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    Csrp3 cysteine and glycine-rich protein 3 [ Mus musculus (house mouse) ]

    Gene ID: 13009, updated on 27-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Muscle LIM Protein Is Expressed in the Injured Adult CNS and Promotes Axon Regeneration.

    Muscle LIM Protein Is Expressed in the Injured Adult CNS and Promotes Axon Regeneration.
    Levin E, Leibinger M, Gobrecht P, Hilla A, Andreadaki A, Fischer D.

    03/7/2020
    our cellular experiments suggest that protein depletion and proteasomal overload also play a role in other HCM-causing CSPR3 mutations that we investigated, indicating that reduced levels of functional MLP may be a common mechanism for HCM-causing CSPR3 mutations.

    Mutant Muscle LIM Protein C58G causes cardiomyopathy through protein depletion.
    Ehsan M, Kelly M, Hooper C, Yavari A, Beglov J, Bellahcene M, Ghataorhe K, Poloni G, Goel A, Kyriakou T, Fleischanderl K, Ehler E, Makeyev E, Lange S, Ashrafian H, Redwood C, Davies B, Watkins H, Gehmlich K., Free PMC Article

    09/14/2019
    we identify a novel role for Csrp3 expression in skeletal muscle in the development of obesity-induced insulin resistance

    Cysteine- and glycine-rich protein 3 regulates glucose homeostasis in skeletal muscle.
    Hernandez-Carretero A, Weber N, LaBarge SA, Peterka V, Doan NYT, Schenk S, Osborn O., Free PMC Article

    07/13/2019
    Ablation of MLP protein (and MYBPC3) protected mice from developing the dilated cardiomyopathy phenotype.

    Sarcomere-based genetic enhancement of systolic cardiac function in a murine model of dilated cardiomyopathy.
    Li J, Gresham KS, Mamidi R, Doh CY, Wan X, Deschenes I, Stelzer JE., Free PMC Article

    03/30/2019
    Cardiac overexpression of muscle LIM protein does not modulate the heart's response to various forms of pathological stress.

    Cardiac remodeling is not modulated by overexpression of muscle LIM protein (MLP).
    Kuhn C, Frank D, Dierck F, Oehl U, Krebs J, Will R, Lehmann LH, Backs J, Katus HA, Frey N.

    07/14/2012
    Loss of MLP leads to dilated cardiomyopathy and hearts of surviving MLP knockout mice show transient changes of intracellular calcium handling.

    Hearts of surviving MLP-KO mice show transient changes of intracellular calcium handling.
    Kemecsei P, Miklós Z, Bíró T, Marincsák R, Tóth BI, Komlódi-Pásztor E, Barnucz E, Mirk E, Van der Vusse GJ, Ligeti L, Ivanics T.

    01/8/2011
    Report a common MLP (muscle LIM protein) variant associated with a hypertrophic cardiomyopathy and heart failure phenotype, and skeletal muscle pathology.

    A common MLP (muscle LIM protein) variant is associated with cardiomyopathy.
    Knöll R, Kostin S, Klede S, Savvatis K, Klinge L, Stehle I, Gunkel S, Kötter S, Babicz K, Sohns M, Miocic S, Didié M, Knöll G, Zimmermann WH, Thelen P, Bickeböller H, Maier LS, Schaper W, Schaper J, Kraft T, Tschöpe C, Linke WA, Chien KR.

    03/29/2010
    MLP binds directly to CFL2 in human cardiac and skeletal muscles.

    Muscle LIM protein interacts with cofilin 2 and regulates F-actin dynamics in cardiac and skeletal muscle.
    Papalouka V, Arvanitis DA, Vafiadaki E, Mavroidis M, Papadodima SA, Spiliopoulou CA, Kremastinos DT, Kranias EG, Sanoudou D., Free PMC Article

    01/21/2010
    Mice with knockout of muscle-LIM protein exhibit prolongation of atrial and ventricular conduction and an increased ventricular vulnerability.

    Reduced delayed rectifier K+ current, altered electrophysiology, and increased ventricular vulnerability in MLP-deficient mice.
    Gardiwal A, Klein G, Kraemer K, Durgac T, Koenig T, Niehaus M, Heineke J, Mohammadi B, Krampfl K, Schaefer A, Wollert KC, Korte T.

    01/21/2010
    Reduced MLP-calcineurin signaling predisposes to adverse remodeling after myocardial infarct.

    Attenuation of cardiac remodeling after myocardial infarction by muscle LIM protein-calcineurin signaling at the sarcomeric Z-disc.
    Heineke J, Ruetten H, Willenbockel C, Gross SC, Naguib M, Schaefer A, Kempf T, Hilfiker-Kleiner D, Caroni P, Kraft T, Kaiser RA, Molkentin JD, Drexler H, Wollert KC., Free PMC Article

    01/21/2010
    This detailed physiological characterization during a phase of rapid anatomical remodeling suggests that systolic function in the MLP(-/-) mice may temporarily improve as a result of alterations in chamber compliance, which are mediated by dilatation.

    Role of diastolic properties in the transition to failure in a mouse model of the cardiac dilatation.
    Costandi PN, Frank LR, McCulloch AD, Omens JH., Free PMC Article

    01/21/2010
    results indicate that the progression to heart failure in the MLPKO model may be driven by diastolic myocardial dysfunction and abnormal passive properties rather than systolic dysfunction

    Young MLP deficient mice show diastolic dysfunction before the onset of dilated cardiomyopathy.
    Lorenzen-Schmidt I, Stuyvers BD, ter Keurs HE, Date MO, Hoshijima M, Chien KR, McCulloch AD, Omens JH., Free PMC Article

    01/21/2010
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