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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 Eye Proteins
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 Molecular mechanism underlying a Cx50-linked congenital cataract.
Academic Article Functional role of the carboxyl terminal domain of human connexin 50 in gap junctional channels.
Academic Article Loss of function and impaired degradation of a cataract-associated mutant connexin50.
Academic Article A novel connexin50 mutation associated with congenital nuclear pulverulent cataracts.
Academic Article Transgenic overexpression of connexin50 induces cataracts.
Academic Article The cytoplasmic accumulations of the cataract-associated mutant, Connexin50P88S, are long-lived and form in the endoplasmic reticulum.
Academic Article The GJA8 allele encoding CX50I247M is a rare polymorphism, not a cataract-causing mutation.
Academic Article A novel GJA8 mutation is associated with autosomal dominant lamellar pulverulent cataract: further evidence for gap junction dysfunction in human cataract.
Academic Article Different consequences of cataract-associated mutations at adjacent positions in the first extracellular boundary of connexin50.
Academic Article A mutant connexin50 with enhanced hemichannel function leads to cell death.
Academic Article Autophagy: a pathway that contributes to connexin degradation.
Academic Article Characterization of the gap junction protein connexin56 in the chicken lens by immunofluorescence and immunoblotting.
Academic Article Chick connexin-56, a novel lens gap junction protein. Molecular cloning and functional expression.
Academic Article Differential expression of two gap junction proteins in corneal epithelium.
Academic Article Cataracts are caused by alterations of a critical N-terminal positive charge in connexin50.
Academic Article Distinct behavior of connexin56 and connexin46 gap junctional channels can be predicted from the behavior of their hemi-gap-junctional channels.
Academic Article An MIP/AQP0 mutation with impaired trafficking and function underlies an autosomal dominant congenital lamellar cataract.
Academic Article A connexin50 mutant, CX50fs, that causes cataracts is unstable, but is rescued by a proteasomal inhibitor.
Academic Article Connexin50D47A decreases levels of fiber cell connexins and impairs lens fiber cell differentiation.
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 Chemical chaperone treatment improves levels and distributions of connexins in Cx50D47A mouse lenses.
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.
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