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16 results on '"Martin Hrabe de Angelis"'

1. Improving laboratory animal genetic reporting: LAG-R guidelines

Author

Lydia Teboul, James Amos-Landgraf, Fernando J. Benavides, Marie-Christine Birling, Steve D. M. Brown, Elizabeth Bryda, Rosie Bunton-Stasyshyn, Hsian-Jean Chin, Martina Crispo, Fabien Delerue, Michael Dobbie, Craig L. Franklin, Ernst-Martin Fuchtbauer, Xiang Gao, Christelle Golzio, Rebecca Haffner, Yann Hérault, Martin Hrabe de Angelis, Kevin C. Kent Lloyd, Terry R. Magnuson, Lluis Montoliu, Stephen A. Murray, Ki-Hoan Nam, Lauryl M. J. Nutter, Eric Pailhoux, Fernando Pardo Manuel de Villena, Kevin Peterson, Laura Reinholdt, Radislav Sedlacek, Je Kyung Seong, Toshihiko Shiroishi, Cynthia Smith, Toru Takeo, Louise Tinsley, Jean-Luc Vilotte, Søren Warming, Sara Wells, C. Bruce Whitelaw, Atsushi Yoshiki, Asian Mouse Mutagenesis Resource Association, CELPHEDIA infrastructure, INFRAFRONTIER consortium, International Mammalian Genome Society, International Mouse Phenotyping Consortium, International Society for Transgenic Technologies, Mutant Mouse Resource and Research Centers, Phenomics Australia, RRRC- Rat Resource and Research Center, and Guillaume Pavlovic

Subjects
Science
Abstract

Abstract The biomedical research community addresses reproducibility challenges in animal studies through standardized nomenclature, improved experimental design, transparent reporting, data sharing, and centralized repositories. The ARRIVE guidelines outline documentation standards for laboratory animals in experiments, but genetic information is often incomplete. To remedy this, we propose the Laboratory Animal Genetic Reporting (LAG-R) framework. LAG-R aims to document animals’ genetic makeup in scientific publications, providing essential details for replication and appropriate model use. While verifying complete genetic compositions may be impractical, better reporting and validation efforts enhance reliability of research. LAG-R standardization will bolster reproducibility, peer review, and overall scientific rigor.

Published
2024
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2. Offspring born to influenza A virus infected pregnant mice have increased susceptibility to viral and bacterial infections in early life

Author

Henning Jacobsen, Kerstin Walendy-Gnirß, Nilgün Tekin-Bubenheim, Nancy Mounogou Kouassi, Isabel Ben-Batalla, Nikolaus Berenbrok, Martin Wolff, Vinicius Pinho dos Reis, Martin Zickler, Lucas Scholl, Annette Gries, Hanna Jania, Andreas Kloetgen, Arne Düsedau, Gundula Pilnitz-Stolze, Aicha Jeridi, Ali Önder Yildirim, Helmut Fuchs, Valerie Gailus-Durner, Claudia Stoeger, Martin Hrabe de Angelis, Tatjana Manuylova, Karin Klingel, Fiona J. Culley, Jochen Behrends, Sonja Loges, Bianca Schneider, Susanne Krauss-Etschmann, Peter Openshaw, and Gülsah Gabriel

Subjects
Science
Abstract

Influenza infection during pregnancy can affect health of offspring but it is not clear how this affects immune responses. Here the authors use a mouse model to show that influenza infection during pregnancy can increase susceptibility to secondary infection and alter immune cell function in offspring.

Published
2021
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3. Endogenous FGF21-signaling controls paradoxical obesity resistance of UCP1-deficient mice

Author

Susanne Keipert, Dominik Lutter, Bjoern O. Schroeder, Daniel Brandt, Marcus Ståhlman, Thomas Schwarzmayr, Elisabeth Graf, Helmut Fuchs, Martin Hrabe de Angelis, Matthias H. Tschöp, Jan Rozman, and Martin Jastroch

Subjects
Science
Abstract

Brown adipose thermogenesis increases energy expenditure and relies on uncoupling protein 1 (UCP1), however, UCP1 knock-out mice show resistance to diet-induced obesity at room temperature. Here, the authors show that this resistance relies on FGF21-signaling, inducing the browning of white adipose tissue.

