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J Immunol. 2004 Jan 1;172(1):651-60.

A novel mechanism of alternative promoter and splicing regulates the epitope generation of tumor antigen CML66-L.

Author information

1
Department of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

Abstract

This report describes the difference in the epitope generation of two isoforms of self-tumor Ag CML66 and the regulation mechanism. We identified a new CML66 short isoform, termed CML66-S. The previously identified long CML66 is referred to as CML66-L. CML66-S shares the C terminus with CML66-L but has its unique N terminus. CML66-S is predominantly expressed in testis, but is also expressed in very low levels in tumor cells, whereas CML66-L is expressed in tumor cells and testis. Differential expression of CML66-L and CML66-S in tumor cells resulted from regulation at transcription, although alternative splicing also participated in the generation of the isoforms. In addition, Ab titers to a CML66-L peptide were significantly higher than that to CML66-S peptide in the sera from patients with tumors. Finally, the Abs to full-length CML66-L in the sera from patients with tumors were correlated with the Abs in the sera from these patients to CML66-L-38, which is a fusion protein with a CML66-L-specific N terminus. This suggests that the CML66-L isoform is mainly responsible for the epitope generation. Our studies have identified the alternative promoter in combination with alternative splicing as a novel mechanism for regulation of the epitope generation of a self-tumor Ag.

PMID:
14688378
PMCID:
PMC3901998
DOI:
10.4049/jimmunol.172.1.651
[Indexed for MEDLINE]
Free PMC Article

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