Recombinant Human CDK5 Protein Catalog Number: ATGP1835

Total Page：16

File Type：pdf, Size：1020Kb

Recombinant human CDK5 protein Catalog Number: ATGP1835 PRODUCT INPORMATION Expression system E.coli Domain 1-292aa UniProt No. Q00535 NCBI Accession No. NP_004926 Alternative Names Cyclin-dependent kinase 5, PSSALRE PRODUCT SPECIFICATION Molecular Weight 35.8 kDa (316aa) Concentration 0.5mg/ml (determined by Bradford assay) Formulation Liquid in. 20mM Tris-HCl buffer (pH 8.0) containing 10% glycerol 0.4M urea Purity > 85% by SDS-PAGE Tag His-Tag Application SDS-PAGE,Denatured Storage Condition Can be stored at +2C to +8C for 1 week. For long term storage, aliquot and store at -20C to -80C. Avoid repeated freezing and thawing cycles. BACKGROUND Description CDK5, also known as cell division protein kinase 5, is a member of the cyclin-dependent kinase family. It is required for proper development of the brain and to be activated, CDK5 must associate with CDK5R1 or CDK5R2. unlike other cyclin dependent kinases, it does not also require phosphorylation on the T loop so that binding with the activator is sufficient to activate the kinase. This protein is involved in the processes of neuronal maturation and migration, phosphorylating the key intracellular adaptor of the reelin signaling chain. Recombinant human CDK5 protein, fused to His-tag at N-terminus, was expressed in E. coli. 1 Recombinant human CDK5 protein Catalog Number: ATGP1835 Amino acid Sequence MGSSHHHHHH SSGLVPRGSH MGSHMQKYEK LEKIGEGTYG TVFKAKNRET HEIVALKRVR LDDDDEGVPS SALREICLLK ELKHKNIVRL HDVLHSDKKL TLVFEFCDQD LKKYFDSCNG DLDPEIVKSF LFQLLKGLGF CHSRNVLHRD LKPQNLLINR NGELKLADFG LARAFGIPVR CYSAEVVTLW YRPPDVLFGA KLYSTSIDMW SAGCIFAELA NAGRPLFPGN DVDDQLKRIF RLLGTPTEEQ WPSMTKLPDY KPYPMYPATT SLVNVVPKLN ATGRDLLQNL LKCNPVQRIS AEEALQHPYF SDFCPP General References Demetrick DJ. et al. (1994) Cytogenet Cell Genet. 66:72-74. Meyerson M. et al. (1992) EMBO J. 11:2909-2917. DATA SDS-PAGE 3ug by SDS-PAGE under reducing condition and visualized by coomassie blue stain. 2.

Copy Link

Recommended publications

Cytotoxic Effects and Changes in Gene Expression Profile
Toxicology in Vitro 34 (2016) 309–320 Contents lists available at ScienceDirect Toxicology in Vitro journal homepage: www.elsevier.com/locate/toxinvit Fusarium mycotoxin enniatin B: Cytotoxic effects and changes in gene expression proﬁle Martina Jonsson a,⁎,MarikaJestoib, Minna Anthoni a, Annikki Welling a, Iida Loivamaa a, Ville Hallikainen c, Matti Kankainen d, Erik Lysøe e, Pertti Koivisto a, Kimmo Peltonen a,f a Chemistry and Toxicology Research Unit, Finnish Food Safety Authority (Evira), Mustialankatu 3, FI-00790 Helsinki, Finland b Product Safety Unit, Finnish Food Safety Authority (Evira), Mustialankatu 3, FI-00790 Helsinki, c The Finnish Forest Research Institute, Rovaniemi Unit, P.O. Box 16, FI-96301 Rovaniemi, Finland d Institute for Molecular Medicine Finland (FIMM), University of Helsinki, P.O. Box 20, FI-00014, Finland e Plant Health and Biotechnology, Norwegian Institute of Bioeconomy, Høyskoleveien 7, NO -1430 Ås, Norway f Finnish Safety and Chemicals Agency (Tukes), Opastinsilta 12 B, FI-00521 Helsinki, Finland article info abstract Article history: The mycotoxin enniatin B, a cyclic hexadepsipeptide produced by the plant pathogen Fusarium,isprevalentin Received 3 December 2015 grains and grain-based products in different geographical areas. Although enniatins have not been associated Received in revised form 5 April 2016 with toxic outbreaks, they have caused toxicity in vitro in several cell lines. In this study, the cytotoxic effects Accepted 28 April 2016 of enniatin B were assessed in relation to cellular energy metabolism, cell proliferation, and the induction of ap- Available online 6 May 2016 optosis in Balb 3T3 and HepG2 cells. The mechanism of toxicity was examined by means of whole genome ex- ﬁ Keywords: pression pro ling of exposed rat primary hepatocytes.
