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One or more keywords matched the following properties of Beyer, Eric C.
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keywords Cataract
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 Cataract Extraction
Academic Article Connexin46 mutations linked to congenital cataract show loss of gap junction channel function.
Academic Article Molecular mechanism underlying a Cx50-linked congenital cataract.
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 Oxidative stress, lens gap junctions, and cataracts.
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 Cataracts are caused by alterations of a critical N-terminal positive charge in connexin50.
Academic Article An aberrant sequence in a connexin46 mutant underlies congenital cataracts.
Academic Article Connexin mutants and cataracts.
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 Connexin46fs380 causes progressive cataracts.
Academic Article The connexin46 mutant, Cx46T19M, causes loss of gap junction function and alters hemi-channel gating.
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 The E368Q Mutant Allele of GJA8 is Associated with Congenital Cataracts with Intrafamilial Variation in a South Indian Family.
Academic Article Chemical chaperone treatment improves levels and distributions of connexins in Cx50D47A mouse lenses.
Academic Article Characterization of a variant of gap junction protein a8 identified in a family with hereditary cataract.
Academic Article The Connexin50D47A Mutant Causes Cataracts by Calcium Precipitation.
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 Connexin Mutants Cause Cataracts Through Deposition of Apatite.
Academic Article Loss of fiber cell communication may contribute to the development of cataracts of many different etiologies.
Academic Article A crystallin mutant cataract with mineral deposits.
Academic Article Pediatric cataracts of different etiologies contain insoluble, calcified particles.
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  • Cataract