Anti-PPP3CB (Aa 63-363) Polyclonal Antibody (DPABH-19613) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use

Total Page：16

File Type：pdf, Size：1020Kb

Anti-PPP3CB (aa 63-363) polyclonal antibody (DPABH-19613) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Antigen Description Calcium-dependent, calmodulin-stimulated protein phosphatase. This subunit may have a role in the calmodulin activation of calcineurin. Immunogen Recombinant fragment, corresponding to a region within amino acids 63-363 of Human PPP3CB (NP_066955). Isotype IgG Source/Host Rabbit Species Reactivity Mouse, Human Purification Immunogen affinity purified Conjugate Unconjugated Applications WB Format Liquid Size 50 μl Buffer Constituents: 10% Glycerol, 0.1M Tris, 0.1M Glycine, pH 7.0 Preservative None Storage Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. GENE INFORMATION Gene Name PPP3CB protein phosphatase 3, catalytic subunit, beta isozyme [ Homo sapiens ] Official Symbol PPP3CB Synonyms PPP3CB; protein phosphatase 3, catalytic subunit, beta isozyme; CALNB, protein phosphatase 3 (formerly 2B), catalytic subunit, beta isoform; protein phosphatase 3 (formerly 2B), catalytic subunit, beta isoform (calcineurin A beta); serine/threonine-protein phosphatase 2B catalytic subunit beta isoform; calcineurin A beta; CALNA2; CNA2; PP2Bbeta; protein phosphatase 2B; 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved catalytic subunit; beta isoform; calcineurin A2; CAM-PRP catalytic subunit; protein phosphatase from PCR fragment H32; calmodulin-dependent calcineurin A subunit beta isoform; protein phosphatase 2B, catalytic subunit, beta isoform; protein phosphatase 3 (formerly 2B), catalytic subunit, beta isoform; CALNB; Entrez Gene ID 5532 Protein Refseq NP_001135825 UniProt ID P16298 Chromosome Location 10q22.2 Pathway Alzheimers disease; Amphetamine addiction; Amyotrophic lateral sclerosis (ALS); Apoptosis; Function calcium ion binding; calcium-dependent protein serine/threonine phosphatase activity; calmodulin binding; calmodulin-dependent protein phosphatase activity; drug binding; enzyme binding; hydrolase activity 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 2 © Creative Diagnostics All Rights Reserved.

Copy Link

Recommended publications

FK506-Binding Protein 12.6/1B, a Negative Regulator of [Ca2+], Rescues Memory and Restores Genomic Regulation in the Hippocampus of Aging Rats
This Accepted Manuscript has not been copyedited and formatted. The final version may differ from this version. A link to any extended data will be provided when the final version is posted online. Research Articles: Neurobiology of Disease FK506-Binding Protein 12.6/1b, a negative regulator of [Ca2+], rescues memory and restores genomic regulation in the hippocampus of aging rats John C. Gant1, Eric M. Blalock1, Kuey-Chu Chen1, Inga Kadish2, Olivier Thibault1, Nada M. Porter1 and Philip W. Landfield1 1Department of Pharmacology & Nutritional Sciences, University of Kentucky, Lexington, KY 40536 2Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294 DOI: 10.1523/JNEUROSCI.2234-17.2017 Received: 7 August 2017 Revised: 10 October 2017 Accepted: 24 November 2017 Published: 18 December 2017 Author contributions: J.C.G. and P.W.L. designed research; J.C.G., E.M.B., K.-c.C., and I.K. performed research; J.C.G., E.M.B., K.-c.C., I.K., and P.W.L. analyzed data; J.C.G., E.M.B., O.T., N.M.P., and P.W.L. wrote the paper. Conflict of Interest: The authors declare no competing financial interests. NIH grants AG004542, AG033649, AG052050, AG037868 and McAlpine Foundation for Neuroscience Research Corresponding author: Philip W. Landfield, [email protected], Department of Pharmacology & Nutritional Sciences, University of Kentucky, 800 Rose Street, UKMC MS 307, Lexington, KY 40536 Cite as: J. Neurosci ; 10.1523/JNEUROSCI.2234-17.2017 Alerts: Sign up at www.jneurosci.org/cgi/alerts to receive customized email alerts when the fully formatted version of this article is published.