[Show full text]
Breed Relationships Facilitate Fine-Mapping Studies: a 7.8-Kb Deletion Cosegregates with Collie Eye Anomaly Across Multiple Dog Breeds
Downloaded from genome.cshlp.org on October 4, 2021 - Published by Cold Spring Harbor Laboratory Press Article Breed relationships facilitate fine-mapping studies: A 7.8-kb deletion cosegregates with Collie eye anomaly across multiple dog breeds Heidi G. Parker,1 Anna V. Kukekova,2 Dayna T. Akey,3 Orly Goldstein,2 Ewen F. Kirkness,4 Kathleen C. Baysac,1 Dana S. Mosher,1 Gustavo D. Aguirre,5 Gregory M. Acland,2 and Elaine A. Ostrander1,6 1Cancer Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA; 2Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853, USA; 3Department of Genome Sciences, School of Medicine, University of Washington, Seattle, Washington 98195, USA; 4The Institute for Genomic Research, Rockville, Maryland 20850, USA; 5Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA The features of modern dog breeds that increase the ease of mapping common diseases, such as reduced heterogeneity and extensive linkage disequilibrium, may also increase the difficulty associated with fine mapping and identifying causative mutations. One way to address this problem is by combining data from multiple breeds segregating the same trait after initial linkage has been determined. The multibreed approach increases the number of potentially informative recombination events and reduces the size of the critical haplotype by taking advantage of shortened linkage disequilibrium distances found across breeds. In order to identify breeds that likely share a trait inherited from the same ancestral source, we have used cluster analysis to divide 132 breeds of dog into five primary breed groups.
[Show full text]
CDK5 Functions As a Tumor Promoter in Human Lung Cancer Jie Zeng1#, Shuanshuan Xie1#, Yang Liu1, Changxing Shen1, Xiaolian Song1, Guo-Lei Zhou2, 3, Changhui Wang1
Journal of Cancer 2018, Vol. 9 3950 Ivyspring International Publisher Journal of Cancer 2018; 9(21): 3950-3961. doi: 10.7150/jca.25967 Research Paper CDK5 Functions as a Tumor Promoter in Human Lung Cancer Jie Zeng1#, Shuanshuan Xie1#, Yang Liu1, Changxing Shen1, Xiaolian Song1, Guo-Lei Zhou2, 3, Changhui Wang1 1. Department of Respiratory Medicine, Shanghai Tenth People’s Hospital, Tongji University, Shanghai 200072, PR China; 2. Department of Biological Sciences, Arkansas State University, State University, AR 72467, USA; 3. Molecular Biosciences Program, Arkansas State University, State University, AR 72467, USA. # These authors have contributed equally to this work. Corresponding author: Changhui Wang, No.301, Mid Yanchang Rd, Department of Respiratory Medicine, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, China, 200072. Email: [email protected], Fax number: 86-021-66301685, Telephone: 86-021-66301685 © Ivyspring International Publisher. This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions. Received: 2018.03.09; Accepted: 2018.08.19; Published: 2018.10.10 Abstract Cyclin-dependent kinase 5 (CDK5), an atypical member of the cyclin-dependent kinase family, plays an important role in the nervous system. Recent studies have shown that CDK5 is also associated with tumors. However, few studies have been done to investigate the mechanism underlying the connection between CDK5 and cancers. To explore the role of CDK5 in cancers by using an extensive bioinformatics data mining process. We mined the transcriptional, survival, functions and structure of CDK5 gene through databases and in vitro experiments.
