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1. Full Text High-throughput discovery of novel developmental phenotypes
by Dickinson, Mary E and Flenniken, Ann M and Ji, Xiao and Teboul, Lydia and Wong, Michael D and White, Jacqueline K and Meehan, Terrence F and Weninger, Wolfgang J and Westerberg, Henrik and Adissu, Hibret and Baker, Candice N and Bower, Lynette and Brown, James M and Brianna Caddle, L and Chiani, Francesco and Clary, Dave and Cleak, James and Daly, Mark J and Denegre, James M and Doe, Brendan and Dolan, Mary E and Edie, Sarah M and Fuchs, Helmut and Gailus-Durner, Valerie and Galli, Antonella and Gambadoro, Alessia and Gallegos, Juan and Guo, Shiying and Horner, Neil R and Hsu, Chih-wei and Johnson, Sara J and Kalaga, Sowmya and Keith, Lance C and Lanoue, Louise and Lawson, Thomas N and Lek, Monkol and Mark, Manuel and Marschall, Susan and Mason, Jeremy and McElwee, Melissa L and Newbigging, Susan and Nutter, Lauryl M.J and Peterson, Kevin A and Ramirez-Solis, Ramiro and Rowland, Douglas J and Ryder, Edward and Samocha, Kaitlin E and Seavitt, John R and Selloum, Mohammed and Szoke-Kovacs, Zsombor and Tamura, Masaru and Trainor, Amanda G and Tudose, Ilinca and Wakana, Shigeharu and Warren, Jonathan and Wendling, Olivia and West, David B and Wong, Leeyean and Yoshiki, Atsushi and MacArthur, Daniel G and Tocchini-Valentini, Glauco P and Gao, Xiang and Flicek, Paul and Bradley, Allan and Skarnes, William C and Justice, Monica J and Parkinson, Helen E and Moore, Mark and Wells, Sara and Braun, Robert E and Svenson, Karen L and Hrabe de Angelis, Martin and Herault, Yann and Mohun, Tim and Mallon, Ann-Marie and Mark Henkelman, R and Brown, Steve D.M and Adams, David J and Kent Lloyd, K.C and McKerlie, Colin and Beaudet, Arthur L and Bucan, Maja and Murray, Stephen A and McKay, Matthew and Urban, Barbara and Lund, Caroline and Froeter, Erin and LaCasse, Taylor and Mehalow, Adrienne and Gordon, Emily and Donahue, Leah Rae and Taft, Robert and Kutney, Peter and Dion, Stephanie and Goodwin, Leslie and Kales, Susan and Urban, Rachel and Palmer, Kristina and Pertuy, Fabien and Bitz, Deborah and ... and Int Mouse Phenotyping Consortium and The International Mouse Phenotyping Consortium
Nature, ISSN 0028-0836, 09/2016, Volume 537, Issue 7621, pp. 508 - 514
Approximately one-third of all mammalian genes are essential for life. Phenotypes resulting from knockouts of these genes in mice have provided tremendous... 
