| First Author | Attaya M | Year | 1992 |
| Journal | Nature | Volume | 355 |
| Issue | 6361 | Pages | 647-9 |
| PubMed ID | 1538753 | Mgi Jnum | J:1767 |
| Mgi Id | MGI:50291 | Doi | 10.1038/355647a0 |
| Citation | Attaya M, et al. (1992) Ham-2 corrects the class I antigen-processing defect in RMA-S cells. Nature 355(6361):647-9 |
| abstractText | The murine major histocompatibility complex (MHC) contains two genes (Ham-1 and Ham-2) that encode members of a super-family of ATP-dependent transport proteins. These genes are believed to mediate the transport of peptide antigen from the cytoplasm into the lumen of the endoplasmic reticulum for binding by MHC class I molecules. Evidence for such a function has come from the rescue of class I surface expression by a cloned copy of the human homologue of Ham-1, PSF-1, in a human cell line that is defective in antigen processing. A mutant murine cell line, RMA-S, has an identical antigen-processing-defective phenotype. Here we show that expression of a cloned copy of the Ham-2 gene in RMA-S cells results in recovery of the ability to process and present class I-restricted antigens to cytotoxic T lymphocytes, and in partial recovery of class I surface expression. Processing defects for classical (H-2 K and D) and non-classical (Qa1 and HMT) class I molecules are corrected by Ham-2. These data indicate that both MHC-linked transporter genes are probably required for class I antigen processing, and that the functional transporter in this pathway may consist of a Ham-1/Ham-2 heterodimer. |
