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  1. Article ; Online: Protocol for detection of ferroptosis in cultured cells.

    Murray, Magdalena B / Leak, Logan B / Lee, Weaverly Colleen / Dixon, Scott J

    STAR protocols

    2023  Volume 4, Issue 3, Page(s) 102457

    Abstract: Mammalian cells can die by apoptosis or by one of several non-apoptotic mechanisms, such as ferroptosis. Here, we present a protocol to distinguish ferroptosis from other cell death mechanisms in cultured cells. We describe steps for seeding cells, ... ...

    Abstract Mammalian cells can die by apoptosis or by one of several non-apoptotic mechanisms, such as ferroptosis. Here, we present a protocol to distinguish ferroptosis from other cell death mechanisms in cultured cells. We describe steps for seeding cells, administering mechanism-specific cell death inducers and inhibitors, and measuring cell death and viability. We then detail the use of molecular markers to verify mechanisms of cell death. This protocol can be used to identify and distinguish ferroptosis in 2D and 3D cultures. For complete details on the use and execution of this protocol, please refer to Ko, et al. (2019),
    MeSH term(s) Animals ; Ferroptosis ; Cell Death ; Apoptosis ; Cells, Cultured ; Mammals
    Language English
    Publishing date 2023-08-08
    Publishing country United States
    Document type Journal Article
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2023.102457
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: NMJ-Analyser identifies subtle early changes in mouse models of neuromuscular disease.

    Mejia Maza, Alan / Jarvis, Seth / Lee, Weaverly Colleen / Cunningham, Thomas J / Schiavo, Giampietro / Secrier, Maria / Fratta, Pietro / Sleigh, James N / Fisher, Elizabeth M C / Sudre, Carole H

    Scientific reports

    2021  Volume 11, Issue 1, Page(s) 12251

    Abstract: The neuromuscular junction (NMJ) is the peripheral synapse formed between a motor neuron axon terminal and a muscle fibre. NMJs are thought to be the primary site of peripheral pathology in many neuromuscular diseases, but innervation/denervation status ... ...

    Abstract The neuromuscular junction (NMJ) is the peripheral synapse formed between a motor neuron axon terminal and a muscle fibre. NMJs are thought to be the primary site of peripheral pathology in many neuromuscular diseases, but innervation/denervation status is often assessed qualitatively with poor systematic criteria across studies, and separately from 3D morphological structure. Here, we describe the development of 'NMJ-Analyser', to comprehensively screen the morphology of NMJs and their corresponding innervation status automatically. NMJ-Analyser generates 29 biologically relevant features to quantitatively define healthy and aberrant neuromuscular synapses and applies machine learning to diagnose NMJ degeneration. We validated this framework in longitudinal analyses of wildtype mice, as well as in four different neuromuscular disease models: three for amyotrophic lateral sclerosis (ALS) and one for peripheral neuropathy. We showed that structural changes at the NMJ initially occur in the nerve terminal of mutant TDP43 and FUS ALS models. Using a machine learning algorithm, healthy and aberrant neuromuscular synapses are identified with 95% accuracy, with 88% sensitivity and 97% specificity. Our results validate NMJ-Analyser as a robust platform for systematic and structural screening of NMJs, and pave the way for transferrable, and cross-comparison and high-throughput studies in neuromuscular diseases.
    MeSH term(s) Animals ; Biomarkers ; Case-Control Studies ; Disease Models, Animal ; Disease Susceptibility ; Fluorescent Antibody Technique ; Machine Learning ; Mice ; Mice, Knockout ; Neuromuscular Diseases/diagnosis ; Neuromuscular Diseases/etiology ; Neuromuscular Diseases/metabolism ; Neuromuscular Junction/metabolism ; Neuromuscular Junction/pathology ; RNA-Binding Protein FUS/genetics ; RNA-Binding Protein FUS/metabolism ; ROC Curve
    Chemical Substances Biomarkers ; FUS protein, mouse ; RNA-Binding Protein FUS
    Language English
    Publishing date 2021-06-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-91094-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: A novel knockout mouse for the small EDRK-rich factor 2 (Serf2) showing developmental and other deficits

    Cleverley, Karen / Lee, Weaverly Colleen / Mumford, Paige / Collins, Toby / Rickman, Matthew / Cunningham, Thomas J / Cleak, James / Mianne, Joffrey / Szoke-Kovacs, Zsombor / Stewart, Michelle / Teboul, Lydia / Maduro, Cheryl / Wells, Sara / Wiseman, Frances K / Fisher, Elizabeth M. C

    Mammalian genome. 2021 Apr., v. 32, no. 2

    2021  

    Abstract: The small EDRK-rich factor 2 (SERF2) is a highly conserved protein that modifies amyloid fibre assembly in vitro and promotes protein misfolding. However, the role of SERF2 in regulating age-related proteotoxicity remains largely unexplored due to a lack ...

