This micrograph shows a cell with a D50Y mutation in connexin26. Cx26 protein (red) and golgin-97 (green) colocalize more frequently than in wildtype cells. D50Y and I30N mutations result in the formation of aberrant hemichannels that might elevate intracellular calcium levels, which may contribute to the hyperproliferative epidermal phenotypes of KID syndrome.
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Articles
Connexin26 mutations and KID syndrome
Aypek et al. BMC Cell Biol. 17:5
Aims and scope
BMC Molecular and Cell Biology, formerly known as BMC Cell Biology, is an open access journal that considers articles on all aspects of both eukaryotic and prokaryotic cell and molecular biology, including structural and functional cell biology, DNA and RNA in a cellular context and biochemistry, as well as research using both the experimental and theoretical aspects of physics to study biological processes and investigations into the structure of biological macromolecules.
Editor
- Alison Cuff, BioMed Central
Manuscript Editor
- Cecilia Pennica, BioMed Central
Assistant Editor
- Alexandria Latto, BioMed Central
Section Editors
- Matthias Falk, Lehigh University
- Xuejun Jiang, Memorial Sloan-Kettering Cancer Center
- Andrew Koff, Memorial Sloan-Kettering Cancer Center
- Andrew Peden, University of Sheffield
Journal Sections
Transcription and translation
Structure and function of macromolecules
Cell cycle and cell division
Signalling
Membrane processes/transport
Protein folding, proteasome, degradation
Cell death
Molecular basis of disease
Metabolism
Matthias Falk, Section Editor
Matthias Falk, PhD is Professor for Cell Biology in the Department of Biological Sciences at Lehigh University, USA. His research investigates the biosynthesis, structure and function of gap junctions, plasma membrane channels that provide direct cell-to-cell communication and physical cell-cell adhesion.
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