The level of K8 expression in carcinomas showed a positive correlation with the degree of malignancy.

All of the papillomas tested were negative for the presence of K8, whereas the carcinomas were positive.

Furthermore, tumors expressing high levels of K8 showed a reduced expression of K13.

Immunoperoxidase staining and immunoblotting were also used on selected tumor samples to further explore for the presence of K8.

Our results demonstrate that K8 expression is a marker of late stages of carcinoma progression in the mouse skin carcinogenesis model.

Deletion of the fragment including this 16-bp consensus abrogated the ART responsiveness of the K8 promoter.

The other two monoclonal antibodies, designated K8 and K9, reacted with a methanol-sensitive restricted component of this complex.

How the ART activation domain activates ORF57 and K8 gene expression through the 16-bp consensus sequence remains to be determined.

Transient expression assays showed that ART strongly activated ORF57 and K8 promoter-directed gene expression in both CV-1 and BJAB cells.

The appearance of the R3 antigen in P3HR-1 superinfected Raji cells occurred approximately 4 h earlier than the antigen detected by K8.

Northern blot analysis using a K8 cDNA probe suggested that control of K8 expression in mouse skin tumors occurs at the transcriptional level.

This 40-bp segment contains a 16-bp consensus sequence which is also found in the K8 promoter region located between nt 74769 to 74784.