Martin Leeb

The paper identifies Wt1 splice isoforms as regulators of lineage-associated transcriptional programs during formative pluripotency, showing that alternative splicing tunes lineage bias.

This study reveals that PHLPP2 is a pseudophosphatase with no catalytic activity, challenges its role as a tumor suppressor, and identifies its non-catalytic functions in Akt signaling.

This study develops a feeder-free serum-coated system for culturing naive human pluripotent stem cells, maintaining their developmental potential and reducing contamination and mutations.

This study identifies FoxO transcription factors as essential for transitioning from naive to formative pluripotency by regulating enhancer activity through AKT signaling.

The paper studies 3D genome structure changes in single mouse ES cells exiting pluripotency, finding reorganization of enhancer-promoter interactions through multiway chromatin hubs.

The paper identifies an enhancer element that amplifies Fgf5 expression by accumulating paused RNA Polymerase II, revealing a new mechanism of enhancer collaboration during differentiation.

The paper identifies novel imprinted genes in mouse blastocysts and shows that their expression is mostly independent of DNA methylation but associated with H3K27me3 marks.

The paper identifies molecular networks driving the transition from naive to formative pluripotency in mammalian cells using genetic and transcriptomic analyses.