[Show full text]
SPATA33 Localizes Calcineurin to the Mitochondria and Regulates Sperm Motility in Mice
SPATA33 localizes calcineurin to the mitochondria and regulates sperm motility in mice Haruhiko Miyataa, Seiya Ouraa,b, Akane Morohoshia,c, Keisuke Shimadaa, Daisuke Mashikoa,1, Yuki Oyamaa,b, Yuki Kanedaa,b, Takafumi Matsumuraa,2, Ferheen Abbasia,3, and Masahito Ikawaa,b,c,d,4 aResearch Institute for Microbial Diseases, Osaka University, Osaka 5650871, Japan; bGraduate School of Pharmaceutical Sciences, Osaka University, Osaka 5650871, Japan; cGraduate School of Medicine, Osaka University, Osaka 5650871, Japan; and dThe Institute of Medical Science, The University of Tokyo, Tokyo 1088639, Japan Edited by Mariana F. Wolfner, Cornell University, Ithaca, NY, and approved July 27, 2021 (received for review April 8, 2021) Calcineurin is a calcium-dependent phosphatase that plays roles in calcineurin can be a target for reversible and rapidly acting male a variety of biological processes including immune responses. In sper- contraceptives (5). However, it is challenging to develop molecules matozoa, there is a testis-enriched calcineurin composed of PPP3CC and that specifically inhibit sperm calcineurin and not somatic calci- PPP3R2 (sperm calcineurin) that is essential for sperm motility and male neurin because of sequence similarities (82% amino acid identity fertility. Because sperm calcineurin has been proposed as a target for between human PPP3CA and PPP3CC and 85% amino acid reversible male contraceptives, identifying proteins that interact with identity between human PPP3R1 and PPP3R2). Therefore, identi- sperm calcineurin widens the choice for developing specific inhibitors. fying proteins that interact with sperm calcineurin widens the choice Here, by screening the calcineurin-interacting PxIxIT consensus motif of inhibitors that target the sperm calcineurin pathway. in silico and analyzing the function of candidate proteins through the The PxIxIT motif is a conserved sequence found in generation of gene-modified mice, we discovered that SPATA33 inter- calcineurin-binding proteins (8, 9).
[Show full text]
(12) Patent Application Publication (10) Pub. No.: US 2003/0170678A1 Tanzi Et Al
US 2003.017O678A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2003/0170678A1 Tanzi et al. (43) Pub. Date: Sep. 11, 2003 (54) GENETIC MARKERS FOR ALZHEIMER'S Related U.S. Application Data DISEASE AND METHODS USING THE SAME (60) Provisional application No. 60/348,065, filed on Oct. (75) Inventors: Rudolph E. Tanzi, Hull, MA (US); 25, 2001. Provisional application No. 60/336,983, Kenneth David Becker, San Diego, CA filed on Nov. 2, 2001. (US); Gonul Velicelebi, San Diego, CA (US); Kathryn J. Elliott, San Diego, Publication Classification CA (US); Xin Wang, San Diego, CA (US); Lars Bertram, Brighton, MA (51) Int. C.7 - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - C12O 1/68 (US); Aleister J. Saunders, (52) U.S. Cl. .................................................................. 435/6 Philadelphia, PA (US); Deborah Lynne Blacker, Newton, MA (US) (57) ABSTRACT Correspondence Address: HELLER EHRMAN WHITE & MCAULIFFE LLP Genetic markers associated with Alzheimer's disease are 4350 LA JOLLAVILLAGE DRIVE provided. Also provided are methods of determining the 7TH FLOOR presence or absence in a Subject of one or more polymor SAN DIEGO, CA 92122-1246 (US) phisms associated with Alzheimer's disease and methods of determining the level of risk for Alzheimer's disease in a (73) Assignee: Neurogenetics, Inc. Subject. Further provided are nucleic acid compositions and kits for use in determining the presence or absence in a (21) Appl. No.: 10/281,456 Subject of one or more polymorphisms associated with Alzheimer's disease and kits for determining the level of (22) Filed: Oct. 25, 2002 risk for Alzheimer's disease in a Subject. Patent Application Publication Sep.
