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StratRe fvsMCF 7- StratRefvs Scramb StratRefvs MCF7- led MCF7- GID UNIQID NAME SiRNA siRNA untreated AID ARRY1X ARRY2XARRY0X GENE137XR21955 R21955::DNM3::Dynamin 3 10.99 -5.371 -5.618 GENE372XAA437224 AA437224::NKX3-1::NK3 transcription factor related, locus 1 (Drosophila) 4.542 -1.942 -2.6 GENE428XAI686398 AI686398::NEFH::Neurofilament, heavy polypeptide 200kDa 4.47 -3.078 -1.391 GENE438XN24046 N24046::Transcribed locus 4.455 -2.147 -2.308 GENE425XW46575 W46575 4.44 -2.12 -2.32 GENE108XAA862465 AA862465::AZGP1::Alpha-2-glycoprotein 1, zinc 4.404 -2.465 -1.939 GENE426XAI658727 AI658727::MSMB::Microseminoprotein, beta- 4.344 -2.53 -1.814 GENE410XAI220580 AI220580::TCF20::Transcription factor 20 (AR1) 4.23 -2.06 -2.17 GENE371XT59658 T59658::ANTXR2::Anthrax toxin receptor 2 3.994 -2.146 -1.848 GENE26X AA490694 AA490694::SPARCL1::SPARC-like 1 (mast9, hevin) 3.925 -2.137 -1.788 GENE80X AA032221 AA032221::STEAP::Six transmembrane epithelial antigen of the prostate 1 3.845 -1.905 -1.941 GENE324XAA446859 AA446859::EDG7::Endothelial differentiation, lysophosphatidic acid G-protein-coupled receptor,3.779 7-1.752 -2.027 GENE422XAA677165 AA677165::Similar to Zinc-alpha-2-glycoprotein precursor (Zn-alpha-2-glycoprotein) (Zn-alpha-2-GP)3.77 -1.938 -1.832 GENE277XAA488070 AA488070 3.712 -2.163 -1.549 GENE38X AA436184 AA436184::KCNJ8::Potassium inwardly-rectifying channel, subfamily J, member 8 3.705 -2.467 -1.238 GENE362XTOPOII TOPOII 3.608 -1.788 -1.819 GENE361XNM_001648NM_001648::KLK3::Kallikrein 3, (prostate specific antigen) 3.507 -1.537 -1.97 GENE224XAA620973 AA620973::Transcribed locus 3.493 -1.213 -2.28 GENE48X R98851 R98851::MME::Membrane metallo-endopeptidase (neutral endopeptidase, enkephalinase,3.438 CALLA,-2.115 CD10) -1.323 GENE16X W70234 W70234::DPP4::Dipeptidylpeptidase 4 (CD26, adenosine deaminase complexing protein 2)3.34 -1.883 -1.457 GENE403XAA159194 AA159194::FAT::FAT tumor suppressor homolog 1 (Drosophila) 3.338 -1.873 -1.465 GENE252XN50880 N50880::TARP::T cell receptor gamma variable 9 3.318 -0.935 -2.384 GENE439XN34288 N34288 3.28 -1.342 -1.938 GENE236XAA883127 AA883127 3.27 -1.982 -1.288 GENE198XH95960 H95960::SPARC::Secreted protein, acidic, cysteine-rich (osteonectin) 3.257 -1.505 -1.752 GENE270XH78999 H78999::DCBLD2::Discoidin, CUB and LCCL domain containing 2 3.229 -1.74 -1.489 GENE322XAI079397 AI079397::Transcribed locus, weakly similar to XP_209041.2 PREDICTED: similar to KIAA15033.148 protein-1.546 [Homo-1.602 sapiens] GENE377XAA877166 AA877166::MYL9::Myosin, light polypeptide 9, regulatory 3.059 -1.755 -1.304 GENE300XH51574 H51574::ALOX5::Arachidonate 5-lipoxygenase 3.017 -1.59 -1.426 GENE174XAA598830 AA598830::NBL1::Neuroblastoma, suppression of tumorigenicity 1 3.001 -1.644 -1.357 GENE328XAI086086 AI086086::MBNL3::Muscleblind-like 3 (Drosophila) 2.988 -1.515 -1.473 GENE52X AA070226 