Rhoj Interacts with the GIT–PIX Complex and Regulates Focal
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Transcriptome Analyses of Rhesus Monkey Pre-Implantation Embryos Reveal A
Downloaded from genome.cshlp.org on September 23, 2021 - Published by Cold Spring Harbor Laboratory Press Transcriptome analyses of rhesus monkey pre-implantation embryos reveal a reduced capacity for DNA double strand break (DSB) repair in primate oocytes and early embryos Xinyi Wang 1,3,4,5*, Denghui Liu 2,4*, Dajian He 1,3,4,5, Shengbao Suo 2,4, Xian Xia 2,4, Xiechao He1,3,6, Jing-Dong J. Han2#, Ping Zheng1,3,6# Running title: reduced DNA DSB repair in monkey early embryos Affiliations: 1 State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650223, China 2 Key Laboratory of Computational Biology, CAS Center for Excellence in Molecular Cell Science, Collaborative Innovation Center for Genetics and Developmental Biology, Chinese Academy of Sciences-Max Planck Partner Institute for Computational Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China 3 Yunnan Key Laboratory of Animal Reproduction, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650223, China 4 University of Chinese Academy of Sciences, Beijing, China 5 Kunming College of Life Science, University of Chinese Academy of Sciences, Kunming, Yunnan 650204, China 6 Primate Research Center, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China * Xinyi Wang and Denghui Liu contributed equally to this work 1 Downloaded from genome.cshlp.org on September 23, 2021 - Published by Cold Spring Harbor Laboratory Press # Correspondence: Jing-Dong J. Han, Email: [email protected]; Ping Zheng, Email: [email protected] Key words: rhesus monkey, pre-implantation embryo, DNA damage 2 Downloaded from genome.cshlp.org on September 23, 2021 - Published by Cold Spring Harbor Laboratory Press ABSTRACT Pre-implantation embryogenesis encompasses several critical events including genome reprogramming, zygotic genome activation (ZGA) and cell fate commitment. -
Title: Therapeutic Potential of HSP90 Inhibition for Neurofibromatosis Type 2
Author Manuscript Published OnlineFirst on May 28, 2013; DOI: 10.1158/1078-0432.CCR-12-3167 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Title: Therapeutic Potential of HSP90 Inhibition for Neurofibromatosis type 2 Karo Tanaka1, Ascia Eskin3, Fabrice Chareyre1, Walter J. Jessen4, Jan Manent5, Michiko Niwa-Kawakita6, Ruihong Chen7, Cory H. White2, Jeremie Vitte1, Zahara M. Jaffer1, Stanley F. Nelson3, Allan E. Rubenstein8, Marco Giovannini1,9§. Authors’ affiliations: House Research Institute, 1Center for Neural Tumor Research and 2Section on Genetics of Hereditary Ear Disorders, Los Angeles, CA; 3Department of Human Genetics, University of California, Los Angeles, CA; 4Informatics, Covance Inc., Princeton, NJ; 5Peter MacCallum Cancer Institute, Melbourne, Australia; 6Inserm U944, CNRS U7212, Université Paris, Institut Universitaire d'Hématologie, Paris, France; 7NexGenix Pharmaceuticals, Burlingame, CA; and 8New York University Langone Medical Center, New York, NY; and Department of Cell and Neurobiology, University of Southern California, Keck School of Medicine, Los Angeles, CA Running title: HSP90 Inhibition for NF2 Keywords: NF2, HSP90 inhibitors, Transcriptome Financial support: This work was supported by a Drug Discovery Initiative Award, Children’s Tumor Foundation, to M.G., and by the House Research Institute. Corresponding author: Marco Giovannini, House Research Institute, Center for Neural Tumor Research, 2100 West 3rd street, Los Angeles, CA90057. Phone: +1-213-989-6708; Fax: +1-213-989-6778; E-mail: [email protected] 1 Downloaded from clincancerres.aacrjournals.org on September 30, 2021. © 2013 American Association for Cancer Research. Author Manuscript Published OnlineFirst on May 28, 2013; DOI: 10.1158/1078-0432.CCR-12-3167 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. -
