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One or more keywords matched the following properties of Beyer, Eric C.
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keywords Lens, Eye
overview Dr. Beyer is a physician scientist who practices pediatric hematology/oncology and has a broad background in basic laboratory and translational research. His laboratory has spent more nearly 30 years investigating intercellular communication (as mediated by the channels contained within gap junctions) and how its disruptions contribute to disease. These studies encompass basic investigations including identification and cloning of the subunit proteins, characterization of structure-function physiological relationships, determination of pathways of biosynthesis and degradation. Dr. Beyer's laboratory has also been pursuing translational examinations of the roles of these proteins in diseases including cataracts, deafness, arrhythmias, cancer, and premature labor. The group has spent many years studying the connexins expressed in the eye lens. They are elucidating the process of cataract development by studying mouse and cell culture models that mimic the pathologies seen in human families with connexin mutants and inherited cataracts. Dr. Beyer has investigated the roles of cardiac connexins in normal cardiac conduction and in the pathogenesis of arrhythmias. He is studying the roles of circulating extracellular vesicles in the vascular pathologies that underlie the crises of patients with sickle cell disease. He has mentored many students and post-doctoral fellows within his laboratory.
One or more keywords matched the following items that are connected to Beyer, Eric C.
Item TypeName
Concept Lens, Crystalline
Academic Article The gap-junction protein connexin 56 is phosphorylated in the intracellular loop and the carboxy-terminal region.
Academic Article Cultured chicken embryo lens cells resemble differentiating fiber cells in vivo and contain two kinetic pools of connexin56.
Academic Article Co-expression of lens fiber connexins modifies hemi-gap-junctional channel behavior.
Academic Article Heteromeric connexons formed by the lens connexins, connexin43 and connexin56.
Academic Article PKC isoenzymes in the chicken lens and TPA-induced effects on intercellular communication.
Academic Article Transgenic overexpression of connexin50 induces cataracts.
Academic Article Oxidative stress, lens gap junctions, and cataracts.
Academic Article Characterization of the gap junction protein connexin56 in the chicken lens by immunofluorescence and immunoblotting.
Academic Article Expression of the gap junction protein connexin43 in embryonic chick lens: molecular cloning, ultrastructural localization, and post-translational phosphorylation.
Academic Article Bovine connexin44, a lens gap junction protein: molecular cloning, immunologic characterization, and functional expression.
Academic Article Electrical properties of mammalian lens epithelial gap junction channels.
Academic Article An MIP/AQP0 mutation with impaired trafficking and function underlies an autosomal dominant congenital lamellar cataract.
Academic Article Roles and regulation of lens epithelial cell connexins.
Academic Article Connexin50D47A decreases levels of fiber cell connexins and impairs lens fiber cell differentiation.
Academic Article Connexin46fs380 causes progressive cataracts.
Academic Article Connexin23 deletion does not affect lens transparency.
Academic Article The Cataract-linked Mutant Connexin50D47A Causes Endoplasmic Reticulum Stress in Mouse Lenses.
Academic Article Disruption of the lens circulation causes calcium accumulation and precipitates in connexin mutant mice.
Academic Article Physiological and Optical Alterations Precede the Appearance of Cataracts in Cx46fs380 Mice.
Academic Article Chemical chaperone treatment improves levels and distributions of connexins in Cx50D47A mouse lenses.
Academic Article The Connexin50D47A Mutant Causes Cataracts by Calcium Precipitation.
Academic Article CHOP is dispensable for lens transparency in wild-type and connexin50 mutant mice.
Academic Article p62/Sequestosome 1 levels increase and phosphorylation is altered in Cx50D47A lenses, but deletion of p62/sequestosome 1 does not improve transparency.
Academic Article Connexin Mutants Compromise the Lens Circulation and Cause Cataracts through Biomineralization.
Academic Article Do Connexin Mutants Cause Cataracts by Perturbing Glutathione Levels and Redox Metabolism in the Lens?
Academic Article Molecular mechanisms underlying enhanced hemichannel function of a cataract-associated Cx50 mutant.
Academic Article Cataract-linked serine mutations in the gap junction protein connexin50 expose a sorting signal that promotes its lysosomal degradation.
Academic Article Levels and Modifications of Both Lens Fiber Cell Connexins Are Affected in Connexin Mutant Mice.
Academic Article A crystallin mutant cataract with mineral deposits.
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