MICRO-CT | MULTIDISCIPLINARY SCIENCES | DISEASE | GENOME-WIDE | MAMMALIAN GENE-FUNCTION | SCREENS | GLYCOGENIN-1 DEFICIENCY | IDENTIFICATION | EXPRESSION | MOUSE EMBRYO | RESOURCE | Genetic research | Phenotype | Research | High-throughput screening (Biochemical assaying) | Methods | Genotype & phenotype | Disease | Developmental biology | Genes | Genomes | Mutation | Embryos | knockout | embryonic lethal | mouse | KOMP | IMPC | EUCOMM
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2. Full Text A large scale hearing loss screen reveals an extensive unexplored genetic landscape for auditory dysfunction
by Bowl, Michael R and Simon, Michelle M and Ingham, Neil J and Greenaway, Simon and Santos, Luis and Cater, Heather and Taylor, Sarah and Mason, Jeremy and Kurbatova, Natalja and Pearson, Selina and Bower, Lynette R and Clary, Dave A and Meziane, Hamid and Reilly, Patrick and Minowa, Osamu and Kelsey, Lois and Allen, Sue and Clementson-Mobbs, Sharon and Codner, Gemma and Fray, Martin and Gardiner, Wendy and Joynson, Russell and Kenyon, Janet and Loeffler, Jorik and Nell, Barbara and Parker, Andrew and Quwailid, Deen and Stewart, Michelle and Walling, Alison and Zaman, Rumana and Chen, Chao-Kung and Conte, Nathalie and Matthews, Peter and Relac, Mike and Tudose, Ilinca and Warren, Jonathan and Le Marchand, Elise and El Amri, Amal and El Fertak, Leila and Ennah, Hamid and Ali-Hadji, Dalila and Ayadi, Abdel and Wattenhofer-Donze, Marie and Moulaert, David and Jacquot, Sylvie and André, Philippe and Birling, Marie-Christine and Pavlovic, Guillaume and Lalanne, Valérie and Lux, Aline and Riet, Fabrice and Mittelhaeuser, Christophe and Bour, Raphael and Guimond, Alain and Bam'Hamed, Chaouki and Leblanc, Sophie and Vasseur, Laurent and Selloum, Mohammed and Sorg, Tania and Ayabe, Shinya and Furuse, Tamio and Kaneda, Hideki and Kobayashi, Kimio and Masuya, Hiroshi and Miura, Ikuo and Obata, Yuichi and Suzuki, Tomohiro and Tamura, Masaru and Tanaka, Nobuhiko and Yamada, Ikuko and Yoshiki, Atsushi and Berberovic, Zorana and Bubshait, Mohammed and Cabezas, Jorge and Carroll, Tracy and Clark, Greg and Clarke, Shannon and Creighton, Amie and Danisment, Ozge and Eskandarian, Mohammad and Feugas, Patricia and Gertsenstein, Marina and Guo, Ruolin and Hunter, Jane and Jacob, Elsa and Lan, Qing and Laurin, Valerie and Law, Napoleon and MacMaster, Sue and Miller, David and Morikawa, Lily and Newbigging, Susan and Owen, Celeste and Penton, Patricia and Pereira, Monica and Qu, Dawei and Shang, Xueyuan and Sleep, Gillian and Sohel, Khondoker and Tondat, Sandra and ... and Int Mouse Phenotyping Consortium and International Mouse Phenotyping Consortium and The International Mouse Phenotyping Consortium
Nature Communications, ISSN 2041-1723, 12/2017, Volume 8, Issue 1, pp. 886 - 11
The developmental and physiological complexity of the auditory system is likely reflected in the underlying set of genes involved in auditory function. In... 
HAIR-CELLS | MUTAGENESIS | PROJECT | OTITIS-MEDIA | MULTIDISCIPLINARY SCIENCES | MOUSE | MUTATION | DISEASE | GENOME-WIDE | IMPAIRMENT | RESOURCE | Hearing Loss - genetics | Phenotype | Animals | Datasets as Topic | Genetic Testing | Protein Interaction Maps - genetics | Hearing Loss - epidemiology | Mice | Hearing Tests | Mice, Knockout | Consortia | Genes | Phenotyping | Auditory system | Hearing protection | Hearing impairment | Hearing loss
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3. Full Text Identification of genetic elements in metabolism by high-throughput mouse phenotyping