[Show full text]
Characterization and Expression Analysis of a CNV at Chromosome
Inês C. Conceição1,2, Catarina Correia1,2,3, Joana I. Coelho1,4, Bárbara Oliveira1,2, Frederico Duque5, Susana Mouga5, Guiomar Oliveira5, Astrid M. Vicente1,2,3 1 Instituto Nacional de Saúde Dr. Ricardo Jorge, 1600 Lisboa, Portugal; 2 Center for Biodiversity, Functional & Integrative Genomics, Lisboa, Portugal; 3 Instituto Gulbenkian de Ciência, Oeiras, Portugal; 4 Faculdade de Ciências, Universidade de Lisboa, Portugal 5 Centro de Desenvolvimento da Criança, Hospital Pediátrico de Coimbra, Coimbra, Portugal Genetics of Autism Spectrum Disorders Autism Spectrum Disorders (ASD) have a strong genetic component, with an estimated heritability of over 90%1. Recent studies carried out by the Autism Genome Project (AGP) consortium suggest that rare Copy Number Variants (CNV), characterized by submicroscopic chromosomal deletions and duplications, are more frequent in ASD compared to controls, and may play an important role in susceptibility to this disorder2-7. However, to adequately assess pathogenicity, a detailed characterization of patients CNVs is required. A de novo deletion encompassing 14 genes We have been characterizing potentially pathogenic rare CNVs identified by the AGP whole genome CNV analysis of 1,275 ASD individuals. CNV validation in patients and parents and characterization were performed by qPCR and Long- range PCR. One autistic patient showed a rare deletion absent in 4964 controls of European ancestry with no psychiatric disease history. This deletion was located at 10q22, and encompassed 14 genes, including ANXA7, ZMYND17, PPP3CB and CAMK2G (Figure 1). We validated this CNV as de novo, and accurate breakpoint determination showed that it is smaller than predicted by CNV identification algorithms, including only part of CAMK2G.
[Show full text]
ANXA7, PPP3CB, DNAJC9, and ZMYND17 Genes at Chromosome
ARCHIVAL REPORTS ANXA7, PPP3CB, DNAJC9, and ZMYND17 Genes at Chromosome 10q22 Associated with the Subgroup of Schizophrenia with Deficits in Attention and Executive Function Chih-Min Liu, Cathy S.-J. Fann, Chien-Yu Chen, Yu-Li Liu, Yen-Jen Oyang, Wei-Chih Yang, Chien-Ching Chang, Chun-Chiang Wen, Wei J. Chen, Tzung-Jeng Hwang, Ming H. Hsieh, Chen-Chung Liu, Stephen V. Faraone, Ming T. Tsuang, and Hai-Gwo Hwu Background: A genome scan of Taiwanese schizophrenia families suggested linkage to chromosome 10q22.3. We aimed to find the candidate genes in this region. Methods: A total of 476 schizophrenia families were included. Hierarchical clustering method was used for clustering families to homoge- neous subgroups according to their performances of sustained attention and executive function. Association analysis was performed using family-based association testing and TRANSMIT. Candidate associated regions were identified using the longest significance run method. The relative messenger RNA expression level was determined using real-time reverse transcriptase polymerase chain reaction. Results: First, we genotyped 18 microsatellite markers between D10S1432 and D10S1239. The maximum nonparametric linkage score was 2.79 on D10S195. Through family clustering, we found the maximum nonparametric linkage score was 3.70 on D10S195 in the family cluster with deficits in attention and executive function. Second, we genotyped 79 single nucleotide polymorphisms between D10S1432 and D10S580 in 90 attention deficit and execution deficit families. Association analysis indicated significant transmission distortion for nine single nucleotide polymorphisms. Using the longest significance run method, we identified a 427-kilobase region as a significant candidate region, which encompasses nine genes.