    Abstract The small EDRK-rich factor 2 (SERF2) is a highly conserved protein that modifies amyloid fibre assembly in vitro and promotes protein misfolding. However, the role of SERF2 in regulating age-related proteotoxicity remains largely unexplored due to a lack of in vivo models. Here, we report the generation of Serf2 knockout mice using an ES cell targeting approach, with Serf2 knockout alleles being bred onto different defined genetic backgrounds. We highlight phenotyping data from heterozygous Serf2⁺/⁻ mice, including unexpected male-specific phenotypes in startle response and pre-pulse inhibition. We report embryonic lethality in Serf2⁻/⁻ null animals when bred onto a C57BL/6 N background. However, homozygous null animals were viable on a mixed genetic background and, remarkably, developed without obvious abnormalities. The Serf2 knockout mice provide a powerful tool to further investigate the role of SERF2 protein in previously unexplored pathophysiological pathways in the context of a whole organism.
    Keywords amyloid ; embryonic mortality ; genetic background ; heterozygosity ; homozygosity ; knockout mutants ; phenotype ; protein folding
    Language English
    Dates of publication 2021-04
    Size p. 94-103.
    Publishing place Springer US
    Document type Article
    Note NAL-AP-2-clean
    ZDB-ID 1058547-3
    ISSN 1432-1777 ; 0938-8990
    ISSN (online) 1432-1777
    ISSN 0938-8990
    DOI 10.1007/s00335-021-09864-6
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3489: 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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  4. Article ; Online: A novel knockout mouse for the small EDRK-rich factor 2 (Serf2) showing developmental and other deficits.

    Cleverley, Karen / Lee, Weaverly Colleen / Mumford, Paige / Collins, Toby / Rickman, Matthew / Cunningham, Thomas J / Cleak, James / Mianne, Joffrey / Szoke-Kovacs, Zsombor / Stewart, Michelle / Teboul, Lydia / Maduro, Cheryl / Wells, Sara / Wiseman, Frances K / Fisher, Elizabeth M C

    Mammalian genome : official journal of the International Mammalian Genome Society

    2021  Volume 32, Issue 2, Page(s) 94–103

    Abstract: The small EDRK-rich factor 2 (SERF2) is a highly conserved protein that modifies amyloid fibre assembly in vitro and promotes protein misfolding. However, the role of SERF2 in regulating age-related proteotoxicity remains largely unexplored due to a lack ...

    Abstract The small EDRK-rich factor 2 (SERF2) is a highly conserved protein that modifies amyloid fibre assembly in vitro and promotes protein misfolding. However, the role of SERF2 in regulating age-related proteotoxicity remains largely unexplored due to a lack of in vivo models. Here, we report the generation of Serf2 knockout mice using an ES cell targeting approach, with Serf2 knockout alleles being bred onto different defined genetic backgrounds. We highlight phenotyping data from heterozygous Serf2
    MeSH term(s) Age Factors ; Alleles ; Alternative Splicing ; Animals ; Cell Line ; Developmental Disabilities/diagnosis ; Developmental Disabilities/genetics ; Disease Models, Animal ; Embryonic Stem Cells/metabolism ; Female ; Gene Expression Regulation ; Genetic Association Studies/methods ; Genetic Background ; Genetic Loci ; Genetic Predisposition to Disease ; Genotype ; Intracellular Signaling Peptides and Proteins/genetics ; Male ; Mice ; Mice, Knockout ; Organ Specificity ; Phenotype ; X-Ray Microtomography
    Chemical Substances Intracellular Signaling Peptides and Proteins ; Serf2 protein, mouse
    Language English
    Publishing date 2021-03-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1058547-3
    ISSN 1432-1777 ; 0938-8990
    ISSN (online) 1432-1777
    ISSN 0938-8990
    DOI 10.1007/s00335-021-09864-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3489: 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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  5. Article ; Online: TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A.

    Brown, Anna-Leigh / Wilkins, Oscar G / Keuss, Matthew J / Hill, Sarah E / Zanovello, Matteo / Lee, Weaverly Colleen / Bampton, Alexander / Lee, Flora C Y / Masino, Laura / Qi, Yue A / Bryce-Smith, Sam / Gatt, Ariana / Hallegger, Martina / Fagegaltier, Delphine / Phatnani, Hemali / Newcombe, Jia / Gustavsson, Emil K / Seddighi, Sahba / Reyes, Joel F /
    Coon, Steven L / Ramos, Daniel / Schiavo, Giampietro / Fisher, Elizabeth M C / Raj, Towfique / Secrier, Maria / Lashley, Tammaryn / Ule, Jernej / Buratti, Emanuele / Humphrey, Jack / Ward, Michael E / Fratta, Pietro

    Nature

    2022  Volume 603, Issue 7899, Page(s) 131–137

    Abstract: Variants of UNC13A, a critical gene for synapse function, increase the risk of amyotrophic lateral sclerosis and frontotemporal ... ...

    Abstract Variants of UNC13A, a critical gene for synapse function, increase the risk of amyotrophic lateral sclerosis and frontotemporal dementia
    MeSH term(s) Alternative Splicing ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Codon, Nonsense ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/metabolism ; Humans ; Nerve Tissue Proteins ; Polymorphism, Single Nucleotide/genetics ; TDP-43 Proteinopathies
    Chemical Substances Codon, Nonsense ; DNA-Binding Proteins ; Nerve Tissue Proteins ; TARDBP protein, human ; UNC13B protein, human
    Language English
    Publishing date 2022-02-23
    Publishing country England
    Document type Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-022-04436-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 26: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 9: Show issues
    Zs.MO 244: Show issues

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