Loss of Rapid Transferrin Receptor Recycling Due to a Mutation in Sec15l1 in Hbd Mice.
From: Department of Biochemistry, School of Medicine and Biomedical Sciences, SUNY, Buffalo, NY 14214, USA. mgarrick@baffalo.edu
Biochimica et biophysica acta
- Publish Date: Feb 2007
- ISSN: 0006-3002
- Volume: 1773
- Issue: 2
- Pages: 105-8
- Medium: Print
- Language: English
- Citation (JAMA): Garrick Michael D, Garrick Laura M, et al. Loss of Rapid Transferrin Receptor Recycling Due to a Mutation in Sec15l1 in Hbd Mice.. Biochim. Biophys. Acta Feb 2007;1773:105-8
Abstract
The hbd (hemoglobin deficit) mutation affects iron trafficking in murine reticulocytes. It is due to a deletion that eliminates exon 8 of Sec15l1, the homolog of a gene that encodes an exocyst component in yeast. We tested the hypothesis that the mutation causes defective slow or rapid receptor recycling by measuring endocytosis and exocytosis of transferrin by hbd reticulocytes. Endocytosis and initial iron incorporation were relatively unaffected, but exocytosis was unexpectedly slowed. These data indicate that rapid transferrin recycling is defective after pSec15l1 has mutated.
Mesh Headings (Keywords): Animals, Endocytosis, Exocytosis, Hemoglobins, Iodine Radioisotopes, Iron, Membrane Proteins, Mice, Mice, Mutant Strains, Mutation, Receptors, Transferrin, Reticulocytes, Time Factors
Check for Full Text / PubMed Unique Identifier (PMID): 17087999
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