[Show full text]
GENETICS Gene Expression Profiles of Two B-Complex Disparate
GENETICS Ii Gene expression profiles of two B-complex disparate, genetically inbred Fayoumi chicken lines that differ in susceptibility to Eimeria maxima D. K. Kinl.* C. H. Kiin.t S. .T. Lanont4 C. L. Keeler .Jr.. and H. S. Lillehoj*I AnzTnai Parasitic Disases Laboratory. Animal and i'vaturai Re,soaices 1i,.t,tatc, 115124, l3e1tsi ;,iie. AID 20705: tKorcan Biom formation Center. Korea Research Ins tit etc of Bioscience and Biotechnoloqy. Doe jeoi. 305-806. Republic of Korea: .f Department of Animal Science. iowa State Uiwersity, Arries 50011: ii o.dI)cparfmrrenf of Aiwaai and Food Sciences. (ni ic csitq of Delaware. Newark 19716 ABSTRACT This stud y Was conducted to compare the clown), and 92 (33 up. 59 down) mnRNA at the 3 time gene ixprussioli profiles, after Emmn crma maxima infection. points. Functional anal ysis using gene ontology catego- between 2 B-complex congcmc lines of Favonnui chick- rized the genes exhibiting the different expression pat- (-'115 that display differeiicis in disease resistance and terns between 2 chicken lines into several gene ontology innate immunity against avian coccidiosis using cD\A terms including imniunlity and defense. In summary, inicroarrav. When compared with uninfected controls transcriptional profiles showed that more gene expres- using a cutoff of >2.0-fold alteration (P < 0.05), l\I5.1 sion changes occurred with E. maxima infection in the demonstrated altered expression of I (downregulate(l). M15.2 than the A15.1 line. The roost gene expression 12 (6 up. 6 down). and 18 (5 up. 13 clown) infINA at 3. (liffmeices between the 2 chicken lines were exhibited 4.
[Show full text]
Genome-Wide Dissection of Microrna Functions and Cotargeting Networks Using Gene-Set Signatures
Genome-wide dissection of microRNA functions and cotargeting networks using gene-set signatures The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation Tsang, John S., Margaret S. Ebert, and Alexander van Oudenaarden. “Genome-wide Dissection of MicroRNA Functions and Cotargeting Networks Using Gene Set Signatures.” Molecular Cell 38.1 (2010): 140–153. As Published http://dx.doi.org/10.1016/j.molcel.2010.03.007 Publisher Elsevier Version Author's final manuscript Citable link http://hdl.handle.net/1721.1/76631 Terms of Use Creative Commons Attribution-Noncommercial-Share Alike 3.0 Detailed Terms http://creativecommons.org/licenses/by-nc-sa/3.0/ NIH Public Access Author Manuscript Mol Cell. Author manuscript; available in PMC 2011 June 9. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Mol Cell. 2010 April 9; 38(1): 140±153. doi:10.1016/j.molcel.2010.03.007. Genome-wide dissection of microRNA functions and co- targeting networks using gene-set signatures John S. Tsang1,2, Margaret S. Ebert3,4, and Alexander van Oudenaarden2,3,4 1 Graduate Program in Biophysics, Harvard University, Cambridge, MA 2 Department of Physics, Massachusetts Institute of Technology, Cambridge, MA 3 Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 4 Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA SUMMARY MicroRNAs are emerging as important regulators of diverse biological processes and pathologies in animals and plants. While hundreds of human miRNAs are known, only a few have known functions.
[Show full text]
Supporting Information
Supporting Information Miller et al. 10.1073/pnas.0914257107 SI Materials and Methods files with 20 to 40 samples and 5,629 to 9,731 genes each and 20 Data Set Acquisition and Filtering. All data sets were downloaded mouse expression files with 18 and 44 samples and 5,176 to 6,157 from the GEO database, and consisted of experiments run on genes each. All preprocessed data files (as well as the resulting either mouse or human brain tissue (Fig. 1A). We filtered out all network data and some associated code and support files) are but a core collection of data sets that were similar enough for available at the WGCNA group Web site (www.genetics.ucla.edu/ useful bioinformatic comparison. First, we removed all data sets labs/horvath/CoexpressionNetwork/MouseHumanBrain). that were not run on an Affymetrix platform, leaving three From these preprocessed expression files we created a human platforms in human (HG-U95A, HG-U133A, HG-U133 Plus 2) and a mouse consensus network (method modified from ref. 4). and two in mouse (MG-U74A, MG-U430A). Second, we ex- For each consensus network we first created correlation matrices cluded all samples in each data set that were not taken from from each data set (obtained by calculating the Pearson correla- brain tissue (for example, in one expression atlas study, more tions between all variable probe sets across all subjects in each than 80% of the samples were excluded). Third, to make the data set), and then weighted them based on the number of sam- correlations between genes more comparable across studies, we ples used in that data set.
