Department of Surgery, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America ; Department of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America ; Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America ; Will Rogers Institute Pulmonary Research Center and Division of Pulmonary and Critical Care Medicine, Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America ; Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Department of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America ; Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America ; Will Rogers Institute Pulmonary Research Center and Division of Pulmonary and Critical Care Medicine, Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Cell-type specific gene regulation is key to gaining a full understanding of how the distinct phenotypes of differentiated cells are achieved and maintained. Here we examined how changes in transcriptional activation during alveolar epithelial cell (AEC) differentiation determine phenotype. We performed transcriptomic profiling using in vitro differentiation of human and rat primary AEC. This model recapitulates in vitro an in vivo process in which AEC transition from alveolar type 2 (AT2) cells to alveolar type 1 (AT1) cells during normal maintenance and regeneration following lung injury. Here we describe in detail the quality control, preprocessing, and normalization of microarray data presented within the associated study [1]. We also include R code for reproducibility of the referenced data and easily accessible processed data tables.
