Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL019737-20
Application #
2215293
Study Section
Heart, Lung, and Blood Research Review Committee A (HLBA)
Project Start
1976-12-01
Project End
1996-11-30
Budget Start
1995-12-01
Budget End
1996-11-30
Support Year
20
Fiscal Year
1996
Total Cost
Indirect Cost
Name
University of Pennsylvania
Department
Physiology
Type
Schools of Medicine
DUNS #
042250712
City
Philadelphia
State
PA
Country
United States
Zip Code
19104
Hawkins, Arie; Guttentag, Susan H; Deterding, Robin et al. (2015) A non-BRICHOS SFTPC mutant (SP-CI73T) linked to interstitial lung disease promotes a late block in macroautophagy disrupting cellular proteostasis and mitophagy. Am J Physiol Lung Cell Mol Physiol 308:L33-47
Chowdhury, Ibrul; Fisher, Aron B; Christofidou-Solomidou, Melpo et al. (2014) Keratinocyte growth factor and glucocorticoid induction of human peroxiredoxin 6 gene expression occur by independent mechanisms that are synergistic. Antioxid Redox Signal 20:391-402
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Rahaman, Hamidur; Zhou, Suiping; Dodia, Chandra et al. (2012) Increased phospholipase A2 activity with phosphorylation of peroxiredoxin 6 requires a conformational change in the protein. Biochemistry 51:5521-30
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Maguire, Jean Ann; Mulugeta, Surafel; Beers, Michael F (2012) Multiple ways to die: delineation of the unfolded protein response and apoptosis induced by Surfactant Protein C BRICHOS mutants. Int J Biochem Cell Biol 44:101-12
Maguire, Jean Ann; Mulugeta, Surafel; Beers, Michael F (2011) Endoplasmic reticulum stress induced by surfactant protein C BRICHOS mutants promotes proinflammatory signaling by epithelial cells. Am J Respir Cell Mol Biol 44:404-14
Beers, Michael F; Hawkins, Arie; Maguire, Jean Ann et al. (2011) A nonaggregating surfactant protein C mutant is misdirected to early endosomes and disrupts phospholipid recycling. Traffic 12:1196-210
Zhang, Linghui; Yu, Kevin; Robert, Kyle W et al. (2011) Rab38 targets to lamellar bodies and normalizes their sizes in lung alveolar type II epithelial cells. Am J Physiol Lung Cell Mol Physiol 301:L461-77

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