Anti-RDBP Polyclonal Antibody (CABT-BL5525) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use

Anti-RDBP polyclonal antibody (CABT-BL5525) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Product Overview Rabbit Anti-RDBP polyclonal Antibody Target RDBP Immunogen Recombinant protein corresponding to amino acids of human RDBP. Isotype IgG Source/Host Rabbit Species Reactivity Human Purification Antigen affinity purification Conjugate Unconjugated Sequence Similarities LLALKKQSSSSTTSQGGVKRSLSEQPVMDTATATEQAKQLVKSGAISAIKAETKNSGFKRSRTLE GKLKDPEKGP VPTFQPFQRSISADDDLQESSRRPQRKSLYESFVSSSDRLRELGPDG Format Liquid Buffer In PBS, pH 7.5 (40% glycerol, 0.02% sodium azide) Preservative 0.02% Sodium Azide Storage Store at 4°C. For long term storage store at -20°C. Aliquot to avoid repeated freezing and thawing. BACKGROUND Introduction The protein encoded by this gene is part of a complex termed negative elongation factor (NELF) which represses RNA polymerase II transcript elongation. This protein bears similarity to nuclear RNA-binding proteins; however, it has not been demonstrated that this protein binds RNA. The protein contains a tract of alternating basic and acidic residues, largely arginine (R) and aspartic acid (D). The gene localizes to the major histocompatibility complex (MHC) class III region on chromosome 6. [provided by RefSeq, Jul 2008] 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 GENE INFORMATION Entrez Gene ID 7936 Protein Refseq NP_002895 UniProt ID P18615 Chromosome Location 6p21.3 Pathway Abortive elongation of HIV-1 transcript in the absence of Tat, organism-specific biosystem; Disease, organism-specific biosystem; Formation of HIV-1 elongation complex containing HIV-1 Tat, organism-specific biosystem; Formation of HIV-1 elongation complex in the absence of HIV- 1 Tat, organism-specific biosystem; Formation of RNA Pol II elongation complex, organism- specific biosystem; Formation of the Early Elongation Complex, organism-specific biosystem; Formation of the HIV-1 Early Elongation Function RNA binding; nucleotide binding; 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.

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Published OnlineFirst March 30, 2015; DOI: 10.1158/1078-0432.CCR-14-2804 Biology of Human Tumors Clinical Cancer Research DNA Methylation Profiling in Pheochromocytoma and Paraganglioma Reveals Diagnostic and Prognostic Markers Aguirre A. de Cubas1, Esther Korpershoek2, Lucia Inglada-Perez 1,3, Eric Letouze4, Maria Curras-Freixes 1, Agustin F. Fernandez 5,Inaki~ Comino-Mendez 1, Francesca Schiavi6, Veronika Mancikova1, Graeme Eisenhofer7,8, Massimo Mannelli9, Guiseppe Opocher6,10, Henri Timmers11, Felix Beuschlein12, Ronald de Krijger13, Alberto Cascon1,3, Cristina Rodríguez-Antona1,3, Mario F. Fraga5,14, Judith Favier15,16, Anne-Paule Gimenez-Roqueplo15,16,17,18, and Mercedes Robledo1,3 Abstract Purpose: Pheochromocytoma and paraganglioma (PPGL) are these, 48 CpGs showed significant associations with time to rare neuroendocrine tumors, associated with highly variable progression even after correcting for SDHB genotype, suggesting postoperative evolution. The scarcity of reliable PPGL prognostic their value as prognostic markers independent of genetic back- markers continues to complicate patient management. In this ground. Hypermethylation of RDBP (negative elongation study, we explored genome-wide DNA methylation patterns in factor complex member E) in metastatic tumors was further the context of PPGL malignancy to identify novel prognostic validated by bisulfite pyrosequencing [Dbmetastatic-benign ¼ 0.29, markers. P ¼ 0.003; HR, 1.4; 95% confidence interval (CI), 1.1–2.0; P ¼ Experimental Design: We retrospectively investigated DNA 0.018] and may alter transcriptional networks involving (RERG, methylation patterns in PPGL with and without metastases using GPX3, and PDZK1) apoptosis, invasion, and maintenance of high-throughput DNA methylation profiling data (Illumina 27K) DNA integrity. from two large, well-characterized discovery (n ¼ 123; 24 met- Conclusions: This is the first large-scale study of DNA methy- astatic) and primary validation (n ¼ 154; 24 metastatic) series.
