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  1. Article ; Online: Mitochondria: A "pacemaker" for species-specific development.

    Liu, Yasmine J / Auwerx, Johan

    Molecular cell

    2023  Volume 83, Issue 6, Page(s) 824–826

    Abstract: We highlight papers by Diaz-Cuadros et al. ...

    Abstract We highlight papers by Diaz-Cuadros et al.
    MeSH term(s) Humans ; Mice ; Animals ; Energy Metabolism ; Oxidation-Reduction ; Mitochondria/genetics ; Mitochondria/metabolism
    Language English
    Publishing date 2023-03-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2023.02.025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5055: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Phalloidin Staining of Actin Filaments for Visualization of Muscle Fibers in

    Romani, Mario / Auwerx, Johan

    Bio-protocol

    2021  Volume 11, Issue 19, Page(s) e4183

    Abstract: ... Advances ... ...

    Abstract Advances in
    Language English
    Publishing date 2021-10-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2833269-6
    ISSN 2331-8325 ; 2331-8325
    ISSN (online) 2331-8325
    ISSN 2331-8325
    DOI 10.21769/BioProtoc.4183
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Mouse Systems Genetics as a Prelude to Precision Medicine.

    Li, Hao / Auwerx, Johan

    Trends in genetics : TIG

    2020  Volume 36, Issue 4, Page(s) 259–272

    Abstract: Mouse models have been instrumental in understanding human disease biology and proposing possible new treatments. The precise control of the environment and genetic composition of mice allows more rigorous observations, but limits the generalizability ... ...

    Abstract Mouse models have been instrumental in understanding human disease biology and proposing possible new treatments. The precise control of the environment and genetic composition of mice allows more rigorous observations, but limits the generalizability and translatability of the results into human applications. In the era of precision medicine, strategies using mouse models have to be revisited to effectively emulate human populations. Systems genetics is one promising paradigm that may promote the transition to novel precision medicine strategies. Here, we review the state-of-the-art resources and discuss how mouse systems genetics helps to understand human diseases and to advance the development of precision medicine, with an emphasis on the existing resources and strategies.
    MeSH term(s) Animals ; Disease Models, Animal ; Genome/genetics ; Genomics ; Humans ; Mice ; Precision Medicine/trends ; Systems Biology
    Language English
    Publishing date 2020-02-06
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 619240-3
    ISSN 1362-4555 ; 0168-9525 ; 0168-9479
    ISSN (online) 1362-4555
    ISSN 0168-9525 ; 0168-9479
    DOI 10.1016/j.tig.2020.01.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2272: Show issues Location:
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  4. Article ; Online: The virtuous cycle of human genetics and mouse models in drug discovery.

    Nadeau, Joseph H / Auwerx, Johan

    Nature reviews. Drug discovery

    2019  Volume 18, Issue 4, Page(s) 255–272

    Abstract: Ongoing studies in many species seek to understand the origins, architecture and consequences of phenotypic variation under normal and dysfunctional conditions, with the aim of identifying targets for intervention that can prevent, stabilize or reverse ... ...

    Abstract Ongoing studies in many species seek to understand the origins, architecture and consequences of phenotypic variation under normal and dysfunctional conditions, with the aim of identifying targets for intervention that can prevent, stabilize or reverse disease. Some suggest that only humans are appropriate for studying these questions and argue that candidate drug targets identified in mouse models are largely unreliable. Here, we review the vast evidence showing that mouse models continue to make fundamental contributions to our understanding of genetic principles, pathogenic mechanisms and therapeutic modalities. We propose a virtuous cycle in which the power of observational studies and natural experiments in humans are closely integrated with the rigour of true experiments in model organisms.
    MeSH term(s) Animals ; Disease Models, Animal ; Drug Discovery/trends ; Genetics/trends ; Human Genetics ; Humans ; Mice/genetics
    Language English
    Publishing date 2019-01-22
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2062954-0
    ISSN 1474-1784 ; 1474-1776
    ISSN (online) 1474-1784
    ISSN 1474-1776
    DOI 10.1038/s41573-018-0009-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5564: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 334: Show issues
    Zs.MG 63: Show issues

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  5. Article ; Online: Mitophagy in human health, ageing and disease.

    Picca, Anna / Faitg, Julie / Auwerx, Johan / Ferrucci, Luigi / D'Amico, Davide

    Nature metabolism

    2023  Volume 5, Issue 12, Page(s) 2047–2061

    Abstract: Maintaining optimal mitochondrial function is a feature of health. Mitophagy removes and recycles damaged mitochondria and regulates the biogenesis of new, fully functional ones preserving healthy mitochondrial functions and activities. Preclinical and ... ...

