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| C/EBPα | |
|---|---|
| Name | C/EBPα |
| Uniprot | P51161 |
| Organism | Homo sapiens |
C/EBPα is a basic leucine zipper transcription factor with central roles in cellular differentiation, metabolic regulation, and lineage commitment. It was characterized in studies involving National Institutes of Health, Cold Spring Harbor Laboratory, and investigators affiliated with Harvard University, Stanford University School of Medicine, and the Max Planck Society. C/EBPα functions at the nexus of signaling pathways influenced by receptors and kinases studied by groups at University of Cambridge, Massachusetts Institute of Technology, and Johns Hopkins University.
C/EBPα was discovered during transcriptional profiling work at institutions such as University of California, San Francisco, Rockefeller University, and Imperial College London and has been the subject of reviews published in journals edited by Nature Publishing Group, Cell Press, and Oxford University Press. Its activity is modulated by interactions described by labs at the European Molecular Biology Laboratory and disease-focused teams at Mayo Clinic and Memorial Sloan Kettering Cancer Center. The protein integrates signals from pathways investigated by research groups at University of Pennsylvania, Yale University School of Medicine, and Karolinska Institutet.
C/EBPα contains a basic region and a leucine zipper motif conserved among proteins studied in structural biology programs at Salk Institute, EMBL-EBI, and Rutherford Appleton Laboratory. Structural analysis has used methods developed at European Synchrotron Radiation Facility, Brookhaven National Laboratory, and Lawrence Berkeley National Laboratory. The gene encodes multiple isoforms produced via alternative translation initiation, a concept characterized in labs at Cold Spring Harbor Laboratory, University of Oxford, and University of Chicago. Post-translational modifications such as phosphorylation and acetylation were elucidated by teams at Weizmann Institute of Science, Johns Hopkins University, and Vanderbilt University Medical Center.
Transcriptional control of the CEBPA locus involves promoter and enhancer elements mapped by consortia including ENCODE and analyzed by groups at Broad Institute, Wellcome Sanger Institute, and European Bioinformatics Institute. Expression is responsive to signaling cascades characterized by researchers at Dana-Farber Cancer Institute, Scripps Research Institute, and CNRS that include inputs from kinases and receptors investigated at Icahn School of Medicine at Mount Sinai, University College London, and University of Toronto. Epigenetic regulation, chromatin remodeling, and DNA methylation of the locus were studied in projects led by Howard Hughes Medical Institute, National Cancer Institute, and Pasteur Institute.
C/EBPα participates in transcriptional networks regulating cell-cycle genes, metabolism, and differentiation, concepts advanced by investigators at Fred Hutchinson Cancer Center, University of Zurich, and University of Melbourne. It cooperates with factors characterized by labs at Columbia University, University of Michigan, and Northwestern University to control targets implicated in lipid metabolism and proliferation. Pathway mapping studies from Kyoto University, Baylor College of Medicine, and Seoul National University placed C/EBPα within broader signaling modules alongside components explored by teams at Max Delbrück Center, University of Barcelona, and King's College London.
Key roles for C/EBPα in granulocytic differentiation and adipocyte development were established through experiments performed at Fred Hutchinson Cancer Center, University of Minnesota, and University of California, San Diego. Its requirement for myeloid lineage commitment was demonstrated in murine models developed by groups at Cold Spring Harbor Laboratory, European Molecular Biology Laboratory, and The Jackson Laboratory. Studies of adipogenesis used assays standardized by researchers at University of Illinois Urbana-Champaign, University of Wisconsin–Madison, and University of Copenhagen, and integrated insights from laboratories at Tokyo Medical and Dental University, Shanghai Jiao Tong University, and University of São Paulo.
Mutations, deletions, and dysregulated expression of the CEBPA gene have been associated with acute myeloid leukemia and metabolic disorders in clinical studies conducted at M.D. Anderson Cancer Center, Cleveland Clinic, and University College London Hospitals. Prognostic and diagnostic implications were assessed in cohorts assembled by International Agency for Research on Cancer, World Health Organization, and consortia coordinated by European LeukemiaNet. Associations with insulin resistance and fatty liver disease were reported in translational studies carried out at Hospital for Sick Children, National University Hospital Singapore, and Aarhus University Hospital.
Research on C/EBPα has employed knockout and knock-in mouse models generated at The Jackson Laboratory, Knockout Mouse Project, and facilities at European Mouse Mutant Archive. In vitro studies use cell lines authenticated by ATCC and methods developed by groups at Wellcome Trust Sanger Institute and Broad Institute including chromatin immunoprecipitation, RNA-seq, and CRISPR approaches first popularized at Howard Hughes Medical Institute and labs associated with Broad Institute and MIT. Proteomics and mass spectrometry analyses were performed in core facilities affiliated with EMBL-EBI, Max Planck Institute for Biochemistry, and National Center for Protein Sciences.
Category:Transcription factors