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Arp40431 P050
Aviva Systems Biology RDBP antibody - N-terminal region (ARP40431_P050) Product Number ARP40431_P050 Product Page http://www.avivasysbio.com/rdbp-antibody-n-terminal-region-arp40431-p050.html Product Name RDBP antibody - N-terminal region (ARP40431_P050) Size 100 ul Gene Symbol NELFE Alias Symbols D6S45, NELF-E, RD, RDP, RDBP Protein Size (# AA) 380 amino acids Molecular Weight 43kDa Product Format Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose. NCBI Gene Id 7936 Host Rabbit Clonality Polyclonal Concentration Batch dependent within range: 100 ul at 0.5 - 1 mg/ml Official Gene Full RD RNA binding protein Name Description This is a rabbit polyclonal antibody against RDBP. It was validated on Western Blot using a cell lysate as a positive control. Aviva Systems Biology strives to provide antibodies covering each member of a whole protein family of your interest. We also use our best efforts to provide you antibodies recognize various epitopes of a target protein. For availability of antibody needed for your experiment, please inquire ([email protected]). Peptide Sequence Synthetic peptide located within the following region: LVIPPGLSEEEEALQKKFNKLKKKKKALLALKKQSSSSTTSQGGVKRSLS Target Reference Rao,J.N., (2008) Biochemistry 47 (12), 3756-3761 Description of RDBP is part of a complex termed negative elongation factor (NELF) which represses Target RNA polymerase II transcript elongation. This protein bears similarity to nuclear RNA- binding proteins; however, it has not been demonstrated that this protein binds RNA. The protein contains a tract of alternating basic and acidic residues, largely arginine (R) and aspartic acid (D).The protein encoded by this gene is part of a complex termed negative elongation factor (NELF) which represses RNA polymerase II transcript elongation.
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COBRA1 Monoclonal Antibody, Clone F7E4
COBRA1 monoclonal antibody, Gene Symbol: COBRA1 clone F7E4 Gene Alias: DKFZp586B0519, KIAA1182, NELF-B, NELFB Catalog Number: MAB8174 Gene Summary: NELFB is a subunit of negative Regulatory Status: For research use only (RUO) elongation factor (NELF), which also includes NELFA (WHSC2; MIM 606026), either NELFC or NELFD (TH1L; Product Description: Mouse monoclonal antibody MIM 605297), and NELFE (RDBP; MIM 154040). NELF raised against full length recombinant COBRA1. acts with DRB sensitivity-inducing factor (DSIF), a Clone Name: F7E4 heterodimer of SPT4 (SUPT4H1; MIM 603555) and SPT5 (SUPT5H; MIM 602102), to cause transcriptional Immunogen: Recombinant protein corresponding to full pausing of RNA polymerase II (see MIM 180660) (Narita length human COBRA1. et al., 2003 [PubMed 12612062]).[supplied by OMIM] Host: Mouse References: 1. COBRA1 inhibits AP-1 transcriptional activity in Theoretical MW (kDa): 62 transfected cells. Zhong H, Zhu J, Zhang H, Ding L, Sun Y, Huang C, Ye Q. Biochem Biophys Res Commun. Reactivity: Human,Mouse,Rat 2004 Dec 10;325(2):568-73. 2. Attenuation of estrogen receptor alpha-mediated Applications: WB-Ti transcription through estrogen-stimulated recruitment of (See our web site product page for detailed applications a negative elongation factor. Aiyar SE, Sun JL, Blair AL, information) Moskaluk CA, Lu YZ, Ye QN, Yamaguchi Y, Mukherjee A, Ren DM, Handa H, Li R. Genes Dev. 2004 Sep Protocols: See our web site at 1;18(17):2134-46. http://www.abnova.com/support/protocols.asp or product page for detailed protocols Specificity: This antibody has been directly tested for reactivity in Western blots with human, mouse and rat tissue.
