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  1. Article ; Online: Does extracellular cardiac troponin I play a pathogenic role independently of autoantibodies?

    Redwood, Charles S

    Clinical science (London, England : 1979)

    2019  Volume 130, Issue 24, Page(s) 2277–2278

    Abstract: Cardiac troponin I (cTnI) is a key component of the ... ...

    Abstract Cardiac troponin I (cTnI) is a key component of the Ca
    Language English
    Publishing date 2019-03-05
    Publishing country England
    Document type Journal Article
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20160493
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article: Fluorescent PSC-Derived Cardiomyocyte Reporter Lines: Generation Approaches and Their Applications in Cardiovascular Medicine.

    Sontayananon, Naeramit / Redwood, Charles / Davies, Benjamin / Gehmlich, Katja

    Biology

    2020  Volume 9, Issue 11

    Abstract: Recent advances have made pluripotent stem cell (PSC)-derived cardiomyocytes an attractive option to model both normal and diseased cardiac function at the single-cell level. However, in vitro differentiation yields heterogeneous populations of ... ...

    Abstract Recent advances have made pluripotent stem cell (PSC)-derived cardiomyocytes an attractive option to model both normal and diseased cardiac function at the single-cell level. However, in vitro differentiation yields heterogeneous populations of cardiomyocytes and other cell types, potentially confounding phenotypic analyses. Fluorescent PSC-derived cardiomyocyte reporter systems allow specific cell lineages to be labelled, facilitating cell isolation for downstream applications including drug testing, disease modelling and cardiac regeneration. In this review, the different genetic strategies used to generate such reporter lines are presented with an emphasis on their relative technical advantages and disadvantages. Next, we explore how the fluorescent reporter lines have provided insights into cardiac development and cardiomyocyte physiology. Finally, we discuss how exciting new approaches using PSC-derived cardiomyocyte reporter lines are contributing to progress in cardiac cell therapy with respect to both graft adaptation and clinical safety.
    Language English
    Publishing date 2020-11-16
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology9110402
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Fluorescent PSC-Derived Cardiomyocyte Reporter Lines: Generation Approaches and Their Applications in Cardiovascular Medicine

    Sontayananon, Naeramit / Redwood, Charles / Davies, Benjamin / Gehmlich, Katja

    Biology. 2020 Nov. 16, v. 9, no. 11

    2020  

    Abstract: Recent advances have made pluripotent stem cell (PSC)-derived cardiomyocytes an attractive option to model both normal and diseased cardiac function at the single-cell level. However, in vitro differentiation yields heterogeneous populations of ... ...

    Abstract Recent advances have made pluripotent stem cell (PSC)-derived cardiomyocytes an attractive option to model both normal and diseased cardiac function at the single-cell level. However, in vitro differentiation yields heterogeneous populations of cardiomyocytes and other cell types, potentially confounding phenotypic analyses. Fluorescent PSC-derived cardiomyocyte reporter systems allow specific cell lineages to be labelled, facilitating cell isolation for downstream applications including drug testing, disease modelling and cardiac regeneration. In this review, the different genetic strategies used to generate such reporter lines are presented with an emphasis on their relative technical advantages and disadvantages. Next, we explore how the fluorescent reporter lines have provided insights into cardiac development and cardiomyocyte physiology. Finally, we discuss how exciting new approaches using PSC-derived cardiomyocyte reporter lines are contributing to progress in cardiac cell therapy with respect to both graft adaptation and clinical safety.
    Keywords cardiac output ; cardiomyocytes ; drug evaluation ; fluorescence ; medicine ; models ; phenotype ; population ; stem cells ; therapeutics ; yields
    Language English
    Dates of publication 2020-1116
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    Note NAL-light
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology9110402
    Database NAL-Catalogue (AGRICOLA)

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  4. Article ; Online: Molecular Mechanisms of Deregulation of Muscle Contractility Caused by the R168H Mutation in TPM3 and Its Attenuation by Therapeutic Agents.

    Karpicheva, Olga E / Avrova, Stanislava V / Bogdanov, Andrey L / Sirenko, Vladimir V / Redwood, Charles S / Borovikov, Yurii S

    International journal of molecular sciences

    2023  Volume 24, Issue 6

    Abstract: The substitution for Arg168His (R168H) in γ-tropomyosin (TPM3 gene, Tpm3.12 isoform) is associated with congenital muscle fiber type disproportion (CFTD) and muscle weakness. It is still unclear what molecular mechanisms underlie the muscle dysfunction ... ...