Published
2020
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4. Irp2 regulates insulin production through iron-mediated Cdkal1-catalyzed tRNA modification

Author

Maria C. Ferreira dos Santos, Cole P. Anderson, Susanne Neschen, Kimberly B. Zumbrennen-Bullough, Steven J. Romney, Melanie Kahle-Stephan, Birgit Rathkolb, Valerie Gailus-Durner, Helmut Fuchs, Eckhard Wolf, Jan Rozman, Martin Hrabe de Angelis, Weiling Maggie Cai, Malini Rajan, Jennifer Hu, Peter C. Dedon, and Elizabeth A. Leibold

Subjects
Science
Abstract

Iron metabolism is linked to type 2 diabetes. Here the authors describe a mechanism through which cellular iron deficiency caused by loss of Irp2 impairs Cdkal1 function, resulting in inaccurate proinsulin translation, impaired proinsulin processing and reduced insulin secretion.

Published
2020
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5. Identification of genetic elements in metabolism by high-throughput mouse phenotyping

Author

Jan Rozman, Birgit Rathkolb, Manuela A. Oestereicher, Christine Schütt, Aakash Chavan Ravindranath, Stefanie Leuchtenberger, Sapna Sharma, Martin Kistler, Monja Willershäuser, Robert Brommage, Terrence F. Meehan, Jeremy Mason, Hamed Haselimashhadi, IMPC Consortium, Tertius Hough, Ann-Marie Mallon, Sara Wells, Luis Santos, Christopher J. Lelliott, Jacqueline K. White, Tania Sorg, Marie-France Champy, Lynette R. Bower, Corey L. Reynolds, Ann M. Flenniken, Stephen A. Murray, Lauryl M. J. Nutter, Karen L. Svenson, David West, Glauco P. Tocchini-Valentini, Arthur L. Beaudet, Fatima Bosch, Robert B. Braun, Michael S. Dobbie, Xiang Gao, Yann Herault, Ala Moshiri, Bret A. Moore, K. C. Kent Lloyd, Colin McKerlie, Hiroshi Masuya, Nobuhiko Tanaka, Paul Flicek, Helen E. Parkinson, Radislav Sedlacek, Je Kyung Seong, Chi-Kuang Leo Wang, Mark Moore, Steve D. Brown, Matthias H. Tschöp, Wolfgang Wurst, Martin Klingenspor, Eckhard Wolf, Johannes Beckers, Fausto Machicao, Andreas Peter, Harald Staiger, Hans-Ulrich Häring, Harald Grallert, Monica Campillos, Holger Maier, Helmut Fuchs, Valerie Gailus-Durner, Thomas Werner, and Martin Hrabe de Angelis

Subjects
Science
Abstract

The genetic basis of metabolic diseases is incompletely understood. Here, by high-throughput phenotyping of 2,016 knockout mouse strains, Rozman and colleagues identify candidate metabolic genes, many of which are associated with unexplored regulatory gene networks and metabolic traits in human GWAS.

Published
2018
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6. A large scale hearing loss screen reveals an extensive unexplored genetic landscape for auditory dysfunction

Author

Michael R. Bowl, Michelle M. Simon, Neil J. Ingham, Simon Greenaway, Luis Santos, Heather Cater, Sarah Taylor, Jeremy Mason, Natalja Kurbatova, Selina Pearson, Lynette R. Bower, Dave A. Clary, Hamid Meziane, Patrick Reilly, Osamu Minowa, Lois Kelsey, The International Mouse Phenotyping Consortium, Glauco P. Tocchini-Valentini, Xiang Gao, Allan Bradley, William C. Skarnes, Mark Moore, Arthur L. Beaudet, Monica J. Justice, John Seavitt, Mary E. Dickinson, Wolfgang Wurst, Martin Hrabe de Angelis, Yann Herault, Shigeharu Wakana, Lauryl M. J. Nutter, Ann M. Flenniken, Colin McKerlie, Stephen A. Murray, Karen L. Svenson, Robert E. Braun, David B. West, K. C. Kent Lloyd, David J. Adams, Jacqui White, Natasha Karp, Paul Flicek, Damian Smedley, Terrence F. Meehan, Helen E. Parkinson, Lydia M. Teboul, Sara Wells, Karen P. Steel, Ann-Marie Mallon, and Steve D. M. Brown

Subjects
Science
Abstract

The full extent of the genetic basis for hearing impairment is unknown. Here, as part of the International Mouse Phenotyping Consortium, the authors perform a hearing loss screen in 3006 mouse knockout strains and identify 52 new candidate genes for genetic hearing loss.