AA070226::SEPP1::Selenoprotein P, plasma, 1 2.983 -1.315 -1.668 GENE302XT98612 T98612::COL3A1::Collagen, type III, alpha 1 (Ehlers-Danlos syndrome type IV, autosomal2.955 dominant)-1.693 -1.262 GENE363XR46712 R46712::SEC31L1::SEC31-like 1 (S. cerevisiae) 2.945 -1.281 -1.664 GENE374XR23270 R23270::Transcribed locus 2.933 -1.387 -1.546 GENE254XN49949 N49949::PDE8B::Phosphodiesterase 8B 2.933 -1.354 -1.579 GENE129XH63077 H63077::ANXA1::Annexin A1 2.931 -1.333 -1.597 GENE456XAI688014 AI688014::CASC3::Cancer susceptibility candidate 3 2.922 -1.838 -1.084 GENE225XAA417956 AA417956::FLJ38973::Hypothetical protein FLJ38973 2.893 -1.951 -0.9414 GENE267XT68892 T68892 2.884 -1.334 -1.55 GENE47X AA774649 AA774649::C1orf24::Chromosome 1 open reading frame 24 2.87 -1.38 -1.49 GENE268XAA931428 AA931428::FLJ36766::Hypothetical protein FLJ36766 2.854 -1.508 -1.346 GENE185XAA456394 AA456394::FHL1::Four and a half LIM domains 1 2.854 -1.615 -1.239 GENE398XH08560 H08560::IGFBP5::Insulin-like growth factor binding protein 5 2.82 -1.483 -1.337 GENE260XAA683077 AA683077::MAPK1::Mitogen-activated protein kinase 1 2.809 -1.381 -1.428 GENE218XAA904872 AA904872 2.804 -1.3 -1.505 GENE91X AA664101 AA664101::ALDH1A1::Aldehyde dehydrogenase 1 family, member A1 2.804 -2.227 -0.5769 GENE197XAA663884 AA663884::SNAP25::Synaptosomal-associated protein, 25kDa 2.791 -1.146 -1.645 GENE11X N29986 N29986 2.779 -1.195 -1.583 GENE119X AA040877 AA040877::C9orf90::Chromosome 9 open reading frame 90 2.778 -1.148 -1.631 GENE117X AA035639 AA035639::SET7::SET domain-containing protein 7 2.774 -1.19 -1.584 GENE32X N40180 N40180 2.764 -1.3 -1.464 GENE294XAA910836 AA910836::ANKH::Ankylosis, progressive homolog (mouse) 2.762 -2.061 -0.7013 GENE304XAA160507 AA160507::KRT5::Keratin 5 (epidermolysis bullosa simplex, Dowling-Meara/Kobner/Weber-Cockayne2.744 -1.407 types)-1.337 GENE366XAA700604 AA700604::Similar to Sorbitol dehydrogenase (L-iditol 2-dehydrogenase) 2.729 -1.02 -1.709 GENE452XAI674349 AI674349::TSPAN1::Tetraspanin 1 2.699 -1.552 -1.147 GENE90X AA668470 AA668470::RGS5::Regulator of G-protein signalling 5 2.696 -1.861 -0.8347 GENE154XAA401433 AA401433::NUDT10::Nudix (nucleoside diphosphate linked moiety X)-type motif 10 2.692 -1.166 -1.526 GENE434XAI301564 AI301564 2.685 -1.831 -0.8537 GENE454XAA732787 AA732787::PDE8B::Phosphodiesterase 8B 2.682 -1.674 -1.008 GENE320XR44353 R44353 2.661 -1.09 -1.572 GENE247XH57273 H57273 2.621 -1.303 -1.318 GENE381XAI214400 AI214400 2.612 -1.454 -1.158 GENE283XAA894557 AA894557::CKB::Creatine kinase, brain 2.61 -1.535 -1.076 GENE212XT57920 T57920::SGCD::Sarcoglycan, delta (35kDa dystrophin-associated glycoprotein) 2.607 -1.347 -1.261 GENE401XR64391 R64391 2.605 -1.568 -1.037 GENE200XAA634028 AA634028::HLA-DPA1::Major histocompatibility complex, class II, DP alpha 1 2.605 -1.244 -1.361 GENE234XAA757723 AA757723 2.602 -1.12 -1.483 GENE367XAI219094 AI219094::ChGn::Chondroitin beta1,4 