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Circulating Plasma Exosomes in Obstructive Sleep Apnea and Reverse-Dipping Blood Pressure
Early View Original article Circulating Plasma Exosomes in Obstructive Sleep Apnea and Reverse-Dipping Blood Pressure Abdelnaby Khalyfa, David Gozal, Wen-Ching Chan, Jorge Andrade, Bharati Prasad Please cite this article as: Khalyfa A, Gozal D, Chan W-C, et al. Circulating Plasma Exosomes in Obstructive Sleep Apnea and Reverse-Dipping Blood Pressure. Eur Respir J 2019; in press (https://doi.org/10.1183/13993003.01072-2019). This manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Copyright ©ERS 2019 Circulating Plasma Exosomes in Obstructive Sleep Apnea and Reverse-Dipping Blood Pressure Abdelnaby Khalyfa1, David Gozal1, Wen-Ching Chan2, Jorge Andrade2, and Bharati Prasad3 1Department of Child Health and the Child Health Research Institute, University of Missouri School of Medicine, Columbia, MO 65201, USA. 2Center for Research Informatics, The University of Chicago, Chicago, Illinois. 3Department of Pulmonary, Critical Care, Sleep and Allergy, University of Illinois at Chicago. Corresponding Author: Bharati Prasad, MD, MS Associate Professor of Medicine Department of Medicine Pulmonary, Critical Care, Sleep, and Allergy University of Illinois Hospital and Health Sciences System 840 S Wood St MC 719; 9th Floor Ph: (312)9968039 Fax: (312)9964665 email: [email protected] Abstract Background: Obstructive Sleep Apnea (OSA) increases the risk of abnormal non- dipping 24-hour blood pressure profile, an independent risk factor for cardiovascular disease (CVD).
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Global DNA Methylation Analysis Identifies Two Discrete Clusters Of
www.nature.com/scientificreports OPEN Global DNA Methylation Analysis Identifies Two Discrete clusters of Pheochromocytoma with Distinct Received: 11 October 2016 Accepted: 14 February 2017 Genomic and Genetic Alterations Published: 22 March 2017 Samuel Backman1, Rajani Maharjan1, Alberto Falk-Delgado1, Joakim Crona1, Kenko Cupisti2, Peter Stålberg1, Per Hellman1 & Peyman Björklund1 Pheochromocytomas and paragangliomas (PPGLs) are rare and frequently heritable neural-crest derived tumours arising from the adrenal medulla or extra-adrenal chromaffin cells respectively. The majority of PPGL tumours are benign and do not recur with distant metastases. However, a sizeable fraction of these tumours secrete vasoactive catecholamines into the circulation causing a variety of symptoms including hypertension, palpitations and diaphoresis. The genetic landscape of PPGL has been well characterized and more than a dozen genes have been described as recurrently mutated. Recent studies of DNA-methylation have revealed distinct clusters of PPGL that share DNA methylation patterns and driver mutations, as well as identified potential biomarkers for malignancy. However, these findings have not been adequately validated in independent cohorts. In this study we use an array-based genome-wide approach to study the methylome of 39 PPGL and 4 normal adrenal medullae. We identified two distinct clusters of tumours characterized by different methylation patterns and different driver mutations. Moreover, we identify genes that are differentially methylated between tumour subcategories, and between tumours and normal tissue. Pheochromocytoma and paraganglioma (PPGL) are neural crest derived chromaffin cell tumours of the adrenal medulla and paraganglia, respectively. The tumours may secrete catecholamines such as epinephrine, norepi- nephrine and dopamine into the systemic circulation, leading to symptoms of sympathetic hyperactivity.