[Show full text]
RNA Sequencing Reveals a Diverse and Dynamic Repertoire of the Xenopus Tropicalis Transcriptome Over Development
Downloaded from genome.cshlp.org on October 6, 2021 - Published by Cold Spring Harbor Laboratory Press Resource RNA sequencing reveals a diverse and dynamic repertoire of the Xenopus tropicalis transcriptome over development Meng How Tan,1,6,7 Kin Fai Au,2,6 Arielle L. Yablonovitch,1,3,6 Andrea E. Wills,1 Jason Chuang,4 Julie C. Baker,1 Wing Hung Wong,2,5 and Jin Billy Li1,7 1Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA; 2Department of Statistics, School of Humanities and Sciences, Stanford University, Stanford, California 94305, USA; 3Program in Biophysics, School of Humanities and Sciences, Stanford University, Stanford, California 94305, USA; 4Department of Computer Science, School of Engineering, Stanford University, Stanford, California 94305, USA; 5Department of Health Research and Policy, Stanford University School of Medicine, Stanford, California 94305, USA The Xenopus embryo has provided key insights into fate specification, the cell cycle, and other fundamental developmental and cellular processes, yet a comprehensive understanding of its transcriptome is lacking. Here, we used paired end RNA sequencing (RNA-seq) to explore the transcriptome of Xenopus tropicalis in 23 distinct developmental stages. We determined expression levels of all genes annotated in RefSeq and Ensembl and showed for the first time on a genome-wide scale that, despite a general state of transcriptional silence in the earliest stages of development, approximately 150 genes are tran- scribed prior to the midblastula transition. In addition, our splicing analysis uncovered more than 10,000 novel splice junctions at each stage and revealed that many known genes have additional unannotated isoforms.
[Show full text]
PARP Inhibition Suppresses GR–MYCN–CDK5– RB1–E2F1
Published OnlineFirst August 22, 2019; DOI: 10.1158/1078-0432.CCR-19-0317 Translational Cancer Mechanisms and Therapy Clinical Cancer Research PARP Inhibition Suppresses GR–MYCN–CDK5– RB1–E2F1 Signaling and Neuroendocrine Differentiation in Castration-Resistant Prostate Cancer Bo Liu1, Likun Li1, Guang Yang1, Chuandong Geng1, Yong Luo1, Wenhui Wu2, Ganiraju C. Manyam2, Dimitrios Korentzelos1, Sanghee Park1, Zhe Tang1, Cheng Wu1, Zhenyang Dong1, Michael Sigouros3, Andrea Sboner4,5,6, Himisha Beltran7, Yu Chen3,8,9, Paul G. Corn1, Michael T. Tetzlaff10, Patricia Troncoso10, Bradley Broom2, and Timothy C. Thompson1 Abstract Purpose: In this study, we addressed the underlying ing pathway that drives NED in prostatic adenocarcinoma mechanisms for the association between enzalutamide (ENZ) PDX and cell line models. Mechanistically, long-term treatment and neuroendocrine prostate cancer (NEPC), and ENZ treatment transcriptionally upregulates signaling of the critical involvement of MYCN, and loss of RB1 function in the GR–MYCN axis, leading to CDK5R1 and CDK5R2 upre- neuroendocrine differentiation (NED) of prostatic epithelial gulation, Rb1 phosphorylation, and N-Myc–mediated cells, and the development of NEPC. We further sought to and E2F1-mediated NED gene expression. Importantly, determine whether PARP inhibition could suppress NEPC, olaparib (OLA) or talazoparib (TALA) suppressed these and to identify molecular determinants of this therapeutic activities, and the combination of OLA and dinaciclib activity. (DINA), an inhibitor of CDK2 and CDK5, which also Experimental Design: We used a novel prostate cancer inhibits Rb1 phosphorylation, suppressed NED and signif- patient–derived xenograft (PDX) treatment model, prostatic icantly improved therapeutic efﬁciency in NEPC cells in vitro adenocarcinoma and NEPC cell lines, an NEPC organoid line, and in NEPC tumors in vivo.
