Zdeněk Andrysík

This study identifies hyperactive interferon signaling and lymphoid tissue disorganization as drivers of adaptive immune dysfunction in Down syndrome across development and aging.

The paper demonstrates that sulanemadlin, a stapled peptide inhibitor of MDM2, specifically activates p53 in zebrafish without inducing apoptosis, enabling direct in vivo studies of p53 regulation.

The paper shows that correcting interferon receptor gene dosage in a mouse model of trisomy 21 rescues multiple key phenotypes associated with Down syndrome.

This study identifies a translational control mechanism regulated by PCBP2 and DHX30 that determines the outcome of p53 activation by Nutlin, shifting the response from cell cycle arrest to apoptosis.