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Fine-tuning of Drp1/Fis1 availability by AKAP121/Siah2 regulates mitochondrial adaptation to hypoxia.
Defining the mechanisms underlying the control of mitochondrial fusion and fission is critical to understanding cellular adaptation to diverse physiological conditions. Here we demonstrate thatExpand
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APJ ACTS AS A DUAL RECEPTOR IN CARDIAC HYPERTROPHY
Cardiac hypertrophy is initiated as an adaptive response to sustained overload but progresses pathologically as heart failure ensues. Here we report that genetic loss of APJ, a G-protein-coupledExpand
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Disruption of the podosome adaptor protein TKS4 (SH3PXD2B) causes the skeletal dysplasia, eye, and cardiac abnormalities of Frank-Ter Haar Syndrome.
Frank-Ter Haar syndrome (FTHS), also known as Ter Haar syndrome, is an autosomal-recessive disorder characterized by skeletal, cardiovascular, and eye abnormalities, such as increased intraocularExpand
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Targeted Ablation of PINCH1 and PINCH2 From Murine Myocardium Results in Dilated Cardiomyopathy and Early Postnatal Lethality
Background— PINCH proteins are 5 LIM domain–only adaptor proteins that function as key components of the integrin signaling pathway and play crucial roles in multiple cellular processes. Two PINCHExpand
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Apelin receptor: its responsiveness to stretch mechanisms and its potential for cardiovascular therapy
It has recently been demonstrated that the apelin receptor (APJ) plays a significant role in mediating the stretch response within the heart in a G-protein-independent and β-arrestin-dependentExpand
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Syncoilin is required for generating maximum isometric stress in skeletal muscle but dispensable for muscle cytoarchitecture.
  • J. Zhang, M. Bang, +9 authors J. Chen
  • Biology, Medicine
  • American journal of physiology. Cell physiology
  • 1 May 2008
Syncoilin is a striated muscle-specific intermediate filament-like protein, which is part of the dystrophin-associated protein complex (DPC) at the sarcolemma and provides a link between theExpand
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Cardiac-specific overexpression of E40K active Akt prevents pressure overload-induced heart failure in mice by increasing angiogenesis and reducing apoptosis
Cardiac-specific overexpression of E40K active Akt prevents pressure overload-induced heart failure in mice by increasing angiogenesis and reducing apoptosis
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Prothymosin alpha protects cardiomyocytes against ischemia-induced apoptosis via preservation of Akt activation
The human prothymosin alpha (PTα) gene encodes a 12.5 kDa highly acidic nuclear protein that is widely expressed in mammalian tissues including the heart and importantly, is detectable also in bloodExpand
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Cardiovascular gene therapy for myocardial infarction
Introduction: Cardiovascular gene therapy is the third most popular application for gene therapy, representing 8.4% of all gene therapy trials as reported in 2012 estimates. Gene therapy inExpand
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Notch-independent RBPJ controls angiogenesis in the adult heart
Increasing angiogenesis has long been considered a therapeutic target for improving heart function after injury such as acute myocardial infarction. However, gene, protein and cell therapies toExpand
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