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Article

Endothelial deletion of ADAM17 in mice results in defective remodeling of the semilunar valves and cardiac dysfunction in adults

24 Jan 2013

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Source

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 23354118
DOI: 10.1016/j.mod.2013.01.001

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Related research

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Endothelial deletion of ADAM17 in mice results in defective remodeling of the semilunar valves and cardiac dysfunction in adultsPMID 23354118Read ↗

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Adamts18 deletion results in distinct developmental defects and provides a model for congenital disorders of lens, lung, and female reproductive tract developmentSemantic proximity Read ↗

ADAMTS6: Emerging roles in cardiovascular, musculoskeletal and cancer biologySemantic proximity Read ↗

ADAM-17 regulates endothelial cell morphology, proliferation, and in vitro angiogenesisSemantic proximity Read ↗

Endocardial Brg1 Represses ADAMTS1 to Maintain the Microenvironment for Myocardial MorphogenesisSemantic proximity Read ↗

Emerging roles for the ADAMTS-like family of matricellular proteins in cardiovascular disease through regulation of the extracellular microenvironmentSemantic proximity Read ↗

Intraluminal valves: development, function and disease.Semantic proximity Read ↗

The shedding protease ADAM17: Physiology and pathophysiologySemantic proximity Read ↗

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