James P Bridges

Summary

Affiliation: Cincinnati Children's Hospital Medical Center
Country: USA

Publications

  1. pmc Conditional hypoxia inducible factor-1α induction in embryonic pulmonary epithelium impairs maturation and augments lymphangiogenesis
    James P Bridges
    Perinatal Institute, Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, Cincinnati, OH, USA
    Dev Biol 362:24-41. 2012
  2. pmc Meckel-Gruber syndrome protein MKS3 is required for endoplasmic reticulum-associated degradation of surfactant protein C
    Mei Wang
    Division of Pulmonary Biology, Cincinnati Children s Research Foundation, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229 3039, USA
    J Biol Chem 284:33377-83. 2009
  3. pmc ERdj4 and ERdj5 are required for endoplasmic reticulum-associated protein degradation of misfolded surfactant protein C
    Mei Dong
    Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, and the University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA
    Mol Biol Cell 19:2620-30. 2008
  4. pmc Adaptation and increased susceptibility to infection associated with constitutive expression of misfolded SP-C
    James P Bridges
    Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, The University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    J Cell Biol 172:395-407. 2006
  5. pmc LPCAT1 regulates surfactant phospholipid synthesis and is required for transitioning to air breathing in mice
    James P Bridges
    Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio45229, USA
    J Clin Invest 120:1736-48. 2010
  6. ncbi request reprint Use of transgenic mice to study lung morphogenesis and function
    James P Bridges
    Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA
    ILAR J 47:22-31. 2006
  7. doi request reprint Orphan G Protein-Coupled Receptor GPR116 Regulates Pulmonary Surfactant Pool Size
    James P Bridges
    1 Perinatal Institute, Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio and
    Am J Respir Cell Mol Biol 49:348-57. 2013
  8. ncbi request reprint Expression of a human surfactant protein C mutation associated with interstitial lung disease disrupts lung development in transgenic mice
    James P Bridges
    Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
    J Biol Chem 278:52739-46. 2003

Detail Information

Publications8

  1. pmc Conditional hypoxia inducible factor-1α induction in embryonic pulmonary epithelium impairs maturation and augments lymphangiogenesis
    James P Bridges
    Perinatal Institute, Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, Cincinnati, OH, USA
    Dev Biol 362:24-41. 2012
    ..Collectively, these data indicate that HIF-1a protein levels in the pulmonary epithelium must be tightly controlled for proper development of the epithelial and mesenchymal compartments...
  2. pmc Meckel-Gruber syndrome protein MKS3 is required for endoplasmic reticulum-associated degradation of surfactant protein C
    Mei Wang
    Division of Pulmonary Biology, Cincinnati Children s Research Foundation, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229 3039, USA
    J Biol Chem 284:33377-83. 2009
    ..These results support a model in which MKS3 links the ER lumenal quality control machinery with the cytosolic degradation apparatus...
  3. pmc ERdj4 and ERdj5 are required for endoplasmic reticulum-associated protein degradation of misfolded surfactant protein C
    Mei Dong
    Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, and the University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA
    Mol Biol Cell 19:2620-30. 2008
    ..ERdj4 and ERdj5 promote turnover of misfolded SP-C and this activity is dependent on their ability to stimulate BiP ATPase activity...
  4. pmc Adaptation and increased susceptibility to infection associated with constitutive expression of misfolded SP-C
    James P Bridges
    Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, The University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    J Cell Biol 172:395-407. 2006
    ..The wide variability in the age of onset of ILD in patients with SFTPC mutations may be related to environmental insults that ultimately overwhelm the homeostatic cytoprotective response...
  5. pmc LPCAT1 regulates surfactant phospholipid synthesis and is required for transitioning to air breathing in mice
    James P Bridges
    Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio45229, USA
    J Clin Invest 120:1736-48. 2010
    ..Collectively, these data demonstrate that full LPCAT1 activity is required to achieve the levels of SatPC essential for the transition to air breathing...
  6. ncbi request reprint Use of transgenic mice to study lung morphogenesis and function
    James P Bridges
    Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA
    ILAR J 47:22-31. 2006
    ..In this review, selected transgenic mouse models are highlighted to illustrate the power of this technology, which in many cases has provided important insights that otherwise could not have been obtained...
  7. doi request reprint Orphan G Protein-Coupled Receptor GPR116 Regulates Pulmonary Surfactant Pool Size
    James P Bridges
    1 Perinatal Institute, Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio and
    Am J Respir Cell Mol Biol 49:348-57. 2013
    ..Collectively, these data support the concept that GPR116 functions as a molecular sensor of alveolar surfactant lipid pool sizes by regulating surfactant secretion. ..
  8. ncbi request reprint Expression of a human surfactant protein C mutation associated with interstitial lung disease disrupts lung development in transgenic mice
    James P Bridges
    Division of Pulmonary Biology, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
    J Biol Chem 278:52739-46. 2003
    ..1728 G --> A mutation causes misfolding of the SP-C proprotein with subsequent induction of the unfolded protein response and endoplasmic reticulum-associated degradation pathways ultimately resulting in disrupted lung morphogenesis...