Published
2017
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7. Prevalence of sexual dimorphism in mammalian phenotypic traits

Author

Natasha A. Karp, Jeremy Mason, Arthur L. Beaudet, Yoav Benjamini, Lynette Bower, Robert E. Braun, Steve D.M. Brown, Elissa J. Chesler, Mary E. Dickinson, Ann M. Flenniken, Helmut Fuchs, Martin Hrabe de Angelis, Xiang Gao, Shiying Guo, Simon Greenaway, Ruth Heller, Yann Herault, Monica J. Justice, Natalja Kurbatova, Christopher J. Lelliott, K.C. Kent Lloyd, Ann-Marie Mallon, Judith E. Mank, Hiroshi Masuya, Colin McKerlie, Terrence F. Meehan, Richard F. Mott, Stephen A. Murray, Helen Parkinson, Ramiro Ramirez-Solis, Luis Santos, John R. Seavitt, Damian Smedley, Tania Sorg, Anneliese O. Speak, Karen P. Steel, Karen L. Svenson, International Mouse Phenotyping Consortium, Shigeharu Wakana, David West, Sara Wells, Henrik Westerberg, Shay Yaacoby, and Jacqueline K. White

Subjects
Science
Abstract

Systemic dissection of sexually dimorphic phenotypes in mice is lacking. Here, Karp and the International Mouse Phenotype Consortium show that approximately 10% of qualitative traits and 56% of quantitative traits in mice as measured in laboratory setting are sexually dimorphic.

Published
2017
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9. X-linked deletion of Crossfirre, Firre, and Dxz4 in vivo uncovers diverse phenotypes and combinatorial effects on autosomes

Author

Tim P. Hasenbein, Sarah Hoelzl, Zachary D. Smith, Chiara Gerhardinger, Marion O. C. Gonner, Antonio Aguilar-Pimentel, Oana V. Amarie, Lore Becker, Julia Calzada-Wack, Nathalia R. V. Dragano, Patricia da Silva-Buttkus, Lillian Garrett, Sabine M. Hölter, Markus Kraiger, Manuela A. Östereicher, Birgit Rathkolb, Adrián Sanz-Moreno, Nadine Spielmann, Wolfgang Wurst, Valerie Gailus-Durner, Helmut Fuchs, Martin Hrabě de Angelis, Alexander Meissner, Stefan Engelhardt, John L. Rinn, and Daniel Andergassen

Subjects
Science
Abstract

Abstract The lncRNA Crossfirre was identified as an imprinted X-linked gene, and is transcribed antisense to the trans-acting lncRNA Firre. The Firre locus forms an inactive-X-specific interaction with Dxz4, both loci providing the platform for the largest conserved chromatin structures. Here, we characterize the epigenetic profile of these loci, revealing them as the most female-specific accessible regions genome-wide. To address their in vivo role, we perform one of the largest X-linked knockout studies by deleting Crossfirre, Firre, and Dxz4 individually and in combination. Despite their distinct epigenetic features observed on the X chromosome, our allele-specific analysis uncovers these loci as dispensable for imprinted and random X chromosome inactivation. However, we provide evidence that Crossfirre affects autosomal gene regulation but only in combination with Firre. To shed light on the functional role of these sex-specific loci, we perform an extensive standardized phenotyping pipeline and uncover diverse knockout and sex-specific phenotypes. Collectively, our study provides the foundation for exploring the intricate interplay of conserved X-linked loci in vivo.

Published
2024
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10. Myoscape controls cardiac calcium cycling and contractility via regulation of L-type calcium channel surface expression

Author

Eden, Matthias, Meder, Benjamin, Voelkers, Mirko, Poomvanicha, Montatip, Domes, Katrin, Branchereau, M., Marck, P., Will, Rainer, Bernt, Alexander, Rangrez, Ashraf, Busch, Matthias, Martin Hrabe de Angelis, Heymes, Christophe, Rottbauer, Wolfgang, Most, Patrick, Hofmann, Franz, Frey, Norbert, and German Mouse Clinic Consortiumw

Subjects
Calcium Channels, L-Type, Science, General Physics and Astronomy, General Biochemistry, Genetics and Molecular Biology, Article, Rats, Sprague-Dawley, Animals, Humans, Myocytes, Cardiac, Rats, Wistar, Cells, Cultured, Zebrafish, Mice, Knockout, Multidisciplinary, Myocardium, General Chemistry, Myocardial Contraction, Mice, Inbred C57BL, Cytoskeletal Proteins, HEK293 Cells, Animals, Newborn, Gene Expression Regulation, Calcium, Erratum, Carrier Proteins, Protein Binding
Abstract

