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Schonthaler, Helia B.; Guinea-Viniegra, Juan; Wculek, Stefanie K.; Ruppen, Isabel; Ximénez-Embún, Pilar; Guío-Carrión, Ana; Navarro, Raquel; Hogg, Nancy; Ashman, Keith; Wagner, Erwin F.
Immunity (Cambridge, Mass.), 12/2013, Letnik: 39, Številka: 6Journal Article
Psoriasis is a common heterogeneous inflammatory skin disease with a complex pathophysiology and limited treatment options. Here we performed proteomic analyses of human psoriatic epidermis and found S100A8-S100A9, also called calprotectin, as the most upregulated proteins, followed by the complement component C3. Both S100A8-S100A9 and C3 are specifically expressed in lesional psoriatic skin. S100A9 is shown here to function as a chromatin component modulating C3 expression in mouse and human cells by binding to a region upstream of the C3 start site. When S100A9 was genetically deleted in mouse models of skin inflammation, the psoriasis-like skin disease and inflammation were strongly attenuated, with a mild immune infiltrate and decreased amounts of C3. In addition, inhibition of C3 in the mouse model strongly reduced the inflammatory skin disease. Thus, S100A8-S100A9 can regulate C3 at the nuclear level and present potential new therapeutic targets for psoriasis. Display omitted •S100A8-S100A9 regulate complement C3 expression•S100A8-S100A9 binds to chromatin at the C3 promoter•Loss of S100A8-S100A9 and/or C3 improves psoriasis-like symptoms•S100A8-S100A9 and C3 are specifically expressed in psoriasis
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Dostop do baze podatkov JCR je dovoljen samo uporabnikom iz Slovenije. Vaš trenutni IP-naslov ni na seznamu dovoljenih za dostop, zato je potrebna avtentikacija z ustreznim računom AAI.
Leto | Faktor vpliva | Izdaja | Kategorija | Razvrstitev | ||||
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
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Vir: Osebne bibliografije
in: SICRIS
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