparable. Unfortunately, at present a comprehensive coverage of available evidence is still lacking. In the present paper, we summarized results obtained from both linkage and association studies in BP. Further, we indicated new potential interesting genes, located in genome ‘hot regions’ for BP and being expressed in the brain. We reviewed published studies on the subject till December 2007. We precisely localized regions where positive linkage has been found, by the NCBI Map viewer (http://www.ncbi.nlm.nih.gov/mapview/); further, we identified genes located in interesting areas and expressed in the brain, by the Entrez gene, Unigene databases (http://www.ncbi.nlm.nih.gov/entrez/) and Human Protein Reference Database (http://www.hprd.org); these genes could be of interest in future investigations. The review of association studies gave interesting results, as a number of genes seem to be definitively involved in BP, such as SLC6A4, TPH2, DRD4, SLC6A3, DAOA, DTNBP1, NRG1, DISC1 and BDNF. -
Chapter 4.1 a 400 Kb Duplication, 2.4 Mb Triplication and 130 Kb
High-resolution karyotyping by oligonucleotide microarrays : the next revolution in cytogenetics Gijsbers, A.C.J. Citation Gijsbers, A. C. J. (2010, November 30). High-resolution karyotyping by oligonucleotide microarrays : the next revolution in cytogenetics. Retrieved from https://hdl.handle.net/1887/16187 Version: Corrected Publisher’s Version Licence agreement concerning inclusion of doctoral thesis in the License: Institutional Repository of the University of Leiden Downloaded from: https://hdl.handle.net/1887/16187 Note: To cite this publication please use the final published version (if applicable). Chapter 4.1 A 400 kb duplication, 2.4 Mb triplication and 130 kb duplication of 9q34.3 in a patient with severe mental retardation Antoinet CJ Gijsbers, Emilia K Bijlsma, Marjan M Weiss, Egbert Bakker, Martijn H Breuning, Mariëtte JV Hoffer and Claudia AL Ruivenkamp Center for Human and Clinical Genetics; Leiden University Medical Center (LUMC), Leiden, The Netherlands Eur J Med Genet 2008;51:479-487 Chapter 4 Abstract The presence of a duplication as well as a triplication in one chromosome is a rare rearrangement and not easy to distinguish with routine chromosomal analysis. Recent developments in array technologies, however, not only allow screening of the whole genome at a higher resolution, but also make it possible to characterize complex chromosomal rearrangements in more detail. Here we report a molecular cytogenetic analysis of a 16-year old female with severe mental retardation and an abnormality on the end of the long arm of chromosome 9. Subtelomeric multiplex ligation-dependent probe amplification (MLPA) analysis revealed that the extra material originated from the telomeric end of chromosome 9q.