ERBB SIGNALING IN FETAL TYPE II CELL GROWTH
E Christiane
Tufts Medical Centercity: Boston country: United States (us)
Grant 5R01HL085648-04 from National Heart, Lung, And Blood Institute
Keywords: 1-Phosphatidylinositol 3-Kinase; Address; Birth; Blocking Antibodies; Borderline Personality Disorder; Bronchopulmonary Dysplasia; Cell Differentiation process; cell growth; Cell Nucleus; Cell Proliferation; Cells; Co-Immunoprecipitations; Confocal Microscopy; crosslink; cyclin D2; Development; Developmental Cell Biology; Developmental Process; dimer; Disease; Down-Regulation; Elements; Epidermal Growth Factor; Epidermal Growth Factor Receptor; Epithelial Cells; ErbB Receptor Family Protein; ErbB4 gene; Event; fetal; Fetal Lung; Goals; Growth; Growth and Development function; Indium; inhibitor/antagonist; insight; Ligands; Lung; lung development; Lung diseases; MAP Kinase Activation Pathway; MAP Kinase Gene; MAP Kinase Signaling Pathways; Mediating; member; Messenger RNA; Molecular Chaperones; monomer; Morbidity - disease rate; Mortality Vital Statistics; Mus; mutant; Neuregulins; novel; novel therapeutics; Nuclear; Nuclear Receptors; Pathway interactions; Phosphorylation; Pregnancy; Premature Birth; Process; Production; Pulmonary Surfactant-Associated Protein B; receptor; Receptor Activation; Receptor Signaling; Relative (related person); research study; respiratory distress syndrome; Respiratory physiology; response; Role; Signal Transduction; Small Interfering RNA; surfactant; System; Testing; trafficking; Transgenic Organisms; Type II Epithelial Receptor Cell; Up-Regulation (Physiology)
Relevance: Premature birth disrupts the growth and development of the lung, especially of specialized lung epithelial cells called type 2 cells, causing significant diseases such as the Respiratory Distress Syndrome and Bronchopulmonary Dysplasia, the leading causes of morbidity and mortality following preterm birth. This project will identify the mechanisms controlling growth and function of immature and mature type 2 cells by studying how ErbB receptor proteins regulate fetal type 2 cell growth and differentiation. The results from this study will provide a platform for developing novel treatments to relieve the burden of RDS and BPD
Project start date: 2008-12-10
Project end date: 2012-11-30
Budget start date: 1-DEC-2011
Budget end date: 30-NOV-2012
5R01HL085648-04 (2012): $358628
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