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Abstract

Interactions of genes in intersecting signaling pathways, as well as environmental influences, are required for the development of psoriasis. Peroxisome proliferator-activated receptor gamma (PPAR{gamma}) is a nuclear receptor and transcription factor which inhibits the expression of many proinflammatory genes. We tested the hypothesis that low levels of PPAR{gamma} expression promote the development of psoriatic lesions. We combined experimental results and network functional analysis to reconstruct the model of PPAR{gamma} downregulated signaling in psoriasis. We hypothesize that the expression of IL17, STAT3, FOXP3, and RORC and FOSL1 genes in psoriatic skin are correlated with the level of PPAR{gamma} expression and they belong to the same signaling pathway that regulates the development of psoriasis lesion.

02 /Specification & Classification

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