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Was Gathered from SMR Analysis at the Genome-Wide Significance Level
Supplementary Table 1: Putative functional genes for AMD from the SMR analysis in CAGE. Detailed information of 16 genes (tagged by 21 probes) was gathered from SMR analysis at the genome-wide significance level. probeID Chr Gene Probe bp topSNP topSNP bp A1 A2 Freq GWAS PGWAS eQTL PeQTL SMR PSMR PHEIDI nsnpHEIDI ILMN_1660436 6 HSPA1A 31797709 rs494620 31838713 A G 0.384 0.079 3.71e-07 0.51 1.4e-74 0.155 9.72e-07 2.64e-08 20 ILMN_1765532 6 RDBP 31919892 rs550513 31920687 T C 0.0979 -0.534 9.46e-91 -0.402 1.82e-16 1.33 2.45e-14 2.48e-07 20 ILMN_1679520 6 AGPAT1 32136453 rs41316748 32019512 C T 0.0403 0.246 7.99e-10 -0.72 1.29e-18 -0.341 4.67e-07 4.8e-06 20 ILMN_2044927 6 RNF5 32148208 rs693906 31835164 C G 0.157 0.153 7.05e-12 0.438 6.09e-27 0.349 7.45e-09 0.000454 20 ILMN_1725170 6 CA425595 32624021 rs9274614 32635846 C G 0.241 -0.141 6.5e-16 1.12 3.51e-267 -0.126 3.5e-15 0.00326 20 ILMN_1721636 7 TSC22D4 100064521 rs7792525 99972122 G A 0.188 0.112 1.09e-08 0.323 2.27e-20 0.347 1.16e-06 0.041 20 ILMN_1688279 7 PVRIG 99818960 rs6953580 99825275 G A 0.216 0.090 1.1e-06 -0.951 1.74e-180 -0.0947 1.56e-06 0.051 20 ILMN_1685534 7 PILRB 99947392 rs7792525 99972122 G A 0.188 0.112 1.09e-08 0.345 1.72e-23 0.325 7.01e-07 0.121 20 ILMN_1723984 7 PILRB 99955692 rs73401450 99981859 C G 0.188 0.112 1.07e-08 1.07 3.28e-205 0.105 1.89e-08 0.183 20 ILMN_1768754 7 PILRB 99965148 rs61735533 99955866 A G 0.188 0.111 1.6e-08 1.19 7.93e-255 0.093 2.48e-08 0.257 20 ILMN_1807712 7 PILRB 99951516 rs1964242 99976703 A G 0.186 0.113 7.07e-09 0.649 4.41e-76 0.175
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A High-Throughput Study in Melanoma Identifies Epithelial- Mesenchymal Transition As a Major Determinant of Metastasis
Research Article A High-Throughput Study in Melanoma Identifies Epithelial- Mesenchymal Transition as a Major Determinant of Metastasis Soledad R. Alonso,1 Lorraine Tracey,1 Pablo Ortiz,4 Beatriz Pe´rez-Go´mez,5 Jose´ Palacios,1 Marina Pollań,5 Juan Linares,6 Salvio Serrano,7 Ana I. Saéz-Castillo,6 Lydia Sańchez,2 Raquel Pajares,2 Abel Sańchez-Aguilera,1 Maria J. Artiga,1 Miguel A. Piris,1 and Jose´ L. Rodrı´guez-Peralto3 1Molecular Pathology Programme and 2Histology and Immunohistochemistry Unit, Centro Nacional de Investigaciones Oncolo´gicas; Departments of 3Pathology and 4Dermatology, Hospital Universitario 12 de Octubre; 5Centro Nacional de Epidemiologıá, Instituto de Salud Carlos III, Madrid, Spain; and Departments of 6Pathology and 7Dermatology, Hospital Universitario San Cecilio, Granada, Spain Abstract with a less favorable prognosis as potential candidates for adjuvant Metastatic disease is the primary cause of death in cutaneous or novel therapies. malignant melanoma (CMM) patients. To understand the Currently, the prognosis of primary CMM is mainly based mechanisms of CMM metastasis and identify potential on histopathologic criteria. The most important of these is the predictive markers, we analyzed gene-expression profiles of Breslow index, although it is merely a measure of tumor depth. 34 vertical growth phase melanoma cases using cDNA micro- New molecular markers that correlate with melanoma genesis and/or progression are continuously being identified but, to date, arrays. All patients had a minimum follow-up of 36 months. Twenty-one cases developed nodal metastatic disease and 13 most of them have been obtained in experimental models and did not.