N-acetylgalactosaminyltransferase 2.601 -1.283 -1.318 GENE106XAA972352 AA972352::PDLIM3::PDZ and LIM domain 3 2.598 -1.604 -0.9938 GENE301XT98612 T98612::COL3A1::Collagen, type III, alpha 1 (Ehlers-Danlos syndrome type IV, autosomal2.593 dominant)-1.644 -0.9484 GENE352XAA488466 AA488466::DRG1::Developmentally regulated GTP binding protein 1 2.584 -1.103 -1.481 GENE89X H81907 H81907::ANKH::Ankylosis, progressive homolog (mouse) 2.579 -1.133 -1.446 GENE25X AA043501 AA043501::MAF::V-maf musculoaponeurotic fibrosarcoma oncogene homolog (avian) 2.558 -1.276 -1.282 GENE384XAA131421 AA131421::MARCKS::Myristoylated alanine-rich protein kinase C substrate 2.55 -1.03 -1.52 GENE379XR89356 R89356::GYPA::Glycophorin A (includes MN blood group) 2.527 -1.604 -0.9237 GENE94X N47524 N47524::ANKH::Ankylosis, progressive homolog (mouse) 2.517 -1.375 -1.142 GENE287XAA903389 AA903389::TRIM5::Tripartite motif-containing 5 2.511 -1.325 -1.187 GENE24X H82081 H82081::RAB3-GAP150::Rab3 GTPase-activating protein, non-catalytic subunit (150kD) 2.51 -1.146 -1.364 GENE128XR05336 R05336 2.504 -1.193 -1.311 GENE186XAI242205 AI242205::Transcribed locus 2.495 -1.36 -1.135 GENE157XR24055 R24055 2.492 -1.555 -0.9366 GENE210XN24076 N24076::OSBPL3::Oxysterol binding protein-like 3 2.489 -1.533 -0.9564 GENE411X AI225111 AI225111::GJB3::Gap junction protein, beta 3, 31kDa (connexin 31) 2.488 -1.305 -1.184 GENE349XN62278 N62278 2.487 -1.407 -1.08 GENE98X AA459944 AA459944 2.483 -1.255 -1.228 GENE251XAA872454 AA872454::NOR1::Oxidored-nitro domain-containing protein 2.48 -1.284 -1.196 GENE166XAA701944 AA701944::TRA2A::Transformer-2 alpha 2.475 -1.139 -1.336 GENE330XAA458578 AA458578::NEDD4L::Neural precursor cell expressed, developmentally down-regulated 4-like2.473 -1.312 -1.161 GENE187XAA701285 AA701285 2.472 -1.523 -0.9493 GENE348XAA888213 AA888213::RNASE4::Angiogenin, ribonuclease, RNase A family, 5 2.468 -1.399 -1.068 GENE382XAA702329 AA702329 2.465 -1.471 -0.9934 GENE179XAA706769 AA706769 2.465 -1.341 -1.125 GENE142XT64955 T64955 2.465 -1.42 -1.045 GENE169XN50811 N50811 2.46 -1.008 -1.452 GENE99X AA412049 AA412049::Hypothetical gene supported by AY338954 2.452 -1.44 -1.012 GENE49X AA453712 AA453712::LUM::Lumican 2.437 -1.487 -0.9499 GENE77X AA425947 AA425947::DKK3::Dickkopf homolog 3 (Xenopus laevis) 2.436 -1.444 -0.9923 GENE383XAA142913 AA142913::ARGBP2::Arg/Abl-interacting protein ArgBP2 2.429 -1.101 -1.328 GENE62X AA192547 AA192547::GPD1::Glycerol-3-phosphate dehydrogenase 1 (soluble) 2.426 -1.519 -0.9071 GENE126XAA406242 AA406242::GMPR::Guanosine monophosphate reductase 2.425 -1.267 -1.158 GENE387XH38864 H38864 2.422 -0.985 -1.437 GENE390XAI261505 AI261505::Similar to Ribosome biogenesis protein BMS1 homolog 2.418 -1.179 -1.239 GENE95X H94497 H94497 2.414 -1.297 -1.117 GENE327XAA872383 AA872383::MT1E::Metallothionein 1E (functional) 2.408 -1.328 -1.08 GENE293XAA703519 AA703519 2.406 -1.381 -1.025 GENE414XN51239 