Calcium signalling plays a critical role in the pathogenesis of heart failure. Here we describe a cardiac protein named Myoscape/FAM40B/STRIP2, which directly interacts with the L-type calcium channel. Knockdown of Myoscape in cardiomyocytes decreases calcium transients associated with smaller Ca2+ amplitudes and a lower diastolic Ca2+ content. Likewise, L-type calcium channel currents are significantly diminished on Myoscape ablation, and downregulation of Myoscape significantly reduces contractility of cardiomyocytes. Conversely, overexpression of Myoscape increases global Ca2+ transients and enhances L-type Ca2+ channel currents, and is sufficient to restore decreased currents in failing cardiomyocytes. In vivo, both Myoscape-depleted morphant zebrafish and Myoscape knockout (KO) mice display impairment of cardiac function progressing to advanced heart failure. Mechanistically, Myoscape-deficient mice show reduced L-type Ca2+currents, cell capacity and calcium current densities as a result of diminished LTCC surface expression. Finally, Myoscape expression is reduced in hearts from patients suffering of terminal heart failure, implying a role in human disease., Heart failure is a major public health issue but due to our poor disease understanding the current therapies are symptomatic. Here the authors identify Myoscape as a novel cardiac protein regulating membrane localization of the L-type calcium channel and heart's contractile force, thus promising new therapeutic avenues for heart failure.

Published
2016

11. Deep phenotyping and lifetime trajectories reveal limited effects of longevity regulators on the aging process in C57BL/6J mice

Author

Kan Xie, Helmut Fuchs, Enzo Scifo, Dan Liu, Ahmad Aziz, Juan Antonio Aguilar-Pimentel, Oana Veronica Amarie, Lore Becker, Patricia da Silva-Buttkus, Julia Calzada-Wack, Yi-Li Cho, Yushuang Deng, A. Cole Edwards, Lillian Garrett, Christina Georgopoulou, Raffaele Gerlini, Sabine M. Hölter, Tanja Klein-Rodewald, Michael Kramer, Stefanie Leuchtenberger, Dimitra Lountzi, Phillip Mayer-Kuckuk, Lena L. Nover, Manuela A. Oestereicher, Clemens Overkott, Brandon L. Pearson, Birgit Rathkolb, Jan Rozman, Jenny Russ, Kristina Schaaf, Nadine Spielmann, Adrián Sanz-Moreno, Claudia Stoeger, Irina Treise, Daniele Bano, Dirk H. Busch, Jochen Graw, Martin Klingenspor, Thomas Klopstock, Beverly A. Mock, Paolo Salomoni, Carsten Schmidt-Weber, Marco Weiergräber, Eckhard Wolf, Wolfgang Wurst, Valérie Gailus-Durner, Monique M. B. Breteler, Martin Hrabě de Angelis, and Dan Ehninger

Subjects
Science
Abstract

Lifespan can be affected by both physiological ageing and specific sets of pathologies associated with old age. Here the authors report a resource of large-scale cross-sectional phenotyping of aging male mice at different time points to analyse a large set of phenotypes and molecular markers, including during genetic and diet interventions affecting lifespan.

Published
2022
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12. Human and mouse essentiality screens as a resource for disease gene discovery

Author

Pilar Cacheiro, Violeta Muñoz-Fuentes, Stephen A. Murray, Mary E. Dickinson, Maja Bucan, Lauryl M. J. Nutter, Kevin A. Peterson, Hamed Haselimashhadi, Ann M. Flenniken, Hugh Morgan, Henrik Westerberg, Tomasz Konopka, Chih-Wei Hsu, Audrey Christiansen, Denise G. Lanza, Arthur L. Beaudet, Jason D. Heaney, Helmut Fuchs, Valerie Gailus-Durner, Tania Sorg, Jan Prochazka, Vendula Novosadova, Christopher J. Lelliott, Hannah Wardle-Jones, Sara Wells, Lydia Teboul, Heather Cater, Michelle Stewart, Tertius Hough, Wolfgang Wurst, Radislav Sedlacek, David J. Adams, John R. Seavitt, Glauco Tocchini-Valentini, Fabio Mammano, Robert E. Braun, Colin McKerlie, Yann Herault, Martin Hrabě de Angelis, Ann-Marie Mallon, K. C. Kent Lloyd, Steve D. M. Brown, Helen Parkinson, Terrence F. Meehan, Damian Smedley, The Genomics England Research Consortium, and The International Mouse Phenotyping Consortium

Subjects
Science
Abstract

Discovery of causal variants for monogenic disorders has been facilitated by whole exome and genome sequencing, but does not provide a diagnosis for all patients. Here, the authors propose a Full Spectrum of Intolerance to Loss-of-Function (FUSIL) categorization that integrates gene essentiality information to aid disease gene discovery.

