The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Transgenic coexpression of v-Ha-ras and transforming growth factor alpha increases epidermal hyperproliferation and tumorigenesis and predisposes to malignant conversion via endogenous c-Ha-ras activation.

Previously, transgenic mice were generated that overexpressed v-Ha-ras or human transforming growth factor alpha (TGFalpha) exclusively in the epidermis, by means of a targeting vector based on the human keratin 1 gene ( HK1). Both transgenics exhibited a similar neonatal phenotype of epidermal hyperplasia/hyperkeratosis and, in adults, spontaneous and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced papilloma formation. To assess the synergism in vivo between Ha-ras and TGFalpha, mating experiments were performed. All ras/TGFalpha double genotype progeny ( HK1 less than, with dotras/alpha) exhibited an increased epidermal hyperplasia/hyperkeratosis in neonates and accelerated spontaneous papillomatogenesis, compared with single transgenic siblings. HK1 less than, with dotras/alpha mice from the mild lines of HK1 less than, with dotrasxHK1 less than, with dotTGFalpha developed spontaneous papillomas that were not shown in either their parental mice or single transgenic littermates. Unlika in parental or single-genotype siblings, in which TPA promotion-elicited papillomas remained benign, TPA promotion elicited autonomous papillomas in HK1 less than, with dotras/alpha mice and exhibited a novel susceptibility to malignant conversion. Sequence analysis of the endogenous c-Ha-ras from spontaneous and TPA-induced HK1 less than, with dotras/alpha papillomas revealed wild-type sequence. However, carcinomas exhibited c-Ha-ras mutations at codon 61. All tumors analyzed to date expressed wild-type p53. These data provide in vivo evidence that Ha-ras and TGFalpha cooperate in the induction of epidermal hyperplasia and spontaneous tumor formation and predispose to malignant conversion via endogenous c-Ha-ras activation.[1]


WikiGenes - Universities