Susan E. Rutberg

TL;DR: Experiments in which v-H-ras-expressing keratinocytes were grafted onto nude mice suggest that c-fos-deficient cells have an intrinsic defect that hinders tumorigenesis.

TL;DR: It is shown that AP-1 DNA binding activity is very low in primary cultures of basal keratinocytes, but that this activity is induced 24-48 h after increasing the concentration of extracellular calcium, and this observation provides a link between the obligate activation of PKC during keratinocyte differentiation and the nuclear response required to alter gene expression.

TL;DR: Analysis of AP-1 transcriptional activity in mouse keratinocytes treated with calcium and 12-O-tetradecanoyl phorbol-13-acetate indicates that Fra-2 and c-Fos play opposing roles in regulating AP- 1 activity in Keratinocytes and that multiple inducer-dependent regulatory pathways may exist for the expression of keratinocyte differentiation markers.

TL;DR: The data suggest that modulation of RARs could contribute to the neoplastic phenotype in mouse skin carcinogenesis and may be involved in the differential promoting activity of mezerein and 12-O-tetradecanoylphorbol-13-acetate, particularly for selecting tumors at high risk for malignant conversion.

TL;DR: The increase in CRE reporter activity in the presence of the dominant-negative CREB mutants suggests that CRE-mediated transcriptional activity is suppressed in keratinocytes through protein-protein interactions involving a factor that dimerizes with the CREB leucine zipper.