[Show full text]
Deciphering the Molecular Profile of Plaques, Memory Decline And
ORIGINAL RESEARCH ARTICLE published: 16 April 2014 AGING NEUROSCIENCE doi: 10.3389/fnagi.2014.00075 Deciphering the molecular profile of plaques, memory decline and neuron loss in two mouse models for Alzheimer’s disease by deep sequencing Yvonne Bouter 1†,Tim Kacprowski 2,3†, Robert Weissmann4, Katharina Dietrich1, Henning Borgers 1, Andreas Brauß1, Christian Sperling 4, Oliver Wirths 1, Mario Albrecht 2,5, Lars R. Jensen4, Andreas W. Kuss 4* andThomas A. Bayer 1* 1 Division of Molecular Psychiatry, Georg-August-University Goettingen, University Medicine Goettingen, Goettingen, Germany 2 Department of Bioinformatics, Institute of Biometrics and Medical Informatics, University Medicine Greifswald, Greifswald, Germany 3 Department of Functional Genomics, Interfaculty Institute for Genetics and Functional Genomics, University Medicine Greifswald, Greifswald, Germany 4 Human Molecular Genetics, Department for Human Genetics of the Institute for Genetics and Functional Genomics, Institute for Human Genetics, University Medicine Greifswald, Ernst-Moritz-Arndt University Greifswald, Greifswald, Germany 5 Institute for Knowledge Discovery, Graz University of Technology, Graz, Austria Edited by: One of the central research questions on the etiology of Alzheimer’s disease (AD) is the Isidro Ferrer, University of Barcelona, elucidation of the molecular signatures triggered by the amyloid cascade of pathological Spain events. Next-generation sequencing allows the identification of genes involved in disease Reviewed by: Isidro Ferrer, University of Barcelona, processes in an unbiased manner. We have combined this technique with the analysis of Spain two AD mouse models: (1) The 5XFAD model develops early plaque formation, intraneu- Dietmar R. Thal, University of Ulm, ronal Ab aggregation, neuron loss, and behavioral deficits. (2)TheTg4–42 model expresses Germany N-truncated Ab4–42 and develops neuron loss and behavioral deficits albeit without plaque *Correspondence: formation.
[Show full text]
UC San Francisco Previously Published Works
UCSF UC San Francisco Previously Published Works Title FitSNPs: highly differentially expressed genes are more likely to have variants associated with disease. Permalink https://escholarship.org/uc/item/91k8p2km Journal Genome biology, 9(12) ISSN 1474-7596 Authors Chen, Rong Morgan, Alex A Dudley, Joel et al. Publication Date 2008 DOI 10.1186/gb-2008-9-12-r170 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Open Access Research2008ChenetVolume al. 9, Issue 12, Article R170 FitSNPs: highly differentially expressed genes are more likely to have variants associated with disease Rong Chen*†‡, Alex A Morgan*†‡, Joel Dudley*†‡, Tarangini Deshpande§, Li Li†, Keiichi Kodama*†‡, Annie P Chiang*†‡ and Atul J Butte*†‡ Addresses: *Stanford Center for Biomedical Informatics Research, 251 Cmpus Drive, Stanford, CA 94305, USA. †Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA. ‡Lucile Packard Children's Hospital, 725 Welch Road, Palo Alto, CA 94304, USA. §NuMedii Inc., Menlo Park, CA 94025, USA. Correspondence: Atul J Butte. Email: [email protected] Published: 5 December 2008 Received: 17 June 2008 Revised: 26 September 2008 Genome Biology 2008, 9:R170 (doi:10.1186/gb-2008-9-12-r170) Accepted: 5 December 2008 The electronic version of this article is the complete one and can be found online at http://genomebiology.com/2008/9/12/R170 © 2008 Chen 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.
