<HashMap><database>bioimages</database><scores/><additional><omics_type>Unknown</omics_type><submitter/><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-BIAD661</full_dataset_link><repository>bioimages</repository><figure_sub>Specimen</figure_sub><figure_sub>Image analysis</figure_sub><figure_sub>Study Component</figure_sub><figure_sub>organisation</figure_sub><figure_sub>Biosample</figure_sub><figure_sub>Image correlation</figure_sub><figure_sub>Associations</figure_sub><figure_sub>Image acquisition</figure_sub><pubmed_authors>Agnes Csiszar</pubmed_authors></additional><is_claimable>false</is_claimable><name>FAM3C/ILEI protein is elevated in psoriatic lesions and triggers psoriasiform hyperproliferation in mice</name><description>FAM3C/ILEI is an important cytokine for tumor progression and metastasis. However, its involvement in inflammation remains elusive. Here, we show that ILEI protein is highly expressed in psoriatic lesions. Inducible keratinocyte-specific ILEI overexpression in mice (K5-ILEIind) recapitulates many aspects of psoriasis following TPA challenge, primarily manifested by impaired epidermal differentiation and increased neutrophil recruitment. Mechanistically, ILEI triggers Erk and Akt signaling, which then activate STAT3 via Ser727 phosphorylation. Keratinocyte-specific ILEI deletion ameliorates TPA-induced skin inflammation. A transcriptomic ILEI signature obtained from the K5-ILEIind model shows enrichment in several signaling pathways also found in psoriasis and identifies urokinase as a targ</description><dates><release>2023-03-17T00:00:00Z</release><modification>2023-04-24T15:22:30.197Z</modification><creation>2023-03-27T19:45:31.458Z</creation></dates><accession>S-BIAD661</accession><cross_references/></HashMap>