Decreased vitamin B12 availability induces ER stress through impaired SIRT1-deacetylation of HSF1

@inproceedings{Ghemrawi2013DecreasedVB,
  title={Decreased vitamin B12 availability induces ER stress through impaired SIRT1-deacetylation of HSF1},
  author={Rose Ghemrawi and Shabnam Pooya and S Lorentz and G Gauchotte and Carole Arnold and Jean-Louis Gu{\'e}ant and S-F Battaglia-Hsu},
  booktitle={Cell Death and Disease},
  year={2013}
}
Vitamin B12 (cobalamin) is a key determinant of S-adenosyl methionine (SAM)-dependent epigenomic cellular regulations related to methylation/acetylation and its deficiency produces neurodegenerative disorders by elusive mechanisms. Sirtuin 1 deacetylase (SIRT1) triggers cell response to nutritional stress through endoplasmic reticulum (ER) stress. Recently, we have established a N1E115 dopaminergic cell model by stable expression of a transcobalamin–oleosin chimera (TO), which impairs cellular… CONTINUE READING

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Recently , we have established a N1E115 dopaminergic cell model by stable expression of a transcobalamin – oleosin chimera ( TO ) , which impairs cellular availability of vitamin B12 , decreases methionine synthase activity and SAM level , and reduces cell proliferation .
Recently , we have established a N1E115 dopaminergic cell model by stable expression of a transcobalamin – oleosin chimera ( TO ) , which impairs cellular availability of vitamin B12 , decreases methionine synthase activity and SAM level , and reduces cell proliferation .
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