1 Genome-Wide Comparisons of Variation in Linkage Disequilibrium
Downloaded from genome.cshlp.org on September 30, 2021 - Published by Cold Spring Harbor Laboratory Press Genome-wide comparisons of variation in linkage disequilibrium Yik Y. Teo1,*, Andrew E. Fry1, Kanishka Bhattacharya1, Kerrin S. Small1, Dominic P. Kwiatkowski1,2, Taane G. Clark1,2 1 Wellcome Trust Centre for Human Genetics, University of Oxford, United Kingdom 2 Wellcome Trust Sanger Institute, Hinxton, United Kingdom Running title: Genome-wide comparisons of LD Keywords: linkage disequilibrium, imputation, positive selection, meta-analysis, genome-wide association study * Corresponding author: Wellcome Trust Centre for Human Genetics, Roosevelt Drive, Oxford OX3 7BN, United Kingdom. Email: [email protected], phone: +44 1865 287712, fax: +44 1865 287 501. ABSTRACT Current genome-wide surveys of common diseases and complex traits fundamentally aim to detect indirect associations where the SNPs carrying the association signals are not biologically active but are in linkage disequilibrium (LD) with some unknown functional polymorphisms. Reproducing any novel discoveries from these genome-wide scans in independent studies is now a prerequisite for the putative findings to be accepted. Significant differences in patterns of LD between populations can affect the portability of phenotypic associations when the replication effort or meta-analyses are attempted in populations that are distinct from the original population which the genome-wide study is performed in. Here we introduce a novel method for genome-wide analyses of LD variations between populations that allow the identification of candidate regions with different patterns of LD. The evidence of LD variation provided by the introduced method correlated with the degree of differences in the frequencies of the most common haplotype across the populations. -
A Novel De Novo Microdeletion at 17Q11.2 Adjacent to NF1 Gene
Xie et al. Molecular Cytogenetics (2016) 9:41 DOI 10.1186/s13039-016-0251-y CASEREPORT Open Access A novel de novo microdeletion at 17q11.2 adjacent to NF1 gene associated with developmental delay, short stature, microcephaly and dysmorphic features Bobo Xie1, Xin Fan1, Yaqin Lei1, Rongyu Chen1, Jin Wang1, Chunyun Fu1, Shang Yi1, Jingsi Luo1, Shujie Zhang1, Qi Yang1, Shaoke Chen1* and Yiping Shen1,2* Abstract Background: Microdeletions at 17q11.2 often encompass NF1 gene, is the cause for NF1 microdeletion syndrome. Microdeletion at 17q11.2 without the involvement of NF1 gene is rarely reported. Case presentation: Here we reported a patient carrying a novel de novo deletion at 17q11.2 adjacent to NF1 gene, who presented with developmental delay, short stature, postnatal microcephaly, underweight and dysmorphic features including flat facial profile, dolicocephaly, hypertelorism, short philtrum, flat nasal bridge and posteriorly rotated and low set ears. Chromosomal microarray analysis revealed a 1.69 Mb de novo deletion at 17q11.2 adjacent to NF1 gene, which involves 43 RefSeq genes. We compared this with four overlapping deletions at this interval. Conclusions: Ararede novo microdeletion at 17q11.2 not involving NF1 gene is associated with developmental delay and dysmorphic features. Seven genes, TAOK1, PHF12, NUFIP2, SLC26A4, SEZ6, GIT1 and TRAF4 are possible candidates for the clinical features of our patient. The delineation of this rare deletion and description of associated clinical phenotypes will help to understand the genotype-phenotype correlation of genomic imbalances at this locus. Keywords: Developmental delay, Short stature, Microcephaly, Chromosomal microarray, SNP array, 17q11.2, Microdeletion Background 1 (NF1) [4]. -