[Show full text]
1 Novel Expression Signatures Identified by Transcriptional Analysis
ARD Online First, published on October 7, 2009 as 10.1136/ard.2009.108043 Ann Rheum Dis: first published as 10.1136/ard.2009.108043 on 7 October 2009. Downloaded from Novel expression signatures identified by transcriptional analysis of separated leukocyte subsets in SLE and vasculitis 1Paul A Lyons, 1Eoin F McKinney, 1Tim F Rayner, 1Alexander Hatton, 1Hayley B Woffendin, 1Maria Koukoulaki, 2Thomas C Freeman, 1David RW Jayne, 1Afzal N Chaudhry, and 1Kenneth GC Smith. 1Cambridge Institute for Medical Research and Department of Medicine, Addenbrooke’s Hospital, Hills Road, Cambridge, CB2 0XY, UK 2Roslin Institute, University of Edinburgh, Roslin, Midlothian, EH25 9PS, UK Correspondence should be addressed to Dr Paul Lyons or Prof Kenneth Smith, Department of Medicine, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Hills Road, Cambridge, CB2 0XY, UK. Telephone: +44 1223 762642, Fax: +44 1223 762640, E-mail: [email protected] or [email protected] Key words: Gene expression, autoimmune disease, SLE, vasculitis Word count: 2,906 The Corresponding Author has the right to grant on behalf of all authors and does grant on behalf of all authors, an exclusive licence (or non-exclusive for government employees) on a worldwide basis to the BMJ Publishing Group Ltd and its Licensees to permit this article (if accepted) to be published in Annals of the Rheumatic Diseases and any other BMJPGL products to exploit all subsidiary rights, as set out in their licence (http://ard.bmj.com/ifora/licence.pdf). http://ard.bmj.com/ on September 29, 2021 by guest. Protected copyright. 1 Copyright Article author (or their employer) 2009.
[Show full text]
CDK5R2(P39) Antibody (N-Term) Blocking Peptide Synthetic Peptide Catalog # Bp7742a
10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 CDK5R2(p39) Antibody (N-term) Blocking Peptide Synthetic peptide Catalog # BP7742a Specification CDK5R2(p39) Antibody (N-term) Blocking CDK5R2(p39) Antibody (N-term) Blocking Peptide Peptide - Background - Product Information CDK5R2(p39) is a neuron-specific activator of Primary Accession Q13319 CDK5 kinase. It associates with CDK5 to form an active kinase. This protein and neuron-specific CDK5 activator CDK5R2(p39) Antibody (N-term) Blocking Peptide - Additional Information CDK5R1/p39NCK5A both share limited similarity to cyclins, and thus may define a distinct family of cyclin-dependent kinase Gene ID 8941 activating proteins. Other Names CDK5R2(p39) Antibody (N-term) Blocking Cyclin-dependent kinase 5 activator 2, Peptide - References CDK5 activator 2, Cyclin-dependent kinase 5 regulatory subunit 2, p39, p39I, CDK5R2, Rademakers,R., Neurobiol. Aging 26 (8), NCK5AI 1145-1151 (2005)Dhavan,R., J. Neurosci. 22 Target/Specificity (18), 7879-7891 (2002)Patzke,H., J. Biol. Chem. The synthetic peptide sequence used to 277 (10), 8054-8060 (2002) generate the antibody <a href=/products/AP7742a>AP7742a</a> was selected from the p39 region of human CDK5R2(p39). A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay. Format Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. Storage Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. Precautions This product is for research use only.
[Show full text]
Detection of Copy Number Alterations in Metastatic Melanoma by a DNA
Human Cancer Biology Detection of Copy Number Alterations in Metastatic Melanoma by aDNAFluorescenceIn situ Hybridization Probe Panel and Array Comparative Genomic Hybridization: A Southwest Oncology Group Study (S9431) Stephen R. Moore,1Diane L. Persons,2 Jeffrey A. Sosman,3 Dolores Bobadilla,1Victoria Bedell,1 David D. Smith,1Sandra R.Wolman,4 Ralph J. Tuthill,5 Jim Moon,6 Vernon K. Sondak,7 and Marilyn L. Slovak1 Abstract Purpose: Gene copy number alteration (CNA) is common in malignant melanoma and is associated with tumor development and progression. The concordance between molecular cytogenetic techniques used to determine CNA has not been evaluated on a large set of loci in malignant melanoma. Experimental Design: A panel of 16 locus-specific fluorescence in situ hybridization (FISH) probes located on eight chromosomes was used to identify CNA in touch preparations of frozen tissue samples from19 patients with metastaticmelanoma (SWOG-9431). A subset ( n =11)was analyzed using bacterial artificial chromosome (BAC) array comparative genomic hybridization (aCGH) of DNA isolated directly from touch-preparation slides. Results: By FISH, most samples showed loss near or at WISP3 /6p21, CCND3/6q22, and CDKN2A /9p21 (>75% of samples tested). More than one third of CDKN2A /9p21losses were biallelic. Gains of NEDD9/6p24, MET/7q31, and MYC/8q24 were common (57%, 47%, and 41%, respectively) and CNA events involving 9p21/7p12.3 and MET were frequently coincident, suggesting gain of the whole chromosome 7. Changes were confirmed by aCGH, which also uncovered many discreet regions of change, larger than a single BAC. Overlapping segments observed in >45% of samples included many of the loci analyzed in the FISH study, in addition to other WNT pathway members, and genes associated withTP53 pathways and DNA damage response, repair, and stability.