    Abstract Maintaining optimal mitochondrial function is a feature of health. Mitophagy removes and recycles damaged mitochondria and regulates the biogenesis of new, fully functional ones preserving healthy mitochondrial functions and activities. Preclinical and clinical studies have shown that impaired mitophagy negatively affects cellular health and contributes to age-related chronic diseases. Strategies to boost mitophagy have been successfully tested in model organisms, and, recently, some have been translated into clinics. In this Review, we describe the basic mechanisms of mitophagy and how mitophagy can be assessed in human blood, the immune system and tissues, including muscle, brain and liver. We outline mitophagy's role in specific diseases and describe mitophagy-activating approaches successfully tested in humans, including exercise and nutritional and pharmacological interventions. We describe how mitophagy is connected to other features of ageing through general mechanisms such as inflammation and oxidative stress and forecast how strengthening research on mitophagy and mitophagy interventions may strongly support human health.
    MeSH term(s) Humans ; Mitophagy/physiology ; Aging/physiology ; Mitochondria/metabolism ; Oxidative Stress
    Language English
    Publishing date 2023-11-30
    Publishing country Germany
    Document type Journal Article ; Review
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-023-00930-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Pleiotropic effects of mitochondria in aging.

    Lima, Tanes / Li, Terytty Yang / Mottis, Adrienne / Auwerx, Johan

    Nature aging

    2022  Volume 2, Issue 3, Page(s) 199–213

    Abstract: Aging is typified by a progressive decline in mitochondrial activity and stress resilience. Here, we review how mitochondrial stress pathways have pleiotropic effects on cellular and systemic homeostasis, which can comprise protective or detrimental ... ...

    Abstract Aging is typified by a progressive decline in mitochondrial activity and stress resilience. Here, we review how mitochondrial stress pathways have pleiotropic effects on cellular and systemic homeostasis, which can comprise protective or detrimental responses during aging. We describe recent evidence arguing that defects in these conserved adaptive pathways contribute to aging and age-related diseases. Signaling pathways regulating the mitochondrial unfolded protein response, mitochondrial membrane dynamics, and mitophagy are discussed, emphasizing how their failure contributes to heteroplasmy and de-regulation of key metabolites. Our current understanding of how these processes are controlled and interconnected explains how mitochondria can widely impact fundamental aspects of aging.
    MeSH term(s) Mitochondria/genetics ; Mitophagy ; Mitochondrial Dynamics ; Signal Transduction
    Language English
    Publishing date 2022-03-17
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ISSN 2662-8465
    ISSN (online) 2662-8465
    DOI 10.1038/s43587-022-00191-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Mass Spectrometry-Based Multi-omics Integration with a Single Set of C. elegans Samples

    Zhu, Yunyun / Jen, Annie / Overmyer, Katherine A. / Gao, Arwen W. / Shishkova, Evgenia / Auwerx, Johan / Coon, Joshua J.

    Analytical Chemistry. 2023 July 11, v. 95, no. 29 p.10930-10938

    2023  

    Abstract: Mass spectrometry-based large-scale multi-omics research has proven to be powerful in answering biological questions; nonetheless, it faces many challenges from sample preparation to downstream data integration. To efficiently extract biomolecules of ... ...

    Abstract Mass spectrometry-based large-scale multi-omics research has proven to be powerful in answering biological questions; nonetheless, it faces many challenges from sample preparation to downstream data integration. To efficiently extract biomolecules of different physicochemical properties, preparation of various sample type needs specific tailoring, especially of difficult ones, such as Caenorhabditis elegans. In this study, we sought to develop a multi-omics sample preparation method starting with a single set ofC. elegans samples to save time, minimize variability, expand biomolecule coverage, and promote multi-omics integration. We investigated tissue disruption methods to effectively release biomolecules and optimized extraction strategies to achieve broader and more reproducible biomolecule coverage in proteomics, lipidomics, and metabolomics workflows. In our assessment, we also considered speediness and usability of the approaches. The developed method was validated through a study of 16C. elegans samples designed to shine light on mitochondrial unfolded protein response (UPRmt), induced by three unique stressors—knocking down electron transfer chain element cco-1, mitochondrial ribosome protein S5 mrps-5, and antibiotic treatment Doxycycline. Our findings suggested that the method achieved great coverage of proteome, lipidome, and metabolome with high reproducibility and validated that all stressors triggered UPRmt in C. elegans, although generating unique molecular signatures. Innate immune response was activated, and triglycerides were decreased under all three stressor conditions. Additionally, Doxycycline treatment elicited more distinct proteomic, lipidomic, and metabolomic response than the other two treatments. This method has been successfully used to process Saccharomyces cerevisiae (data not shown) and can likely be applied to other organisms for multi-omics research.
    Keywords Caenorhabditis elegans ; Saccharomyces cerevisiae ; analytical chemistry ; biochemical compounds ; doxycycline ; electron transport chain ; innate immunity ; lipidomics ; mass spectrometry ; metabolome ; mitochondria ; multiomics ; proteome ; proteomics ; ribosomes ; unfolded protein response
    Language English
    Dates of publication 2023-0711
    Size p. 10930-10938.
    Publishing place American Chemical Society
    Document type Article ; Online
    ZDB-ID 1508-8
    ISSN 1520-6882 ; 0003-2700
    ISSN (online) 1520-6882
    ISSN 0003-2700
    DOI 10.1021/acs.analchem.3c00734
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 4' 52/94: Show issues
    Z 2.9: Show issues

