A new article from Dc. Paloma Pérez’s group has been published describing that functional interactions between the glucocorticoid receptor (GR) and p63 play a key role in the pathogenesis of atopic dermatitis.

The group of Dr. Paloma Pérez, in collaboration with the Proteomics Service of CIC bioGUNE, Bilbao, has published a new article in the journal “Cell Death & Disease” entitled: Glucocorticoid receptor controls atopic dermatitis inflammation via functional interactions with P63 and autocrine signaling in epidermal keratinocytes.

In this work, the GR interactome (protein complexes formed by GR in chromatin) has been identified in keratinocytes treated with the synthetic ligand dexamethasone. This interactome includes transcription factors with a key role in atopic dermatitis (AD), such as p63. Using human epidermal equivalents and an experimental model of AD, the authors demonstrate that GR inactivation leads to a constitutive increase in p63 and an increase in the autocrine production of TH2-/TH1-/TH17-TH22 factors, which recapitulate the phenotypic alterations and inflammation characteristic of this disease.

You can read the full article by clicking on the following link.