Multidimensional Informatic Deconvolution Defines Gender
Mechanisms of Ageing and Development 184 (2019) 111150 Contents lists available at ScienceDirect Mechanisms of Ageing and Development journal homepage: www.elsevier.com/locate/mechagedev Multidimensional informatic deconvolution defines gender-specific roles of hypothalamic GIT2 in aging trajectories T Jaana van Gastela, Huan Caib, Wei-Na Congb, Wayne Chadwickc, Caitlin Daimonb, Hanne Leysena, Jhana O. Hendrickxa, Robin De Scheppera, Laura Vangenechtena, Jens Van Turnhouta, Jasper Verswyvela, Kevin G. Beckerd, Yongqing Zhangd, Elin Lehrmannd, William H. Wood IIId, Bronwen Martinb,e,**,1, Stuart Maudsleya,c,*,1 a Receptor Biology Lab, Department of Biomedical Sciences, University of Antwerp, 2610, Wilrijk, Belgium b Metabolism Unit, Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Biomedical Research Center, 251 Bayview Boulevard, Baltimore, MD, 21224, United States c Receptor Pharmacology Unit, Laboratory of Neuroscience, National Institute on Aging, National Institutes of Health, Biomedical Research Center, 251 Bayview Boulevard, Baltimore, MD, 21224, United States d Gene Expression and Genomics Unit, Laboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Biomedical Research Center, 251 Bayview Boulevard, Baltimore, MD, 21224, United States e Faculty of Pharmacy, Biomedical and Veterinary Sciences, University of Antwerp, 2610, Wilrijk, Belgium ARTICLE INFO ABSTRACT Keywords: In most species, females live longer than males. An understanding of this female longevity advantage will likely GIT2 uncover novel anti-aging therapeutic targets. Here we investigated the transcriptomic responses in the hy- Longevity pothalamus – a key organ for somatic aging control – to the introduction of a simple aging-related molecular Aging perturbation, i.e. GIT2 heterozygosity. Our previous work has demonstrated that GIT2 acts as a network con- Female troller of aging. -
NRF1) Coordinates Changes in the Transcriptional and Chromatin Landscape Affecting Development and Progression of Invasive Breast Cancer
Florida International University FIU Digital Commons FIU Electronic Theses and Dissertations University Graduate School 11-7-2018 Decipher Mechanisms by which Nuclear Respiratory Factor One (NRF1) Coordinates Changes in the Transcriptional and Chromatin Landscape Affecting Development and Progression of Invasive Breast Cancer Jairo Ramos [email protected] Follow this and additional works at: https://digitalcommons.fiu.edu/etd Part of the Clinical Epidemiology Commons Recommended Citation Ramos, Jairo, "Decipher Mechanisms by which Nuclear Respiratory Factor One (NRF1) Coordinates Changes in the Transcriptional and Chromatin Landscape Affecting Development and Progression of Invasive Breast Cancer" (2018). FIU Electronic Theses and Dissertations. 3872. https://digitalcommons.fiu.edu/etd/3872 This work is brought to you for free and open access by the University Graduate School at FIU Digital Commons. It has been accepted for inclusion in FIU Electronic Theses and Dissertations by an authorized administrator of FIU Digital Commons. For more information, please contact [email protected]. FLORIDA INTERNATIONAL UNIVERSITY Miami, Florida DECIPHER MECHANISMS BY WHICH NUCLEAR RESPIRATORY FACTOR ONE (NRF1) COORDINATES CHANGES IN THE TRANSCRIPTIONAL AND CHROMATIN LANDSCAPE AFFECTING DEVELOPMENT AND PROGRESSION OF INVASIVE BREAST CANCER