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  8. Book ; Online: Data integration in systems genetics and aging research

    Rapin, Alexis / Sleiman, Maroun Bou / Auwerx, Johan

    2022  

    Abstract: Human life expectancy has dramatically improved over the course of the last century. Although this reflects a global improvement in sanitation and medical care, this also implies that more people suffer from diseases that typically manifest later in life, ...

    Abstract Human life expectancy has dramatically improved over the course of the last century. Although this reflects a global improvement in sanitation and medical care, this also implies that more people suffer from diseases that typically manifest later in life, like Alzheimer and atherosclerosis. Increasing healthspan by delaying or reverting the development of these age-related diseases has therefore become an urgent challenge in biomedical research. Research in this field is complicated by the multi-factorial nature of age-related diseases. They are rooted in complex physiological mechanisms impacted by heritable, environment and life-style factors that can be unique to each individual. Although technological advances in high-throughput biomolecular assays have enabled researchers to investigate individual physiology at the molecular level, integrating information about its different components, and accounting for individual variations remains a challenge. We are using a large collection of omics and phenotype data derived from the BXD mouse genetic diversity panel to explore how good data management practices, as fostered by the FAIR principles, paired with an explainable artificial intelligence framework, can provide solutions to decipher the complex roots of age-related diseases. These developments will help to propose innovative approaches to extend healthspan in the aging global population.

    Comment: 7 pages, 3 figures, Proceedings of the Swiss Research Data Day 2020, Oct. 22 2020. For full conference proceedings see http://www.ressi.ch/sites/default/files/No_special_DLCM.pdf
    Keywords Quantitative Biology - Other Quantitative Biology
    Publishing date 2022-07-07
    Publishing country us
    Document type Book ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Confounding factors from inducible systems for spatiotemporal gene expression regulation.

    Wüst, Rob C I / Houtkooper, Riekelt H / Auwerx, Johan

    The Journal of cell biology

    2020  Volume 219, Issue 7

    Abstract: Spatiotemporally regulated targeted gene manipulation is a common way to study the effect of gene variants on phenotypic traits, but the Cre/loxP and Tet-On/Tet-Off systems can affect whole-organism physiology and function due to off-target effects. We ... ...

    Abstract Spatiotemporally regulated targeted gene manipulation is a common way to study the effect of gene variants on phenotypic traits, but the Cre/loxP and Tet-On/Tet-Off systems can affect whole-organism physiology and function due to off-target effects. We highlight some of these adverse effects, including whole-body endocrinology and disturbances in the gut microbiome and in mitochondrial and metabolic function.
    MeSH term(s) Animals ; Artifacts ; CRISPR-Cas Systems ; Doxycycline/adverse effects ; Gene Editing/methods ; Gene Expression Regulation ; Genome ; Integrases/genetics ; Integrases/metabolism ; Mice ; Mice, Transgenic ; Mitochondria/drug effects ; Mitochondria/metabolism ; Receptors, Estrogen/genetics ; Receptors, Estrogen/metabolism ; Response Elements/drug effects ; Tamoxifen/adverse effects ; Tetracycline/adverse effects ; Transfection/methods
    Chemical Substances Receptors, Estrogen ; Tamoxifen (094ZI81Y45) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-) ; Tetracycline (F8VB5M810T) ; Doxycycline (N12000U13O)
    Language English
    Publishing date 2020-05-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202003031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ub I Zs.190: Show issues Location:
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  10. Article ; Online: NAD

    Katsyuba, Elena / Romani, Mario / Hofer, Dina / Auwerx, Johan

    Nature metabolism

    2020  Volume 2, Issue 1, Page(s) 9–31

    Abstract: The conceptual evolution of nicotinamide adenine dinucleotide ( ... ...

    Abstract The conceptual evolution of nicotinamide adenine dinucleotide (NAD
    MeSH term(s) Animals ; Disease ; Glycolysis ; Homeostasis ; Humans ; Longevity ; Metabolism/physiology ; NAD/metabolism ; NADP/metabolism ; Oxidation-Reduction ; Phosphorylation ; Sirtuins/metabolism ; Subcellular Fractions/metabolism
    Chemical Substances NAD (0U46U6E8UK) ; NADP (53-59-8) ; Sirtuins (EC 3.5.1.-)
    Language English
    Publishing date 2020-01-20
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-019-0161-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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