N51239::CDNA FLJ45259 fis, clone BRHIP2020695 2.401 -1.807 -0.5933 GENE124XAA419108 AA419108::ANXA4::Annexin A4 2.395 -1.52 -0.8757 GENE272XAA988630 AA988630::Full length insert cDNA clone ZD69D05 2.385 -1.572 -0.8128 GENE18X H80749 H80749::ZNF532::Zinc finger protein 532 2.385 -1.191 -1.194 GENE165XAA055440 AA055440::SPRY1::Sprouty homolog 1, antagonist of FGF signaling (Drosophila) 2.375 -1.51 -0.8652 GENE265XAA456135 AA456135::CDNA FLJ37631 fis, clone BRCOC2015944 2.37 -1.223 -1.147 GENE402Xmissing361 missing361 2.368 -0.79 -1.579 GENE343XAA701475 AA701475::FMO5::Flavin containing monooxygenase 5 2.356 -1.461 -0.8948 GENE449XAI675889 AI675889::NPY::Neuropeptide Y 2.349 -1.414 -0.9353 GENE275XR51354 R51354::CNTNAP2::Contactin associated protein-like 2 2.349 -1.248 -1.101 GENE451XAI675311 AI675311::TPSB2::Tryptase alpha/beta 1 2.347 -1.127 -1.22 GENE468XH53340 H53340::MT1G::Metallothionein
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  • Non-Muscle Myosin 2A (NM2A): Structure, Regulation and Function

    Non-Muscle Myosin 2A (NM2A): Structure, Regulation and Function

    cells Review Non-Muscle Myosin 2A (NM2A): Structure, Regulation and Function Cláudia Brito 1,2 and Sandra Sousa 1,* 1 Group of Cell Biology of Bacterial Infections, i3S-Instituto de Investigação e Inovação em Saúde, IBMC, Universidade do Porto, 4200-135 Porto, Portugal; [email protected] 2 Programa Doutoral em Biologia Molecular e Celular (MCBiology), Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, 4099-002 Porto, Portugal * Correspondence: [email protected] Received: 19 May 2020; Accepted: 29 June 2020; Published: 1 July 2020 Abstract: Non-muscle myosin 2A (NM2A) is a motor cytoskeletal enzyme with crucial importance from the early stages of development until adulthood. Due to its capacity to convert chemical energy into force, NM2A powers the contraction of the actomyosin cytoskeleton, required for proper cell division, adhesion and migration, among other cellular functions. Although NM2A has been extensively studied, new findings revealed that a lot remains to be discovered concerning its spatiotemporal regulation in the intracellular environment. In recent years, new functions were attributed to NM2A and its activity was associated to a plethora of illnesses, including neurological disorders and infectious diseases. Here, we provide a concise overview on the current knowledge regarding the structure, the function and the regulation of NM2A. In addition, we recapitulate NM2A-associated diseases and discuss its potential as a therapeutic target. Keywords: non-muscle myosin 2A (NM2A); NM2A activity regulation; NM2A filament assembly; actomyosin cytoskeleton; cell migration; cell adhesion; plasma membrane blebbing 1. Superfamily of Myosins The cell cytoskeleton is an interconnected and dynamic network of filaments essential for intracellular organization and cell shape maintenance.
