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Molecular consequences of Dlx3 deletion by tamoxifen inducible K14 Cre in adult mouse epidermis (P42-P46) as determined by RNASeq analysis

ABSTRACT: DLX3 is a homeodomain transcription factor involved in epidermal and hair follicle differentiation. Epidermal specific deletion of DLX3 leads to IL17 related inflammation. However, the downstream signals from DLX3-deficient keratinocytes that initiates IL17 associated inflammation is not well-characterized. Therefore we performed acute Dlx3 deletion to identify the initial molecular changes causing the skin inflammatory reponse and tried to rescue the immune phenotype by STAT3 inhibitor treatment (Cryptotanshinone). In this study, we compared the epidermal and dermal transcriptome from Dlx3 wild-type (WT) and K14CreERT;DLX3 fl/fl (icKO).

ORGANISM(S): Mus musculus

PROVIDER: GSE104022 | GEO | 2018/03/01

REPOSITORIES: GEO

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DLX3 binding sites in Supabasal Keratinocytes

Project description:DLX3 is a homeodomain transcription factor involved in epidermal differentiation. Here we investigated the distribution of DLX3 DNA binding sites in suprabasal differentiating keratinocytes using ChIP-seq.

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Dlx3 Regulates Lifr and Chrdl1 Expression in Mouse Embryonic Stem Cell Differentiation

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Molecular consequences of Dlx3 deletion in mouse enamel organ as determined by RNASeq analysis

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Gene expression profiles of dental follicle cells after 48 hours of transfection in vitro with a DLX3 plasmid and an empty vector

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Loss of DLX3 tumor suppressive function promotes progression of SCC through EGFR-ERBB2 pathway.

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