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    Aging of mesenchymal stem cell in vitro

    Mandana Mohyeddin Bonab, Kamran Alimoghaddam, Fatemeh Talebian, Syed Hamid Ghaffari, Ardeshir Ghavamzadeh and Behrouz Nikbin

    Published on: 10 March 2006

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Connexin26 mutations and KID syndrome

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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Aims and scope

BMC Cell Biology is an open access, peer-reviewed journal that considers articles on all aspects of the biology of cells, including organelles and cellular compartments, trafficking and turnover, signaling, motility, adhesion, cell division, differentiation and programmed cell death.    


  1. Christopher Foote, 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
  • Howard J Worman, College of Physicians and Surgeons, Columbia University

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