Sylwia Chelstowska

TL;DR: Molecular adaptations that enable retinoid storage are described and mechanisms in which mutations found in selective proteins might influence vitamin A homeostasis in affected patients are delineated.

TL;DR: The first structure of CRBP1 in a ligand-free form as well as ultra-high resolution structures of this protein bound to either all-trans-retinol or retinylamine are reported, suggesting a mechanism of induced fit upon ligand binding by mammalian cellular retinol-binding proteins.

TL;DR: It is reported that the genetic deletion of Acyl‐CoA:wax alcohol acyltransferase 2 (AWAT2) causes the obstruction of MGs and symptoms of evaporative DED in mice and establishes Awat2−/− mice as a model for DED syndrome that can be used in studies on tear film‐oriented therapies.

TL;DR: It is demonstrated that abn-CBD modulates the flux of retinoids via the retinoid cycle in vivo and targeting selected CRBPs with a small-molecule inhibitor can potentially lead to the development of new therapeutic agents to counteract diseases with etiologies involving imbalance in Retinoid metabolism or signaling.

TL;DR: Evidence is provided for an allosteric modulation of the enzymatic activity by 11-cis retinoids, independent from cellular retinaldehyde-binding protein (CRALBP), that leads to decreased esterification rates for 9-Cis, 13-c is, or all-trans retinols and thus enables preferential synthesis of 11- cis-retinyl esters.