by Rozman, Jan and Rathkolb, Birgit and Oestereicher, Manuela A and Schütt, Christine and Ravindranath, Aakash Chavan and Leuchtenberger, Stefanie and Sharma, Sapna and Kistler, Martin and Willershäuser, Monja and Brommage, Robert and Meehan, Terrence F and Mason, Jeremy and Haselimashhadi, Hamed and Aguilar-Pimentel, Antonio and Becker, Lore and Treise, Irina and Moreth, Kristin and Garrett, Lillian and Hölter, Sabine M and Zimprich, Annemarie and Marschall, Susan and Amarie, Oana V and Calzada-Wack, Julia and Neff, Frauke and Brachthäuser, Laura and Lengger, Christoph and Stoeger, Claudia and Zapf, Lilly and Cho, Yi-Li and Da Silva-Buttkus, Patricia and Kraiger, Markus J and Mayer-Kuckuk, Philipp and Gampe, Karen Kristine and Wu, Moya and Conte, Nathalie and Warren, Jonathan and Chen, Chao-Kung and Tudose, Ilinca and Relac, Mike and Matthews, Peter and Cater, Heather L and Natukunda, Helen P and Cleak, James and Teboul, Lydia M and Clementson-Mobbs, Sharon and Szoke-Kovacs, Zsombor and Walling, Alison P and Johnson, Sara J and Codner, Gemma F and Fiegel, Tanja and Ring, Natalie and Westerberg, Henrik and Greenaway, Simon and Sneddon, Duncan and Morgan, Hugh and Loeffler, Jorik and Stewart, Michelle E and Ramirez-Solis, Ramiro and Bradley, Allan and Skarnes, William C and Steel, Karen P and Maguire, Simon A and Dench, Joshua and Lafont, David and Vancollie, Valerie E and Pearson, Selina A and Gates, Amy S and Sanderson, Mark and Shannon, Carl and Anthony, Lauren F. E and Sumowski, Maksymilian T and McLaren, Robbie S. B and Doe, Brendan and Wardle-Jones, Hannah and Griffiths, Mark N. D and Galli, Antonella and Swiatkowska, Agnieszka and Isherwood, Christopher M and Speak, Anneliese O and Cambridge, Emma L and Wilson, Heather M and Caetano, Susana S and Maguire, Anna Karin B and Adams, David J and Bottomley, Joanna and Ryder, Ed and Gleeson, Diane and Pouilly, Laurent and Rousseau, Stephane and Auburtin, Aurélie and Reilly, Patrick and Ayadi, Abdel and Selloum, Mohammed and Wood, Joshua A and Clary, Dave and Havel, Peter and Tolentino, Todd and Tolentino, Heather and Schuchbauer, Mike and Pedroia, Sheryl and ... and IMPC Consortium
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 288 - 16
Metabolic diseases are a worldwide problem but the underlying genetic factors and their relevance to metabolic disease remain incompletely understood.... 
DIABETES-MELLITUS | CONSORTIUM | PATHWAYS | VARIANTS | INSULIN-RESISTANCE | MULTIDISCIPLINARY SCIENCES | DISEASE | BIOLOGY | GLYCEMIC TRAITS | ARCHITECTURE | ASSOCIATION | Genome-Wide Association Study | Basal Metabolism - genetics | Area Under Curve | Diabetes Mellitus, Type 2 - genetics | Humans | Gene Regulatory Networks | Body Weight - genetics | Obesity - genetics | Mice, Knockout | Triglycerides - metabolism | Phenotype | Animals | High-Throughput Screening Assays | Oxygen Consumption - genetics | Metabolic Diseases - genetics | Mice | Blood Glucose - metabolism | Consortia | Annotations | Genes | Phenotyping | Data processing | Genomes | Regulatory sequences | Genetic factors | Metabolism | Binding sites | Metabolic disorders
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4. Full Text The bulk of autotaxin activity is dispensable for adult mouse life
by Katsifa, Aggeliki and Kaffe, Eleanna and Nikolaidou-Katsaridou, Nefeli and Economides, Aris N and Newbigging, Susan and McKerlie, Colin and Aidinis, Vassilis
PLoS ONE, ISSN 1932-6203, 11/2015, Volume 10, Issue 11, pp. e0143083 - e0143083
Autotaxin (ATX, Enpp2) is a secreted lysophospholipase D catalysing the production of lysophosphatidic acid, a pleiotropic growth factor-like lysophospholipid.... 