A dissertation submitted in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY in PUBLIC HEALTH by Jairo Ramos 2018 To: Dean Tomás R. Guilarte Robert Stempel College of Public Health and Social Work This dissertation, Written by Jairo Ramos, and entitled Decipher Mechanisms by Which Nuclear Respiratory Factor One (NRF1) Coordinates Changes in the Transcriptional and Chromatin Landscape Affecting Development and Progression of Invasive Breast Cancer, having been approved in respect to style and intellectual content, is referred to you for judgment. -
The Human Gene Connectome As a Map of Short Cuts for Morbid Allele Discovery
The human gene connectome as a map of short cuts for morbid allele discovery Yuval Itana,1, Shen-Ying Zhanga,b, Guillaume Vogta,b, Avinash Abhyankara, Melina Hermana, Patrick Nitschkec, Dror Friedd, Lluis Quintana-Murcie, Laurent Abela,b, and Jean-Laurent Casanovaa,b,f aSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065; bLaboratory of Human Genetics of Infectious Diseases, Necker Branch, Paris Descartes University, Institut National de la Santé et de la Recherche Médicale U980, Necker Medical School, 75015 Paris, France; cPlateforme Bioinformatique, Université Paris Descartes, 75116 Paris, France; dDepartment of Computer Science, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel; eUnit of Human Evolutionary Genetics, Centre National de la Recherche Scientifique, Unité de Recherche Associée 3012, Institut Pasteur, F-75015 Paris, France; and fPediatric Immunology-Hematology Unit, Necker Hospital for Sick Children, 75015 Paris, France Edited* by Bruce Beutler, University of Texas Southwestern Medical Center, Dallas, TX, and approved February 15, 2013 (received for review October 19, 2012) High-throughput genomic data reveal thousands of gene variants to detect a single mutated gene, with the other polymorphic genes per patient, and it is often difficult to determine which of these being of less interest. This goes some way to explaining why, variants underlies disease in a given individual. However, at the despite the abundance of NGS data, the discovery of disease- population level, there may be some degree of phenotypic homo- causing alleles from such data remains somewhat limited. geneity, with alterations of specific physiological pathways under- We developed the human gene connectome (HGC) to over- come this problem. -
And Calcium PIX Proteins Β the Concerted Action of GIT1/ Derived Mast Cells Is Regulated by − Marrow Microtubule Nucleation I
Published March 27, 2015, doi:10.4049/jimmunol.1402459 The Journal of Immunology Microtubule Nucleation in Mouse Bone Marrow–Derived Mast Cells Is Regulated by the Concerted Action of GIT1/ bPIX Proteins and Calcium Vadym Sulimenko,* Zuzana Ha´jkova´,*,† Marke´ta Cernohorska ´,*,† Tetyana Sulimenko,* Vladimı´ra Sla´dkova´,* Lubica Dra´berova´,‡ Stanislav Vinopal,* Eduarda Dra´berova´,* and Pavel Dra´ber* Ag-mediated activation of mast cells initiates signaling events leading to Ca2+ response, release of allergic mediators from cytoplasmic granules, and synthesis of cytokines and chemokines. Although microtubule rearrangement during activation has been described, the molecular mechanisms that control their remodeling are largely unknown. Microtubule nucleation is mediated by complexes that are formed by g-tubulin and g-tubulin complex proteins. In this study, we report that, in bone marrow–derived mast cells (BMMCs), g-tubulin interacts with p21-activated kinase interacting exchange factor b (bPIX) and G protein–coupled receptor kinase-interacting protein (GIT)1. Microtubule regrowth experiments showed that the depletion of bPIX in BMMCs stimulated microtubule