  • Homozygous Deletion in MYL9 Expands the Molecular Basis of Megacystis–Microcolon–Intestinal Hypoperistalsis Syndrome

    Homozygous Deletion in MYL9 Expands the Molecular Basis of Megacystis–Microcolon–Intestinal Hypoperistalsis Syndrome

    European Journal of Human Genetics (2018) 26:669–675 https://doi.org/10.1038/s41431-017-0055-5 ARTICLE Homozygous deletion in MYL9 expands the molecular basis of megacystis–microcolon–intestinal hypoperistalsis syndrome 1 2 3 3 2 1 Carolina Araujo Moreno ● Nara Sobreira ● Elizabeth Pugh ● Peng Zhang ● Gary Steel ● Fábio Rossi Torres ● Denise Pontes Cavalcanti1 Received: 16 June 2017 / Revised: 14 November 2017 / Accepted: 18 November 2017 / Published online: 16 February 2018 © European Society of Human Genetics 2018 Abstract Megacystis–microcolon–intestinal hypoperistalsis syndrome (MMIHS) is a severe disease characterized by functional obstruction in the urinary and gastrointestinal tract. The molecular basis of this condition started to be defined recently, and the genes related to the syndrome (ACTG2—heterozygous variant in sporadic cases; and MYH11 (myosin heavy chain 11), LMOD1 (leiomodin 1) and MYLK (myosin light chain (MLC) kinase)—autosomal recessive inheritance), encode proteins involved in the smooth muscle contraction, supporting a myopathic basis for the disease. In the present article, we described a family with two affected siblings with MMIHS born to consanguineous parents and the molecular investigation performed fi 1234567890 to de ne the genetic etiology. Previous whole exome sequencing of the affected child and parents did not identify a candidate gene for the disease in this family, but now we present a reanalysis of the data that led to the identification of a homozygous deletion encompassing the last exon of MYL9 (myosin regulatory light chain 9) in the affected individual. MYL9 gene encodes a regulatory myosin MLC and the phosphorylation of this protein is a crucial step in the contraction process of smooth muscle cell.
  • Identification of the Fatty Acid Synthase Interaction Network Via Itraq-Based Proteomics Indicates the Potential Molecular Mecha

    Identification of the Fatty Acid Synthase Interaction Network Via Itraq-Based Proteomics Indicates the Potential Molecular Mecha

    Huang et al. Cancer Cell Int (2020) 20:332 https://doi.org/10.1186/s12935-020-01409-2 Cancer Cell International PRIMARY RESEARCH Open Access Identifcation of the fatty acid synthase interaction network via iTRAQ-based proteomics indicates the potential molecular mechanisms of liver cancer metastasis Juan Huang1, Yao Tang1, Xiaoqin Zou1, Yi Lu1, Sha She1, Wenyue Zhang1, Hong Ren1, Yixuan Yang1,2* and Huaidong Hu1,2* Abstract Background: Fatty acid synthase (FASN) is highly expressed in various types of cancer and has an important role in carcinogenesis and metastasis. To clarify the mechanisms of FASN in liver cancer invasion and metastasis, the FASN protein interaction network in liver cancer was identifed by targeted proteomic analysis. Methods: Wound healing and Transwell assays was performed to observe the efect of FASN during migration and invasion in liver cancer. Isobaric tags for relative and absolute quantitation (iTRAQ)-based mass spectrometry were used to identify proteins interacting with FASN in HepG2 cells. Diferential expressed proteins were validated by co-immunoprecipitation, western blot analyses and confocal microscopy. Western blot and reverse transcription- quantitative polymerase chain reaction (RT-qPCR) were performed to demonstrate the mechanism of FASN regulating metastasis. Results: FASN knockdown inhibited migration and invasion of HepG2 and SMMC7721 cells. A total of, 79 proteins interacting with FASN were identifed. Additionally, gene ontology term enrichment analysis indicated that the majority of biological regulation and cellular processes that the FASN-interacting proteins were associated with. Co- precipitation and co-localization of FASN with fascin actin-bundling protein 1 (FSCN1), signal-induced proliferation- associated 1 (SIPA1), spectrin β, non-erythrocytic 1 (SPTBN1) and CD59 were evaluated.
