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Evidence for the multimeric structure of ferroportin
| Content Provider | Scilit |
|---|---|
| Author | Domenico, Ivana De Ward, Diane McVey Musci, Giovanni Kaplan, Jerry |
| Copyright Year | 2006 |
| Description | Ferroportin (Fpn) (IREG1, SLC40A1, MTP1) is an iron transporter, and mutations in Fpn result in a genetically dominant form of iron overload disease. Previously, we demonstrated that Fpn is a multimer and that mutations in Fpn are dominant negative. Other studies have suggested that Fpn is not a multimer and that overexpression or epitope tags might affect the localization, topology, or multimerization of Fpn. We generated wild-type Fpn with 3 different epitopes, GFP, FLAG, and c-myc, and expressed these constructs in cultured cells. Co-expression of any 2 different epitope-tagged proteins in the same cell resulted in their quantitative coimmunoprecipitation. Treatment of Fpn-GFP/Fpn-FLAG–expressing cells with crosslinking reagents resulted in the crosslinking of Fpn-GFP and Fpn-FLAG. Western analysis of rat glioma C6 cells or mouse bone marrow macrophages exposed to crosslinking reagents showed that endogenous Fpn is a dimer. These results support the hypothesis that the dominant inheritance of Fpn–iron overload disease is due to the dominant-negative effects of mutant Fpn proteins. |
| Related Links | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1801059/pdf |
| Ending Page | 2209 |
| Page Count | 5 |
| Starting Page | 2205 |
| DOI | 10.1182/blood-2006-06-032516 |
| Journal | Blood |
| Issue Number | 5 |
| Volume Number | 109 |
| Language | English |
| Publisher | American Society of Hematology |
| Publisher Date | 2006-10-31 |
| Access Restriction | Open |
| Subject Keyword | Biochemistry and Molecular Biology Bone Marrow Proteins Crosslinking Ferroportin Multimer Cultured Cells Reagents Fpn Iron Overload Disease Journal: Blood (Vol- 84, Issue- 5) |
| Content Type | Text |
| Resource Type | Article |