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Supporting Information
Supporting Information Poulogiannis et al. 10.1073/pnas.1009941107 SI Materials and Methods Loss of Heterozygosity (LOH) Analysis of PARK2. Seven microsatellite Bioinformatic Analysis of Genome and Transcriptome Data. The markers (D6S1550, D6S253, D6S305, D6S955, D6S980, D6S1599, aCGH package in R was used to identify significant DNA copy and D6S396) were amplified for LOH analysis within the PARK2 number (DCN) changes in our collection of 100 sporadic CRCs locus using primers that were previously described (8). (1) (Gene Expression Omnibus, accession no. GSE12520). The MSP of the PARK2 Promoter. CpG sites within the PARK2 promoter aCGH analysis of cell lines and liver metastases was derived region were detected using the Methprimer software (http://www. from published data (2, 3). Chromosome 6 tiling-path array- urogene.org/methprimer/index.html). Methylation-specificand CGH was used to identify the smallest and most frequently al- control primers were designed using the Primo MSP software tered regions of DNA copy number change on chromosome 6. (http://www.changbioscience.com/primo/primom.html); bisulfite An integrative approach was used to correlate expression pro- modification of genomic DNA was performed as described pre- files with genomic copy number data from a SNP array from the viously (9). All tumor DNA samples from primary CRC tumors same tumors (n = 48) (4) (GSE16125), using Pearson’s corre- (n = 100) and CRC lines (n = 5), as well as those from the leukemia lation coefficient analysis to identify the relationships between cell lines KG-1a (acute myeloid leukemia, AML), U937 (acute DNA copy number changes and gene expression of those genes lymphoblastic leukemia, ALL), and Raji (Burkitt lymphoma, BL) SssI located within the small frequently altered regions of DCN were screened as part of this analysis.
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The Neurodegenerative Diseases ALS and SMA Are Linked at The
Nucleic Acids Research, 2019 1 doi: 10.1093/nar/gky1093 The neurodegenerative diseases ALS and SMA are linked at the molecular level via the ASC-1 complex Downloaded from https://academic.oup.com/nar/advance-article-abstract/doi/10.1093/nar/gky1093/5162471 by [email protected] on 06 November 2018 Binkai Chi, Jeremy D. O’Connell, Alexander D. Iocolano, Jordan A. Coady, Yong Yu, Jaya Gangopadhyay, Steven P. Gygi and Robin Reed* Department of Cell Biology, Harvard Medical School, 240 Longwood Ave. Boston MA 02115, USA Received July 17, 2018; Revised October 16, 2018; Editorial Decision October 18, 2018; Accepted October 19, 2018 ABSTRACT Fused in Sarcoma (FUS) and TAR DNA Binding Protein (TARDBP) (9–13). FUS is one of the three members of Understanding the molecular pathways disrupted in the structurally related FET (FUS, EWSR1 and TAF15) motor neuron diseases is urgently needed. Here, we family of RNA/DNA binding proteins (14). In addition to employed CRISPR knockout (KO) to investigate the the RNA/DNA binding domains, the FET proteins also functions of four ALS-causative RNA/DNA binding contain low-complexity domains, and these domains are proteins (FUS, EWSR1, TAF15 and MATR3) within the thought to be involved in ALS pathogenesis (5,15). In light RNAP II/U1 snRNP machinery. We found that each of of the discovery that mutations in FUS are ALS-causative, these structurally related proteins has distinct roles several groups carried out studies to determine whether the with FUS KO resulting in loss of U1 snRNP and the other two members of the FET family, TATA-Box Bind- SMN complex, EWSR1 KO causing dissociation of ing Protein Associated Factor 15 (TAF15) and EWS RNA the tRNA ligase complex, and TAF15 KO resulting in Binding Protein 1 (EWSR1), have a role in ALS.
