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CARP, a cardiac ankyrin repeat protein, is downstream in the Nkx2-5 homeobox gene pathway.
TLDR
CARP is a YB-1 associated factor and represents the first identified cardiac-restricted downstream regulatory gene in the homeobox gene Nkx2-5 pathway and may serve as a negative regulator of HF-1-dependent pathways for ventricular muscle gene expression.
Ventricular muscle-restricted targeting of the RXRalpha gene reveals a non-cell-autonomous requirement in cardiac chamber morphogenesis.
TLDR
It is suggested that RXRalpha functions in a neighboring compartment of the developing heart to generate a signal that is required for ventricular cardiomyocyte development and chamber maturation.
Control of segmental expression of the cardiac-restricted ankyrin repeat protein gene by distinct regulatory pathways in murine cardiogenesis.
TLDR
The mouse cardiac-restricted ankyrin repeat protein (CARP) gene is used as a model system to study the molecular mechanisms that control regional specification of cardiomyocytes in the developing heart and identifies distinct 5' cis regulatory elements of the gene that can direct heart segment-specific transgene expression, such as atrial versus ventricular and left versus right.
Absence of pressure overload induced myocardial hypertrophy after conditional inactivation of Galphaq/Galpha11 in cardiomyocytes.
TLDR
The complete lack of a hypertrophic response proves that the Gq/G11-mediated pathway is essential for cardiac hypertrophy induced by pressure overload and makes this signaling process an interesting target for interventions to prevent myocardialhypertrophy.
Domain-specific gene disruption reveals critical regulation of neuregulin signaling by its cytoplasmic tail.
  • X. Liu, H. Hwang, M. Zhou
  • Biology
    Proceedings of the National Academy of Sciences…
  • 27 October 1998
TLDR
Proteolytic processing of the membrane-bound neuregulin isoforms involved in cranial ganglia and heart embryogenesis is likely developmentally regulated and is critically controlled by their intracellular domain, suggesting a unique temporally and spatially regulated "inside-out" signaling process for processing and release of the extracellular-domain ligand.
Exercise-induced alterations and loss of sarcomeric M-line organization in the diaphragm muscle of obscurin knockout mice.
TLDR
Results suggest that obscurin is required for the maintenance of morphological and ultrastructural integrity of skeletal muscle fibers against damage induced by intense mechanical stress and point to the diaphragm as the skeletal muscle most severely affected in obscur in-deficient mice.
Complexity in simplicity: monogenic disorders and complex cardiomyopathies.
TLDR
To perform force-generating contraction, and to accommodate the repetitive changes in cell geometry that occur during each cardiac cycle, cardiac myocytes have evolved an abundant and highly specialized cytoskeleton, whose components can be classified into the following 3 groups.
A Post-transcriptional Compensatory Pathway in Heterozygous Ventricular Myosin Light Chain 2-Deficient Mice Results in Lack of Gene Dosage Effect during Normal Cardiac Growth or Hypertrophy*
TLDR
It is suggested that post-transcriptional compensatory mechanisms play a major role in maintaining the level of MLC-2v protein in murine hearts and that heterozygous mutants show neither a molecular nor a physiological cardiac phenotype either at base line or following hypertrophic stimuli.
Ankrd2 is a modulator of NF-κB-mediated inflammatory responses during muscle differentiation
TLDR
In a genome-wide expression study on Ankrd2-knockout or -overexpressing primary proliferating or differentiating myoblasts, an inverse correlation between AnkRD2 levels and the expression of proinflammatory genes is found and Ankrd3β is identified as a novel direct target of the p50/Ankrd2 repressosome dimer.
XII Annual Meeting of the Interuniversity Institute of Myology
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