| First Author | Garrick MD | Year | 2007 |
| Journal | Biochim Biophys Acta | Volume | 1773 |
| Issue | 2 | Pages | 105-8 |
| PubMed ID | 17087999 | Mgi Jnum | J:120624 |
| Mgi Id | MGI:3707305 | Doi | 10.1016/j.bbamcr.2006.09.032 |
| Citation | Garrick MD, et al. (2007) Loss of rapid transferrin receptor recycling due to a mutation in Sec15l1 in hbd mice. Biochim Biophys Acta 1773(2):105-8 |
| abstractText | 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. |
