Genetic and pharmacological evidence that a retinoic acid cannot be the RXR- activating ligand in mouse epidermis keratinocytes

Article Abstract:

Transcriptional corepressor complexes associated with histone deacetylase activity are recruited to RAREs by unliganded or retinoid antagonist-bound RAR/RXR heterodimers, resulting in chromatin condensation and transcriptional silencing. Subordination of RXR transcriptional activity to that of its RAR partner plays a crucial role in vivo, because it allows RXRs to act convomitantly, within the same cell, as heterodimerization partners for repression, as well as for activation events in which they are transcriptionally active.

United States, Genetic transcription, Transcription (Genetics), Keratinocytes, Tretinoin

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Skin epidermis lacking the c-myc is resistant to Ras-driven tumorigenesis but can reacquire sensitivity upon additional loss of the [p21.sup.Cip1] gene

Article Abstract:

The target genes required for Myc-mediated tumorigenesis are vague and it is shown that while endogenous c-Myc is dispensable for skin homeostatis and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced hyperplasia, c-Myc-deficient epidermis is resistant to Ras-mediated 7.2-dimethylbenzanthracene/TPA-induced tumorigenesis. This shows c-Myc-mediated repression of [p21.sup.Cip.1] as a vital step for Ras-driven epidermal tumorigenesis.

Tumor suppressor genes, Carcinogenesis, Epidermis, Rats as laboratory animals, Laboratory rats, Tumour suppressor genes

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Specific deletion of focal adhesion kinase suppresses tumor formation and blocks malignant progression

Article Abstract:

The role of focal adhesion kinase (FAK) during the formation and formation of skin tumors is investigated using Cre/IoxP technology to target the introduction of conditional mutations into the FAK gene in mice. Results reveal that FAK modulates the efficiency of benign tumor formation and plays a vital role in malignant conversion.

Gene mutations, Gene mutation, Genetic research, Skin tumors, Skin tumours

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