    Abstract The substitution for Arg168His (R168H) in γ-tropomyosin (TPM3 gene, Tpm3.12 isoform) is associated with congenital muscle fiber type disproportion (CFTD) and muscle weakness. It is still unclear what molecular mechanisms underlie the muscle dysfunction seen in CFTD. The aim of this work was to study the effect of the R168H mutation in Tpm3.12 on the critical conformational changes that myosin, actin, troponin, and tropomyosin undergo during the ATPase cycle. We used polarized fluorescence microscopy and ghost muscle fibers containing regulated thin filaments and myosin heads (myosin subfragment-1) modified with the 1,5-IAEDANS fluorescent probe. Analysis of the data obtained revealed that a sequential interdependent conformational-functional rearrangement of tropomyosin, actin and myosin heads takes place when modeling the ATPase cycle in the presence of wild-type tropomyosin. A multistep shift of the tropomyosin strands from the outer to the inner domain of actin occurs during the transition from weak to strong binding of myosin to actin. Each tropomyosin position determines the corresponding balance between switched-on and switched-off actin monomers and between the strongly and weakly bound myosin heads. At low Ca
    MeSH term(s) Humans ; Actins/metabolism ; Tropomyosin/metabolism ; Myosins/metabolism ; Mutation ; Adenosine Triphosphatases/metabolism ; Muscle Fibers, Skeletal/metabolism ; Myopathies, Structural, Congenital/metabolism ; Troponin/genetics ; Troponin/metabolism ; Calcium/metabolism
    Chemical Substances Actins ; Tropomyosin ; Myosins (EC 3.6.4.1) ; Adenosine Triphosphatases (EC 3.6.1.-) ; Troponin ; Calcium (SY7Q814VUP) ; TPM3 protein, human
    Language English
    Publishing date 2023-03-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24065829
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  5. Article ; Online: Genetics Matters: Voyaging from the Past into the Future of Humanity and Sustainability.

    Cheng, Acga / Harikrishna, Jennifer Ann / Redwood, Charles S / Lit, Lei Cheng / Nath, Swapan K / Chua, Kek Heng

    International journal of molecular sciences

    2022  Volume 23, Issue 7

    Abstract: The understanding of how genetic information may be inherited through generations was established by Gregor Mendel in the 1860s when he developed the fundamental principles of inheritance. The science of genetics, however, began to flourish only during ... ...

    Abstract The understanding of how genetic information may be inherited through generations was established by Gregor Mendel in the 1860s when he developed the fundamental principles of inheritance. The science of genetics, however, began to flourish only during the mid-1940s when DNA was identified as the carrier of genetic information. The world has since then witnessed rapid development of genetic technologies, with the latest being genome-editing tools, which have revolutionized fields from medicine to agriculture. This review walks through the historical timeline of genetics research and deliberates how this discipline might furnish a sustainable future for humanity.
    MeSH term(s) Databases, Genetic ; Heredity ; Inheritance Patterns
    Language English
    Publishing date 2022-04-02
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23073976
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  6. Article ; Online: Looking for Targets to Restore the Contractile Function in Congenital Myopathy Caused by Gln

    Karpicheva, Olga E / Simonyan, Armen O / Rysev, Nikita A / Redwood, Charles S / Borovikov, Yurii S

    International journal of molecular sciences

    2020  Volume 21, Issue 20

    Abstract: We have used the technique of polarized microfluorimetry to obtain new insight into the pathogenesis of skeletal muscle disease caused by the ... ...

    Abstract We have used the technique of polarized microfluorimetry to obtain new insight into the pathogenesis of skeletal muscle disease caused by the Gln
    MeSH term(s) Actins/chemistry ; Adenosine Triphosphate/metabolism ; Amino Acid Substitution ; Animals ; Calcium/chemistry ; Calcium/metabolism ; Cells, Cultured ; Humans ; Molecular Dynamics Simulation ; Muscle Contraction ; Myosins/chemistry ; Myosins/metabolism ; Myotonia Congenita/genetics ; Protein Domains ; Rabbits ; Tropomyosin/chemistry ; Tropomyosin/genetics ; Tropomyosin/metabolism ; Troponin/chemistry ; Troponin/metabolism
    Chemical Substances Actins ; TPM2 protein, human ; Tropomyosin ; Troponin ; Adenosine Triphosphate (8L70Q75FXE) ; Myosins (EC 3.6.4.1) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-10-14
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21207590
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  7. Article ; Online: New mechanisms and concepts for cardiac-resynchronization therapy.

    Neubauer, Stefan / Redwood, Charles

    The New England journal of medicine

    2014  Volume 370, Issue 12, Page(s) 1164–1166

    MeSH term(s) Animals ; Cardiac Resynchronization Therapy ; Disease Models, Animal ; Dogs ; Glycogen Synthase Kinase 3/metabolism ; Heart Failure/enzymology ; Heart Failure/therapy ; Humans ; Myocardial Contraction ; Phosphorylation ; Sarcomeres/metabolism ; Troponin/metabolism
    Chemical Substances Troponin ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
    Language English
    Publishing date 2014-03-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMcibr1315508
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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.34: Show issues Location:
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  8. Article ; Online: Mavacamten rescues increased myofilament calcium sensitivity and dysregulation of Ca

    Sparrow, Alexander J / Watkins, Hugh / Daniels, Matthew J / Redwood, Charles / Robinson, Paul

    American journal of physiology. Heart and circulatory physiology

    2020  Volume 318, Issue 3, Page(s) H715–H722

    Abstract: Thin filament hypertrophic cardiomyopathy (HCM) mutations increase myofilament ... ...