nucleation, whereas depletion of GIT1 led to the inhibition of nucleation compared with control cells. Phenotypic rescue experiments confirmed that bPIX and GIT1 represent negative and positive regulators of microtubule nucle- ation in BMMCs, respectively. Live-cell imaging disclosed that both proteins are associated with centrosomes. Immunoprecipi- tation and pull-down experiments revealed that an enhanced level of free cytosolic Ca2+ affects g-tubulin properties and stimulates the association of GIT1 and g-tubulin complex proteins with g-tubulin. Microtubule nucleation also was affected by Ca2+ level. Moreover, in activated BMMCs, g-tubulin formed complexes with tyrosine-phosphorylated GIT1. -
GIT2 (NM 139201) Human Tagged ORF Clone – RC200045 | Origene
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for RC200045 GIT2 (NM_139201) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: GIT2 (NM_139201) Human Tagged ORF Clone Tag: Myc-DDK Symbol: GIT2 Synonyms: CAT-2; CAT2; PKL Vector: pCMV6-Entry (PS100001) E. coli Selection: Kanamycin (25 ug/mL) Cell Selection: Neomycin This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 6 GIT2 (NM_139201) Human Tagged ORF Clone – RC200045 ORF Nucleotide >RC200045 ORF sequence Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGTCGAAACGGCTCCGGAGCAGCGAGGTGTGCGCTGACTGCAGCGGGCCGGATCCTTCCTGGGCATCAG TAAATAGGGGAACGTTTTTATGTGATGAGTGCTGCAGTGTCCATCGGAGTCTAGGGCGCCATATCTCCCA AGTGAGGCATCTGAAACACACACCGTGGCCTCCAACACTGCTTCAGATGGTTGAGACCTTGTATAATAAC GGTGCTAACTCTATATGGGAGCATTCTTTGCTGGACCCTGCGTCTATTATGAGTGGAAGACGTAAAGCTA ATCCACAGGATAAAGTACATCCCAATAAAGCGGAATTCATCAGAGCCAAGTATCAGATGTTAGCGTTCGT CCATCGCTTGCCCTGCCGGGATGACGATAGTGTGACTGCCAAAGATCTTAGCAAGCAACTCCATTCGAGC GTGAGAACAGGGAATCTTGAAACCTGTTTGAGACTGTTATCTTTAGGAGCACAAGCCAACTTCTTTCATC CTGAAAAAGGAAACACCCCACTCCATGTTGCCTCCAAAGCAGGGCAGATTTTACAGGCTGAATTATTGGC AGTATATGGAGCAGACCCAGGCACACAGGATTCTAGTGGGAAAACTCCCGTTGATTATGCAAGGCAAGGA -
Oxidized Phospholipids Regulate Amino Acid Metabolism Through MTHFD2 to Facilitate Nucleotide Release in Endothelial Cells
ARTICLE DOI: 10.1038/s41467-018-04602-0 OPEN Oxidized phospholipids regulate amino acid metabolism through MTHFD2 to facilitate nucleotide release in endothelial cells Juliane Hitzel1,2, Eunjee Lee3,4, Yi Zhang 3,5,Sofia Iris Bibli2,6, Xiaogang Li7, Sven Zukunft 2,6, Beatrice Pflüger1,2, Jiong Hu2,6, Christoph Schürmann1,2, Andrea Estefania Vasconez1,2, James A. Oo1,2, Adelheid Kratzer8,9, Sandeep Kumar 10, Flávia Rezende1,2, Ivana Josipovic1,2, Dominique Thomas11, Hector Giral8,9, Yannick Schreiber12, Gerd Geisslinger11,12, Christian Fork1,2, Xia Yang13, Fragiska Sigala14, Casey E. Romanoski15, Jens Kroll7, Hanjoong Jo 10, Ulf Landmesser8,9,16, Aldons J. Lusis17, 1234567890():,; Dmitry Namgaladze18, Ingrid Fleming2,6, Matthias S. Leisegang1,2, Jun Zhu 3,4 & Ralf P. Brandes1,2 Oxidized phospholipids (oxPAPC) induce endothelial dysfunction and atherosclerosis. Here we show that oxPAPC induce a gene network regulating serine-glycine metabolism with the mitochondrial methylenetetrahydrofolate dehydrogenase/cyclohydrolase (MTHFD2) as a cau- sal regulator using integrative network modeling and Bayesian network analysis in human aortic endothelial cells. The cluster is activated in human plaque material and by atherogenic lipo- proteins isolated from plasma of patients with coronary artery disease (CAD). Single nucleotide polymorphisms (SNPs) within the MTHFD2-controlled cluster associate with CAD. The MTHFD2-controlled cluster redirects metabolism to glycine synthesis to replenish purine nucleotides. Since endothelial cells secrete purines in response to oxPAPC, the MTHFD2- controlled response maintains endothelial ATP. Accordingly, MTHFD2-dependent glycine synthesis is a prerequisite for angiogenesis. Thus, we propose that endothelial cells undergo MTHFD2-mediated reprogramming toward serine-glycine and mitochondrial one-carbon metabolism to compensate for the loss of ATP in response to oxPAPC during atherosclerosis. -