  • Bioinformatic Analysis Reveals the Importance of Epithelial-Mesenchymal Transition in the Development of Endometriosis

    Bioinformatic Analysis Reveals the Importance of Epithelial-Mesenchymal Transition in the Development of Endometriosis

    www.nature.com/scientificreports OPEN Bioinformatic analysis reveals the importance of epithelial- mesenchymal transition in the development of endometriosis Meihong Chen1,6, Yilu Zhou2,3,6, Hong Xu4, Charlotte Hill2, Rob M. Ewing2,3, Deming He1, Xiaoling Zhang1 ✉ & Yihua Wang2,3,5 ✉ Background: Endometriosis is a frequently occurring disease in women, which seriously afects their quality of life. However, its etiology and pathogenesis are still unclear. Methods: To identify key genes/ pathways involved in the pathogenesis of endometriosis, we recruited 3 raw microarray datasets (GSE11691, GSE7305, and GSE12768) from Gene Expression Omnibus database (GEO), which contain endometriosis tissues and normal endometrial tissues. We then performed in-depth bioinformatic analysis to determine diferentially expressed genes (DEGs), followed by gene ontology (GO), Hallmark pathway enrichment and protein-protein interaction (PPI) network analysis. The fndings were further validated by immunohistochemistry (IHC) staining in endometrial tissues from endometriosis or control patients. Results: We identifed 186 DEGs, of which 118 were up-regulated and 68 were down-regulated. The most enriched DEGs in GO functional analysis were mainly associated with cell adhesion, infammatory response, and extracellular exosome. We found that epithelial-mesenchymal transition (EMT) ranked frst in the Hallmark pathway enrichment. EMT may potentially be induced by infammatory cytokines such as CXCL12. IHC confrmed the down-regulation of E-cadherin (CDH1) and up-regulation of CXCL12 in endometriosis tissues. Conclusions: Utilizing bioinformatics and patient samples, we provide evidence of EMT in endometriosis. Elucidating the role of EMT will improve the understanding of the molecular mechanisms involved in the development of endometriosis. Endometriosis is a frequently occurring gynaecological disease characterised by chronic pelvic pain, dysmenor- rhea and infertility1.
  • Pflugers Final

    Pflugers Final

    CORE Metadata, citation and similar papers at core.ac.uk Provided by Serveur académique lausannois A comprehensive analysis of gene expression profiles in distal parts of the mouse renal tubule. Sylvain Pradervand2, Annie Mercier Zuber1, Gabriel Centeno1, Olivier Bonny1,3,4 and Dmitri Firsov1,4 1 - Department of Pharmacology and Toxicology, University of Lausanne, 1005 Lausanne, Switzerland 2 - DNA Array Facility, University of Lausanne, 1015 Lausanne, Switzerland 3 - Service of Nephrology, Lausanne University Hospital, 1005 Lausanne, Switzerland 4 – these two authors have equally contributed to the study to whom correspondence should be addressed: Dmitri FIRSOV Department of Pharmacology and Toxicology, University of Lausanne, 27 rue du Bugnon, 1005 Lausanne, Switzerland Phone: ++ 41-216925406 Fax: ++ 41-216925355 e-mail: [email protected] and Olivier BONNY Department of Pharmacology and Toxicology, University of Lausanne, 27 rue du Bugnon, 1005 Lausanne, Switzerland Phone: ++ 41-216925417 Fax: ++ 41-216925355 e-mail: [email protected] 1 Abstract The distal parts of the renal tubule play a critical role in maintaining homeostasis of extracellular fluids. In this review, we present an in-depth analysis of microarray-based gene expression profiles available for microdissected mouse distal nephron segments, i.e., the distal convoluted tubule (DCT) and the connecting tubule (CNT), and for the cortical portion of the collecting duct (CCD) (Zuber et al., 2009). Classification of expressed transcripts in 14 major functional gene categories demonstrated that all principal proteins involved in maintaining of salt and water balance are represented by highly abundant transcripts. However, a significant number of transcripts belonging, for instance, to categories of G protein-coupled receptors (GPCR) or serine-threonine kinases exhibit high expression levels but remain unassigned to a specific renal function.