Published
2020
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13. Bacterial encapsulins as orthogonal compartments for mammalian cell engineering

Author

Felix Sigmund, Christoph Massner, Philipp Erdmann, Anja Stelzl, Hannes Rolbieski, Mitul Desai, Sarah Bricault, Tobias P. Wörner, Joost Snijder, Arie Geerlof, Helmut Fuchs, Martin Hrabĕ de Angelis, Albert J. R. Heck, Alan Jasanoff, Vasilis Ntziachristos, Jürgen Plitzko, and Gil G. Westmeyer

Subjects
Science
Abstract

Artificial compartments have been expressed in prokaryotes and yeast, but similar capabilities have been missing for mammalian cell engineering. Here the authors use bacterial encapsulins to engineer genetically controlled multifunctional orthogonal compartments in mammalian cells.

Published
2018
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14. Every-other-day feeding extends lifespan but fails to delay many symptoms of aging in mice

Author

Kan Xie, Frauke Neff, Astrid Markert, Jan Rozman, Juan Antonio Aguilar-Pimentel, Oana Veronica Amarie, Lore Becker, Robert Brommage, Lillian Garrett, Kristin S. Henzel, Sabine M. Hölter, Dirk Janik, Isabelle Lehmann, Kristin Moreth, Brandon L. Pearson, Ildiko Racz, Birgit Rathkolb, Devon P. Ryan, Susanne Schröder, Irina Treise, Raffi Bekeredjian, Dirk H. Busch, Jochen Graw, Gerhard Ehninger, Martin Klingenspor, Thomas Klopstock, Markus Ollert, Michael Sandholzer, Carsten Schmidt-Weber, Marco Weiergräber, Eckhard Wolf, Wolfgang Wurst, Andreas Zimmer, Valerie Gailus-Durner, Helmut Fuchs, Martin Hrabě de Angelis, and Dan Ehninger

Subjects
Science
Abstract

Dietary restriction can extend the life of various model organisms. Here, Xie et al. show that intermittent periods of fasting achieved through every-other-day feeding protect mice against neoplastic disease but do not broadly delay organismal aging in animals.

Published
2017
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15. Myoscape controls cardiac calcium cycling and contractility via regulation of L-type calcium channel surface expression

Author

Matthias Eden, Benjamin Meder, Mirko Völkers, Montatip Poomvanicha, Katrin Domes, M. Branchereau, P. Marck, Rainer Will, Alexander Bernt, Ashraf Rangrez, Matthias Busch, German Mouse Clinic Consortium, Martin Hrabě de Angelis, Christophe Heymes, Wolfgang Rottbauer, Patrick Most, Franz Hofmann, and Norbert Frey

Subjects
Science
Abstract

Heart failure is a major public health issue but due to our poor disease understanding the current therapies are symptomatic. Here the authors identify Myoscape as a novel cardiac protein regulating membrane localization of the L-type calcium channel and heart's contractile force, thus promising new therapeutic avenues for heart failure.

Published
2016
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16. Erratum: Myoscape controls cardiac calcium cycling and contractility via regulation of L-type calcium channel surface expression

Author

Matthias Eden, Benjamin Meder, Mirko Völkers, Montatip Poomvanicha, Katrin Domes, M. Branchereau, P. Marck, Rainer Will, Alexander Bernt, Ashraf Rangrez, Matthias Busch, Martin Hrabě de Angelis, Christophe Heymes, Wolfgang Rottbauer, Patrick Most, Franz Hofmann, and Norbert Frey

Subjects
Science
Abstract

Nature Communications 7, Article number: 11317 (2016); Published: 28 April 2016; Updated: 26 May 2016 The original version of this Article contained an error in the doi number, which was incorrectly given as 15.13155/ncomms11317. This has now been corrected in both the PDF and HTML versions of the Article.

Published
2016
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