| First Author | Nakajima T | Year | 1996 |
| Journal | Life Sci | Volume | 58 |
| Issue | 9 | Pages | 761-8 |
| PubMed ID | 8632723 | Mgi Jnum | J:31708 |
| Mgi Id | MGI:79193 | Doi | 10.1016/0024-3205(95)02354-2 |
| Citation | Nakajima T, et al. (1996) A new alternative splice variant of the mouse Fas antigen with a deletion in the N-terminal portion of the extracellular domain. Life Sci 58(9):761-8 |
| abstractText | The Fas antigen (Fas/APO-1/CD95) has been shown to induce apoptosis when bound to a monoclonal anti-Fas antibody or Fas ligands. Recently, a new soluble human Fas isoform which lacks the transmembrane domain due to alternative splicing has been isolated; however, no mouse Fas isoforms have been reported so far. Analysis of Fas transcripts by RT-PCR detected no Fas transcripts corresponding, to the human soluble Fas isoform iii mouse thymus, spleen, and liver. However, we detected a new isoform with a 117-bp deletion in the second exon in various mouse tissues and cell lines. This isoform, termed truncated Fas (T-Fas), can be generated by alternative splicing and lacks the N- terminal portion of the extracellular domain just after the signal sequence. Since the deletion involves the first cysteine-rich motif believed to be necessary for binding to the Fas ligand, the T-Fas protein may lack the ability to induce apoptosis. The expression of T-Fas relative to that of the normal Fas varies considerably among mouse tissues and cell lines, suggesting preferential transcription of the T-Fas isoform in certain cell types. |
