Deletion of Scap in alveolar type II cells influences lung lipid homeostasis and identifies a compensatory role for pulmonary lipofibroblasts.

@article{Besnard2009DeletionOS,
  title={Deletion of Scap in alveolar type II cells influences lung lipid homeostasis and identifies a compensatory role for pulmonary lipofibroblasts.},
  author={Val{\'e}rie Besnard and Susan E. Wert and Mildred T. Stahlman and Anthony D Postle and Yan Xu and Machiko Ikegami and Jeffrey A. Whitsett},
  journal={The Journal of biological chemistry},
  year={2009},
  volume={284 6},
  pages={4018-30}
}
Pulmonary function after birth is dependent upon surfactant lipids that reduce surface tension in the alveoli. The sterol-responsive element-binding proteins (SREBPs) are transcription factors regulating expression of genes controlling lipid homeostasis in many tissues. To identify the role of SREBPs in the lung, we conditionally deleted the SREBP cleavage-activating protein gene, Scap, in respiratory epithelial cells (ScapDelta/Delta) in vivo. Prior to birth (E18.5), deletion of Scap decreased… CONTINUE READING

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