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HLA-DPB1-COL11A2 and Three Additional Xmhc Loci Are Independently Associated with RA in a UK Cohort
Genes and Immunity (2011) 12, 169–175 & 2011 Macmillan Publishers Limited All rights reserved 1466-4879/11 www.nature.com/gene ORIGINAL ARTICLE HLA-DPB1-COL11A2 and three additional xMHC loci are independently associated with RA in a UK cohort G Orozco1, A Barton1, S Eyre1, B Ding2, J Worthington1,XKe1,3,4 and W Thomson1,4 1Arthritis Research UK Epidemiology Unit, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; 2Karolinska Institute, Stockholm, Sweden and 3Institute of Child Health, University College London, London, UK The aim of this study was to investigate the complex association pattern of the extended major histocompatibility complex (xMHC) region with rheumatoid arthritis (RA) susceptibility to identify effects independent of HLA-DRB1. A total of 1804 RA cases and 1474 controls were included. High-resolution HLA-DRB1 typing was performed. Subjects were genotyped for 1546 single-nucleotide polymorphisms (SNPs) using Affymetrix GeneChip 500 K (Santa Clara, CA, USA) as part of the Wellcome Trust Case Control Consortium Study. Statistical analysis was carried out using PLINK. To avoid confounding by RA- associated HLA-DRB1 alleles, we analyzed xMHC SNPs using a data set with pairwise matching of cases and controls on DRB1 genotypes. A total of 594 case–control pairs with identical DRB1 genotypes were identified. After this adjustment, 104 SNPs remained significantly associated with RA (Po0.05), suggesting that additional RA loci independent of HLA-DRB1 can be found in the xMHC region. Of these, four loci showed the strongest associations with RA (Po0.005): ZNF391, the olfactory receptor (OR) gene cluster, C6orf26-RDBP and HLA-DPB1-COL11A2.
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Hormone and Inhibitor Treatment T47DM Cells Were Used for All Experiments Unless Otherwise Stated
Extended Data Extended Materials Methods Cell culture; hormone and inhibitor treatment T47DM cells were used for all experiments unless otherwise stated. For hormone induction experiments, cells were grown in RPMI medium without Phenol Red, supplemented with 10% dextran-coated charcoal-treated FBS (DCC/FBS) after 24 h in serum-free conditions; cells were incubated with R5020 (10 nM) or vehicle (ethanol) as described (Vicent et al. 2011). For hormone induction experiments in MCF7 cells a similar procedure was performed; cells were grown in DMEM medium without Phenol Red, supplemented with 10% dextran-coated charcoal-treated FBS (DCC/FBS) after 24 h in serum-free conditions; cells were incubated with Estradiol (10 nM) or vehicle (ethanol). PARG and PARP inhibition were carried out via incubating cells with 5uM TA (tannic acid) or 10uM 3AB (3-amino-benzamide) respectively 1 hour prior to hormone treatment. All transfections were performed using Lipofectamine2000 (Invitrogen) according to manufacturers instructions. PAR-capture ELISA Hormone and or inhibitor treatments were carried out as described, and sample preparation was carried out as follows: At the required time point, cells were washed twice with ice-cold PBS and scraped in lysis buffer (0.4 M NaCl, 1% Triton X-100) plus protease inhibitors. Cell suspensions were then incubated for 30 min on ice with periodic vortexing. The disrupted cell suspension was centrifuged at 10,000g for 10 min at 4°C, and the supernatant was recovered, snap-frozen, and stored at 80°C until required. Ninety-six-well black-walled plates were incubated with 2 ng/mL anti-PAR monoclonal antibody (Trevigen) in 50 mM sodium carbonate (pH 7.6) overnight at 4°C.
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Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress
University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations Fall 2010 Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress Renuka Nayak University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Computational Biology Commons, and the Genomics Commons Recommended Citation Nayak, Renuka, "Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress" (2010). Publicly Accessible Penn Dissertations. 1559. https://repository.upenn.edu/edissertations/1559 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/1559 For more information, please contact [email protected]. Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress Abstract Genes interact in networks to orchestrate cellular processes. Here, we used coexpression networks based on natural variation in gene expression to study the functions and interactions of human genes. We asked how these networks change in response to stress. First, we studied human coexpression networks at baseline. We constructed networks by identifying correlations in expression levels of 8.9 million gene pairs in immortalized B cells from 295 individuals comprising three independent samples. The resulting networks allowed us to infer interactions between biological processes. We used the network to predict the functions of poorly-characterized human genes, and provided some experimental support. Examining genes implicated in disease, we found that IFIH1, a diabetes susceptibility gene, interacts with YES1, which affects glucose transport. Genes predisposing to the same diseases are clustered non-randomly in the network, suggesting that the network may be used to identify candidate genes that influence disease susceptibility.
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