GIT/PIX Condensates Are Modular and Ideal for Distinct Compartmentalized Cell Signaling
Article GIT/PIX Condensates Are Modular and Ideal for Distinct Compartmentalized Cell Signaling Graphical Abstract Authors Jinwei Zhu, Qingqing Zhou, Yitian Xia, ..., Mengjuan Peng, Rongguang Zhang, Mingjie Zhang Correspondence [email protected] (J.Z.), [email protected] (R.Z.), [email protected] (M.Z.) In Brief Cells often concentrate limited amounts of enzymes at specific subcellular regions for distinct functions. Zhu et al. show that the small GTPase regulatory enzymes GIT and PIX autonomously form phase- separated condensates without the need for scaffolding molecules. GIT/PIX condensates are modular and positioned at specific cellular compartments for distinct signaling. Highlights d Small GTPase regulatory enzymes GIT and PIX bind to each other very tightly d The GIT/PIX complex forms highly concentrated condensates via phase separation d Formation of GIT/PIX condensates does not require other scaffold molecules d GIT/PIX condensates are modular for signaling in distinct cellular compartments Zhu et al., 2020, Molecular Cell 79, 1–15 September 3, 2020 ª 2020 Elsevier Inc. https://doi.org/10.1016/j.molcel.2020.07.004 ll Please cite this article in press as: Zhu et al., GIT/PIX Condensates Are Modular and Ideal for Distinct Compartmentalized Cell Signaling, Molecular Cell (2020), https://doi.org/10.1016/j.molcel.2020.07.004 ll Article GIT/PIX Condensates Are Modular and Ideal for Distinct Compartmentalized Cell Signaling Jinwei Zhu,1,2,6,* Qingqing Zhou,3,6 Yitian Xia,1 Lin Lin,1,2 Jianchao Li,3 Mengjuan Peng,1,4 Rongguang Zhang,1,4,* -
Toward an Understanding of the Protein Interaction Network of the Human Liver
Molecular Systems Biology 7; Article number 536; doi:10.1038/msb.2011.67 Citation: Molecular Systems Biology 7: 536 & 2011 EMBO and Macmillan Publishers Limited All rights reserved 1744-4292/11 www.molecularsystemsbiology.com REPORT Toward an understanding of the protein interaction network of the human liver Jian Wang1,6, Keke Huo2,6, Lixin Ma3,6, Liujun Tang1,6, Dong Li1,6, Xiaobi Huang1, Yanzhi Yuan1, Chunhua Li3, Wei Wang2, Wei Guan1, Hui Chen1, Chaozhi Jin1, Junchen Wei1, Wanqiao Zhang1, Yongsheng Yang1, Qiongming Liu1, Ying Zhou1, Cuili Zhang1, Zhihao Wu1, Wangxiang Xu1, Ying Zhang1, Tao Liu1, Donghui Yu1, Yaping Zhang1, Liang Chen3, Dewu Zhu3, Xing Zhong3, Lixin Kang3, Xiang Gan3, Xiaolan Yu3,QiMa2, Jing Yan2, Li Zhou2, Zhongyang Liu1, Yunping Zhu1, Tao Zhou4, Fuchu He1,5,* and Xiaoming Yang1,* 1 State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China, 2 State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China, 3 Institute of Biochemistry and Molecular Biology, Hubei University, Wuhan, China, 4 National Center of Biomedical Analysis, Beijing, China and 5 Institutes of Biomedical Sciences, Fudan University, Shanghai, China 6 These authors contributed equally to this work * Corresponding author. X Yang or F He, State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, No. 33, Life Science Park Road, Changping District, Beijing 102206, China. Tel.:/Fax: þ 86 106 817 6833; E-mail: [email protected] or Tel.:/Fax: þ 86 108 070 5155; E-mail: [email protected] Received 4.4.11; accepted 5.8.11 Proteome-scale protein interaction maps are available for many organisms, ranging from bacteria, yeast, worms and flies to humans.