| First Author | King PD | Year | 1995 |
| Journal | J Immunol | Volume | 154 |
| Issue | 11 | Pages | 6080-93 |
| PubMed ID | 7751650 | Mgi Jnum | J:25530 |
| Mgi Id | MGI:73246 | Doi | 10.4049/jimmunol.154.11.6080 |
| Citation | King PD, et al. (1995) Novel isoforms of murine intercellular adhesion molecule-1 generated by alternative RNA splicing. J Immunol 154(11):6080-6093 |
| abstractText | Intercellular adhesion molecule-1 (ICAM-1)-deficient mice, produced by homologous recombination and previously recognized to be devoid of the common form of ICAM-1, are shown to express residual amounts of ICAM-1 Ag in thymus and lung. We demonstrate that this expression of ICAM-1 is possible because the mutated exon 5 in these animals has been skipped by alternative splicing of RNA. Three different alternative isoforms of ICAM-1 are expressed in mutant mice. Moreover, two of these isoforms are expressed in wild-type mice together with two additional alternative isoforms that cannot be produced in mutant mice. All alternatively spliced isoforms of ICAM-1 detected are missing complete extracellular Ig domains. In both mutant and wild-type mice, expression of alternatively spliced isoforms is up-regulated following stimulation of animals with LPS. Furthermore, all alternative isoforms of ICAM-1, except one, retain the ability to bind to the well- recognized ICAM-1 counter-receptor LFA-1. These findings, along with the restricted tissue distribution in mutant mice, indicate that alternative isoforms of ICAM-1 are significant physiologic adhesion structures which could play a distinct role in the functioning of the immune system of intact animals. |