LYSOPHOSPHOLIPASE-D | BREAST-CANCER | RECOMBINATION | MULTIDISCIPLINARY SCIENCES | RECEPTOR | GENERATION | REGRESSION IN-VIVO | LPA | EXPRESSION | LYSOPHOSPHATIDIC ACID PRODUCTION | PULMONARY-FIBROSIS | Benzoxazoles - pharmacology | Animals | Phosphoric Diester Hydrolases - metabolism | Aging - physiology | Mice, Inbred C57BL | Phosphoric Diester Hydrolases - blood | Tamoxifen - pharmacology | Integrases - metabolism | Enzyme Activation - drug effects | Piperazines - pharmacology | Mice | Genetic aspects | Research | G proteins | Autotomy | Medical research | Laboratories | Toxicity | Pathogenesis | Therapeutic applications | Pharmacology | Inflammation | Breast cancer | Arthritis | Lethality | Metastasis | Embryos | Inflammatory diseases | Medicine | Receptors | Immunology | Acids | Lysophospholipase | Clonal deletion | Lysophosphatidic acid | Deletion | Physiology | Cancer | Index Medicus
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5. Full Text Disease model discovery from 3,328 gene knockouts by the International Mouse Phenotyping Consortium
by Meehan, Terrence F and Conte, Nathalie and West, David B and Jacobsen, Julius O and Mason, Jeremy and Warren, Jonathan and Chen, Chao-Kung and Tudose, Ilinca and Relac, Mike and Matthews, Peter and Karp, Natasha and Santos, Luis and Fiegel, Tanja and Ring, Natalie and Westerberg, Henrik and Greenaway, Simon and Sneddon, Duncan and Morgan, Hugh and Codner, Gemma F and Stewart, Michelle E and Brown, James and Horner, Neil and Haendel, Melissa and Washington, Nicole and Mungall, Christopher J and Reynolds, Corey L and Gallegos, Juan and Gailus-Durner, Valerie and Sorg, Tania and Pavlovic, Guillaume and Bower, Lynette R and Moore, Mark and Morse, Iva and Gao, Xiang and Tocchini-Valentini, Glauco P and Obata, Yuichi and Cho, Soo Young and Seong, Je Kyung and Seavitt, John and Beaudet, Arthur L and Dickinson, Mary E and Herault, Yann and Wurst, Wolfgang and De Angelis, Martin Hrabe and Kent Lloyd, K.C and Flenniken, Ann M and Nutter, Lauryl M J and Newbigging, Susan and McKerlie, Colin and Justice, Monica J and Murray, Stephen A and Svenson, Karen L and Braun, Robert E and White, Jacqueline K and Bradley, Allan and Flicek, Paul and Wells, Sara and Skarnes, William C and Adams, David J and Parkinson, Helen and Mallon, Ann-Marie and Brown, Steve D.M and Smedley, Damian and Int Mouse Phenotyping Consortium and International Mouse Phenotyping Consortium and The International Mouse Phenotyping Consortium
Nature Genetics, ISSN 1061-4036, 08/2017, Volume 49, Issue 8, pp. 1231 - 1238
Although next-generation sequencing has revolutionized the ability to associate variants with human diseases, diagnostic rates and development of new therapies... 