[Show full text]
Peripheral Nerve Single-Cell Analysis Identifies Mesenchymal Ligands That Promote Axonal Growth
Research Article: New Research Development Peripheral Nerve Single-Cell Analysis Identifies Mesenchymal Ligands that Promote Axonal Growth Jeremy S. Toma,1 Konstantina Karamboulas,1,ª Matthew J. Carr,1,2,ª Adelaida Kolaj,1,3 Scott A. Yuzwa,1 Neemat Mahmud,1,3 Mekayla A. Storer,1 David R. Kaplan,1,2,4 and Freda D. Miller1,2,3,4 https://doi.org/10.1523/ENEURO.0066-20.2020 1Program in Neurosciences and Mental Health, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada, 2Institute of Medical Sciences University of Toronto, Toronto, Ontario M5G 1A8, Canada, 3Department of Physiology, University of Toronto, Toronto, Ontario M5G 1A8, Canada, and 4Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5G 1A8, Canada Abstract Peripheral nerves provide a supportive growth environment for developing and regenerating axons and are es- sential for maintenance and repair of many non-neural tissues. This capacity has largely been ascribed to paracrine factors secreted by nerve-resident Schwann cells. Here, we used single-cell transcriptional profiling to identify ligands made by different injured rodent nerve cell types and have combined this with cell-surface mass spectrometry to computationally model potential paracrine interactions with peripheral neurons. These analyses show that peripheral nerves make many ligands predicted to act on peripheral and CNS neurons, in- cluding known and previously uncharacterized ligands. While Schwann cells are an important ligand source within injured nerves, more than half of the predicted ligands are made by nerve-resident mesenchymal cells, including the endoneurial cells most closely associated with peripheral axons. At least three of these mesen- chymal ligands, ANGPT1, CCL11, and VEGFC, promote growth when locally applied on sympathetic axons.
[Show full text]
Extracting Unrecognized Gene Relationships from the Biomedical Literature Via Matrix Factorizations
Extracting Unrecognized Gene Relationships from the Biomedical Literature via Matrix Factorizations Hyunsoo Kim∗1, Haesun Park∗1 and Barry L. Drake1 1 College of Computing, Georgia Institute of Technology, 266 Ferst Drive, Atlanta, GA 30332, USA. Email: H. Kim∗- [email protected]; H. Park∗- [email protected]; B. L. Drake - [email protected]; ∗Corresponding author Abstract Background: The construction of literature-based networks of gene-gene interactions is one of the most important applications of text mining in bioinformatics. Extracting potential gene relationships from the biomedical literature may be helpful in building biological hypotheses that can be explored further experimentally. Recently, latent semantic indexing based on the singular value decomposition (LSI/SVD) has been applied to gene retrieval. However, the determination of the number of factors k used in the reduced rank matrix is still an open problem. Results: In this paper, we introduce a way to incorporate a priori knowledge of gene relationships into LSI/SVD to determine the number of factors. We also explore the utility of the non-negative matrix factorization (NMF) to extract unrecognized gene relationships from the biomedical literature by taking advantage of known gene relationships. A gene retrieval method based on NMF (GR/NMF) showed comparable performance with LSI/SVD. Conclusions: Using known gene relationships of a given gene, we can determine the number of factors used in the reduced rank matrix and retrieve unrecognized genes related with the given gene by LSI/SVD or GR/NMF. 1 Background Latent semantic indexing based on the singular value decomposition (LSI/SVD) [1, 2] uses the truncated singular value decomposition as a low-rank approximation of a term-by-document matrix.
[Show full text]