1. Department of Medicine, Division of Hematology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA;2. Lady Davis Institute for Medical Research, Jewish General Hospital and Department of Physiology, McGill University, Montreal, QC H3G 1Y6, Canada;3. Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84312, USA;4. Department of Pediatrics, Center for Pediatric Biomedical Research, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA;5. Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA;6. Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA;7. Department of Medicine, Division of Hematology-Oncology, Boston Children’s Hospital, Harvard Medical School, Boston, MA 02115, USA;8. Whitehead Institute for Biomedical Research and Massachusetts Institute of Technology, Cambridge, MA 02142, USA
Abstract:
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Highlights? Snx3 is highly expressed in vertebrate hematopoietic tissues ? Silencing of Snx3 results in anemia and hemoglobin defects in vertebrates ? Snx3 and Vps35 physically interact with Tfrc ? Snx3 is required for endosomal recycling of Tf-Tfrc complex