RESOURCES | DATABASE | GENETICS & HEREDITY | GENOME-WIDE | ONTOLOGY | MICE | GENERATION | EXPRESSION ATLAS | MUTATIONS | ASSOCIATION | ORGANISM | Genetic Predisposition to Disease | Phenotype | Animals | Humans | Female | Genetic Diseases, Inborn | Male | Mice | Gene Knockout Techniques | Disease Models, Animal | Mice, Knockout | Usage | Genetic aspects | Research | Animal models in research | Genomics | Heart | Animal models | Ontology | Disease | Genes | Disorders | Genomes | Statistical methods | Data bases | Gene sequencing | Consortia | Signal transduction | Annotations | Rodents | Right ventricular dysplasia | Dysplasia | Automation | Gene expression | Ventricular dysplasia | Diseases | Studies | Acids | Phenotyping | Diagnostic systems | Mutation | Ventricle
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6. Full Text Peptide-MHC-based nanomedicines for autoimmunity function as T-cell receptor microclustering devices
by Singha, Santiswarup and Shao, Kun and Yang, Yang and Clemente-Casares, Xavier and Solé, Patricia and Clemente, Antonio and Blanco, Jesús and Dai, Qin and Song, Fayi and Liu, Shang Wan and Yamanouchi, Jun and Umeshappa, Channakeshava Sokke and Nanjundappa, Roopa Hebbandi and Detampel, Pascal and Amrein, Matthias and Fandos, César and Tanguay, Robert and Newbigging, Susan and Serra, Pau and Khadra, Anmar and Chan, Warren C. W and Santamaria, Pere
Nature Nanotechnology, ISSN 1748-3387, 07/2017, Volume 12, Issue 7, pp. 701 - 710
We have shown that nanoparticles (NPs) can be used as ligand-multimerization platforms to activate specific cellular receptors in vivo. Nanoparticles coated... 
IRON-OXIDE NANOPARTICLES | TCR | ACTIVATION | CYTOKINE PRODUCTION | MACROPHAGES | MATERIALS SCIENCE, MULTIDISCIPLINARY | SIZE | COMPLEXES | NANOSCIENCE & NANOTECHNOLOGY | BIOMEDICAL APPLICATIONS | MICE | AVIDITY MATURATION | Formulations | Antigens | Hematology | Toxicity | Immunoregulation | Abnormalities | Zebrafish | Lymphocytes T | T cell receptors | Embryos | Biological activity | Nanoparticles | T-cell receptor | Engineering | Phagocytes | Receptors | Major histocompatibility complex | Lymphocytes | Ligands | Biocompatibility | Differentiation | Histocompatibility | Nanotechnology | Index Medicus
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7. Full Text In vivo Quantum‐Dot Toxicity Assessment
by Hauck, Tanya S and Anderson, Robin E and Fischer, Hans C and Newbigging, Susan and Chan, Warren C. W
Small, ISSN 1613-6810, 01/2010, Volume 6, Issue 1, pp. 138 - 144
Quantum dots have potential in biomedical applications, but concerns persist about their safety. Most toxicology data is derived from in vitro studies and may... 
toxicity | quantum dots | biodistribution | nanostructures | Nanostructures | Quantum dots | Toxicity | Biodistribution | CLEARANCE | PHYSICS, CONDENSED MATTER | PHYSICS, APPLIED | SINGLE | MATERIALS SCIENCE, MULTIDISCIPLINARY | RATS | CHEMISTRY, PHYSICAL | NANOSCIENCE & NANOTECHNOLOGY | CDS NANOCRYSTALS | CDTE | CHEMISTRY, MULTIDISCIPLINARY | NANOPARTICLES | CADMIUM | MICE | NANOTECHNOLOGY | CYTOTOXICITY | Selenium - toxicity | Rats | Selenium Compounds - toxicity | Materials Testing | Metabolic Clearance Rate | Organ Specificity | Rats, Sprague-Dawley | Tissue Distribution | Sulfides | Animals | Quantum Dots | Selenium Compounds - pharmacokinetics | Cadmium Compounds - toxicity | Cadmium Compounds - pharmacokinetics | Selenium - pharmacokinetics | Index Medicus
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8. Full Text Noonan Syndrome Cardiac Defects Are Caused by PTPN11 Acting in Endocardium to Enhance Endocardial-Mesenchymal Transformation
by Toshiyuki Araki and Gordon Chan and Susan Newbigging and Lily Morikawa and Roderick T. Bronson and Benjamin G. Neel and Tak Wah Mak
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2009, Volume 106, Issue 12, pp. 4736 - 4741
Noonan syndrome (NS), the most common single-gene cause of congenital heart disease, is an autosomal dominant disorder that also features proportionate short... 