    Abstract Thin filament hypertrophic cardiomyopathy (HCM) mutations increase myofilament Ca
    MeSH term(s) Animals ; Benzylamines/pharmacology ; Calcium/metabolism ; Cardiomyopathy, Hypertrophic/genetics ; Cardiomyopathy, Hypertrophic/metabolism ; Heart/drug effects ; Mice ; Mutation ; Myocardium/metabolism ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Sarcomeres/drug effects ; Sarcomeres/metabolism ; Troponin I/genetics ; Troponin I/metabolism ; Troponin T/genetics ; Troponin T/metabolism ; Uracil/analogs & derivatives ; Uracil/pharmacology
    Chemical Substances Benzylamines ; MYK-461 ; Troponin I ; Troponin T ; Uracil (56HH86ZVCT) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-02-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00023.2020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.89: Show issues Location:
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  9. Article ; Online: Low expression of the K280N

    Sequeira, Vasco / Wang, Lili / Wijnker, Paul J M / Kim, Kyungsoo / Pinto, Jose R / Dos Remedios, Cris / Redwood, Charles / Knollmann, Bjorn C / van der Velden, Jolanda

    Journal of molecular and cellular cardiology plus

    2023  Volume 1, Page(s) 100007

    Abstract: Background: Hypertrophic cardiomyopathy (HCM) is an autosomal dominant genetic disorder with patients typically showing heterozygous inheritance of a pathogenic variant in a gene encoding a contractile protein. Here, we study the contractile effects of ... ...

    Abstract Background: Hypertrophic cardiomyopathy (HCM) is an autosomal dominant genetic disorder with patients typically showing heterozygous inheritance of a pathogenic variant in a gene encoding a contractile protein. Here, we study the contractile effects of a rare homozygous mutation using explanted tissue and human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) to gain insight into how the balance between mutant and WT protein expression affects cardiomyocyte function.
    Methods: Force measurements were performed in cardiomyocytes isolated from a HCM patient carrying a homozygous troponin T mutation (cTnT-K280N) and healthy donors. To discriminate between mutation-mediated and phosphorylation-related effects on Ca
    Results: Myofilament Ca
    Conclusions: The cTnT-K280N mutation increases myofilament Ca
    Language English
    Publishing date 2023-05-11
    Publishing country Netherlands
    Document type Journal Article
    ISSN 2772-9761
    ISSN (online) 2772-9761
    DOI 10.1016/j.jmccpl.2022.100007
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  10. Article ; Online: Molecular Mechanisms of the Deregulation of Muscle Contraction Induced by the R90P Mutation in Tpm3.12 and the Weakening of This Effect by BDM and W7.

    Borovikov, Yurii S / Andreeva, Daria D / Avrova, Stanislava V / Sirenko, Vladimir V / Simonyan, Armen O / Redwood, Charles S / Karpicheva, Olga E

    International journal of molecular sciences

    2021  Volume 22, Issue 12

    Abstract: Point mutations in the genes encoding the skeletal muscle isoforms of tropomyosin can cause a range of muscle diseases. The amino acid substitution of Arg for Pro residue in the 90th position (R90P) in γ-tropomyosin (Tpm3.12) is associated with ... ...

    Abstract Point mutations in the genes encoding the skeletal muscle isoforms of tropomyosin can cause a range of muscle diseases. The amino acid substitution of Arg for Pro residue in the 90th position (R90P) in γ-tropomyosin (Tpm3.12) is associated with congenital fiber type disproportion and muscle weakness. The molecular mechanisms underlying muscle dysfunction in this disease remain unclear. Here, we observed that this mutation causes an abnormally high Ca
    MeSH term(s) Actins/metabolism ; Animals ; Calcium/metabolism ; Muscle Contraction/drug effects ; Muscle Contraction/genetics ; Muscle Fibers, Skeletal/metabolism ; Mutation/genetics ; Myofibrils/drug effects ; Myofibrils/metabolism ; Myosins/metabolism ; Oximes/pharmacology ; Rabbits ; Sulfonamides/pharmacology ; Tropomyosin/genetics ; Troponin/metabolism
    Chemical Substances Actins ; Oximes ; Sulfonamides ; Tropomyosin ; Troponin ; W 7 (65595-90-6) ; Myosins (EC 3.6.4.1) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2021-06-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22126318
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