[Show full text]
Partial Inhibition of Calcineurin Activity by Rcn2 As a Potential Remedy for Vps13 Deficiency
International Journal of Molecular Sciences Article Partial Inhibition of Calcineurin Activity by Rcn2 as a Potential Remedy for Vps13 Deficiency Patrycja Wardaszka , Piotr Soczewka, Marzena Sienko , Teresa Zoladek and Joanna Kaminska * Institute of Biochemistry and Biophysics Polish Academy of Science, 02-106 Warsaw, Poland; [email protected] (P.W.); [email protected] (P.S.); [email protected] (M.S.); [email protected] (T.Z.) * Correspondence: [email protected]; Tel.: +48-22-592-1316 Abstract: Regulation of calcineurin, a Ca2+/calmodulin-regulated phosphatase, is important for the nervous system, and its abnormal activity is associated with various pathologies, including neurodegenerative disorders. In yeast cells lacking the VPS13 gene (vps13D), a model of VPS13-linked neurological diseases, we recently demonstrated that calcineurin is activated, and its downregulation reduces the negative effects associated with vps13D mutation. Here, we show that overexpression of the RCN2 gene, which encodes a negative regulator of calcineurin, is beneficial for vps13D cells. We studied the molecular mechanism underlying this effect through site-directed mutagenesis of RCN2. The interaction of the resulting Rcn2 variants with a MAPK kinase, Slt2, and subunits of calcineurin was tested. We show that Rcn2 binds preferentially to Cmp2, one of two alternative catalytic subunits of calcineurin, and partially inhibits calcineurin. Rcn2 ability to bind to and reduce the activity of calcineurin was important for the suppression. The binding of Rcn2 to Cmp2 requires two motifs in Rcn2: the previously characterized C-terminal motif and a new N-terminal motif that was discovered in this study. Altogether, our findings can help to better understand calcineurin regulation and to develop new therapeutic strategies against neurodegenerative diseases based on modulation of the activity of selected calcineurin isoforms.
[Show full text]
Original Articles a New Gene (DYX3) for Dyslexia Is Located on Chromosome 2
664 J Med Genet 1999;36:664–669 J Med Genet: first published as 10.1136/jmg.36.9.664 on 1 September 1999. Downloaded from Original articles A new gene (DYX3) for dyslexia is located on chromosome 2 Toril Fagerheim, Peter Raeymaekers, Finn Egil Tønnessen, Marit Pedersen, Lisbeth Tranebjærg, Herbert A Lubs Abstract skills, and adequate schooling.1 In 1950, Developmental dyslexia is a specific read- Hallgren2 reported that more than 80% of chil- ing disability aVecting children and adults dren with dyslexia in Stockholm schools had who otherwise possess normal intelli- other family members with dyslexia. Subse- gence, cognitive skills, and adequate quent studies have shown that there is both a schooling. DiYculties in spelling and physical and genetic basis for many children reading may persist through adult life. and adults with severe reading disability and Possible localisations of genes for dyslexia that the most frequent deficit is in phonological have been reported on chromosomes 15 coding.34This is manifested by decreased abil- (DYX1), 6p21.3-23 (DYX2), and 1p over the ity to pronounce letter strings (or pseudowords) last 15 years. Only the localisation to correctly that have not been encountered previ- 6p21.3-23 has been clearly confirmed and ously. Recent studies using new methods have a genome search has not previously been provided a clearer view of the diVerence in the carried out. We have investigated a large processing of written words in dyslexics and Norwegian family in which dyslexia is non-impaired readers. In none of the studies, inherited as an autosomal dominant trait.