Phenotypes | Receptors | Cell growth | Noonan syndrome | Alleles | Myocardium | Embryos | Genetic mutation | Endothelial cells | Heart valves | Signal transduction protein tyrosine phosphatase | Cardiac development | Cardiac valves | Human disease | CELLS | CUSHION | cardiac valves | ACTIVATION | human disease | signal transduction | protein tyrosine phosphatase | MULTIDISCIPLINARY SCIENCES | HEART | RAS PATHWAY | MOUSE MODEL | GROWTH-FACTOR | MUTATIONS | NEURAL CREST | cardiac development | RECEPTOR TYROSINE KINASE | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Heart Valves - enzymology | Noonan Syndrome - enzymology | Endocardial Cushions - enzymology | Heart Defects, Congenital - pathology | Endocardium - pathology | Mutation - genetics | Heart Valves - abnormalities | Gene Knock-In Techniques | Organogenesis | Endocardial Cushions - pathology | Phenotype | Animals | Heart Defects, Congenital - enzymology | Mesoderm - enzymology | Mice | Endocardium - enzymology | Enzyme Activation | Heart Valves - embryology | Proto-Oncogene Proteins c-akt - metabolism | Mesoderm - pathology | Genetic transformation | Development and progression | Genetic aspects | Properties | Methods | Biological Sciences
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9. Full Text High Resolution Imaging and Histopathological Characterization of Myocardial Infarction
by Lin, Peter and Westreich, Jared and Li, Mengyuan and Gribble, Adam and Newbigging, Susan and Vitkin, Alex and Pop, Mihaela
Biophysical Journal, ISSN 0006-3495, 02/2019, Volume 116, Issue 3, p. 231
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10. Full Text Corrigendum: High-throughput discovery of novel developmental phenotypes
by Dickinson, Mary E and Flenniken, Ann M and Ji, Xiao and Teboul, Lydia and Wong, Michael D and White, Jacqueline K and Meehan, Terrence F and Weninger, Wolfgang J and Westerberg, Henrik and Adissu, Hibret and Baker, Candice N and Bower, Lynette and Brown, James M and Caddle, L Brianna and Chiani, Francesco and Clary, Dave and Cleak, James and Daly, Mark J and Denegre, James M and Doe, Brendan and Dolan, Mary E and Edie Helmut Fuchs, Sarah M and Gailus-Durner, Valerie and Galli, Antonella and Gambadoro, Alessia and Gallegos, Juan and Guo, Shiying and Horner, Neil R and Hsu, Chih-Wei and Johnson, Sara J and Kalaga, Sowmya and Keith, Lance C and Lanoue, Louise and Lawson, Thomas N and Lek, Monkol and Mark, Manuel and Marschall, Susan and Mason, Jeremy and McElwee, Melissa L and Nutter, Susan Newbigging Lauryl M J and Peterson, Kevin A and Ramirez-Solis, Ramiro and Rowland, Douglas J and Ryder, Edward and Samocha, Kaitlin E and Seavitt, John R and Selloum, Mohammed and Szoke-Kovacs, Zsombor and Tamura, Masaru and Trainor, Amanda G and Tudose, Ilinca and Wakana, Shigeharu and Warren, Jonathan and Wendling, Olivia and West, David B and Wong, Leeyean and Yoshiki, Atsushi and Wurst, Wolfgang and MacArthur, Daniel G and Tocchini-Valentini, Glauco P and Gao, Xiang and Flicek, Paul and Bradley, Allan and Skarnes, William C and Justice, Monica J and Parkinson, Helen E and Moore, Mark and Wells, Sara and Braun, Robert E and Svenson, Karen L and de Angelis, Martin Hrabe and Herault, Yann and Mohun, Tim and Mallon, Ann-Marie and Henkelman, R Mark and Brown, Steve D M and Adams, David J and Lloyd, K C Kent and McKerlie, Colin and Beaudet, Arthur L and Murray, Maja Bućan Stephen A and International Mouse Phenotyping Consortium
Nature, ISSN 0028-0836, 11/2017, Volume 551, Issue 7680, pp. 398 - 398
This corrects the article DOI: 10.1038/nature19356. 
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