Surviving Endoplasmic Reticulum Stress Is Coupled to Altered Chondrocyte Differentiation and Function

@article{Tsang2007SurvivingER,
  title={Surviving Endoplasmic Reticulum Stress Is Coupled to Altered Chondrocyte Differentiation and Function },
  author={Kwok Yeung Tsang and Danny Chan and Deborah Cheslett and Wilson C W Chan and Chi Leong So and Ian G. Melhado and Tori W. Y. Chan and Kin Ming Kwan and Ernst Bruno Hunziker and Yoshihiko Yamada and John F Bateman and Kenneth Man-Chee Cheung and Kathryn S E Cheah},
  journal={PLoS Biology},
  year={2007},
  volume={5},
  pages={20 - 28}
}
In protein folding and secretion disorders, activation of endoplasmic reticulum (ER) stress signaling (ERSS) protects cells, alleviating stress that would otherwise trigger apoptosis. Whether the stress-surviving cells resume normal function is not known. We studied the in vivo impact of ER stress in terminally differentiating hypertrophic chondrocytes (HCs) during endochondral bone formation. In transgenic mice expressing mutant collagen X as a consequence of a 13-base pair deletion in Col10a1… CONTINUE READING

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Hypertrophic chondrocytes can become osteoblasts and osteocytes in endochondral bone formation.

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