[Show full text]
(12) United States Patent (10) Patent No.: US 9,163,078 B2 Rao Et Al
US009 163078B2 (12) United States Patent (10) Patent No.: US 9,163,078 B2 Rao et al. (45) Date of Patent: *Oct. 20, 2015 (54) REGULATORS OF NFAT 2009.0143308 A1 6, 2009 Monk et al. 2009,0186422 A1 7/2009 Hogan et al. (75) Inventors: Anjana Rao, Cambridge, MA (US); 2010.0081129 A1 4/2010 Belouchi et al. Stefan Feske, New York, NY (US); Patrick Hogan, Cambridge, MA (US); FOREIGN PATENT DOCUMENTS Yousang Gwack, Los Angeles, CA (US) CN 1329064 1, 2002 EP O976823. A 2, 2000 (73) Assignee: Children's Medical Center EP 1074617 2, 2001 Corporation, Boston, MA (US) EP 1293569 3, 2003 WO 02A30976 A1 4, 2002 (*) Notice: Subject to any disclaimer, the term of this WO O2/O70539 9, 2002 patent is extended or adjusted under 35 WO O3/048.305 6, 2003 U.S.C. 154(b) by 0 days. WO O3/052049 6, 2003 WO WO2005/O16962 A2 * 2, 2005 This patent is Subject to a terminal dis- WO 2005/O19258 3, 2005 claimer. WO 2007/081804 A2 7, 2007 (21) Appl. No.: 13/161,307 OTHER PUBLICATIONS (22) Filed: Jun. 15, 2011 Skolnicket al., 2000, Trends in Biotech, vol. 18, p. 34-39.* Tomasinsig et al., 2005, Current Protein and Peptide Science, vol. 6, (65) Prior Publication Data p. 23-34.* US 2011 FO269174 A1 Nov. 3, 2011 Smallwood et al., 2002, Virology, vol. 304, p. 135-145.* • - s Chattopadhyay et al., 2004. Virus Research, vol. 99, p. 139-145.* Abbas et al., 2005, computer printout pp. 2-6.* Related U.S.
[Show full text]
Research Article Bioinformatics Identification of Modules Of
SAGE-Hindawi Access to Research International Journal of Alzheimer’s Disease Volume 2011, Article ID 154325, 13 pages doi:10.4061/2011/154325 Research Article Bioinformatics Identification of Modules of Transcription Factor Binding Sites in Alzheimer’s Disease-Related Genes by In Silico Promoter Analysis and Microarrays Regina Augustin,1 Stefan F. Lichtenthaler,2 Michael Greeff,3 Jens Hansen,1 Wolfgang Wurst,1, 2, 4 and Dietrich Trumbach¨ 1, 4 1 Institute of Developmental Genetics, Helmholtz Centre Munich, German Research Centre for Environmental Health (GmbH), Technical University Munich, Ingolstadter¨ Landstraße 1, Munich 85764, Neuherberg, Germany 2 DZNE, German Center for Neurodegenerative Diseases, Schillerstraße 44, 80336 Munich, Germany 3 Institute of Bioinformatics and Systems Biology, Helmholtz Centre Munich, German Research Centre for Environmental Health (GmbH), Ingolstadter¨ Landstraße 1, Munich 85764, Neuherberg, Germany 4 Clinical Cooperation Group Molecular Neurogenetics, Max Planck Institute of Psychiatry, Kraepelinstraße, 2-10, 80804 Munich, Germany Correspondence should be addressed to Wolfgang Wurst, [email protected] and Dietrich Trumbach,¨ [email protected] Received 21 December 2010; Accepted 15 February 2011 Academic Editor: Jeff Kuret Copyright © 2011 Regina Augustin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The molecular mechanisms and genetic risk factors underlying Alzheimer’s disease (AD) pathogenesis are only partly understood. To identify new factors, which may contribute to AD, different approaches are taken including proteomics, genetics, and functional genomics. Here, we used a bioinformatics approach and found that distinct AD-related genes share modules of transcription factor binding sites, suggesting a transcriptional coregulation.
[Show full text]