Kevin I. Watt

High-throughput screening in hiPSC-cardiac models reveals cardiomyocyte-specific cell cycle regulatory mechanisms

The paper identifies a compound that selectively promotes cardiomyocyte proliferation through specific cell cycle mechanisms without affecting other cell types.

Proteomics Uncovers Cryptic JPH2 Loss in Paediatric Dilated Cardiomyopathy

This study uses proteomics to identify a cryptic JPH2 loss-of-function in a paediatric DCM patient, revealing a novel mechanism of recessive disease.

Changing the Fate of Dystrophin-Deficient Myoblasts via Hetero ligand Nanoclusters on Biomaterial Surface: Effects of Integrin-Syndecan or Dystroglycan Crosstalk

This paper demonstrates that nanoclusters of integrin-, syndecan-, and dystroglycan-binding peptides on biomaterial surfaces enhance myoblast adhesion, proliferation, and differentiation in dystrophin-deficient cells.

Maturation of human cardiac organoids are required for disease modelling and drug discovery

This study shows that maturing human cardiac organoids enhances disease modeling and drug discovery by mimicking in vivo development and enabling therapeutic testing for DSP cardiomyopathy.

Disparities in spatially variable gene calling highlight the need for benchmarking spatial transcriptomics methods.

This study benchmarks spatial transcriptomics methods by comparing 6 SVG identification tools across 14 datasets, revealing discrepancies in results.

Automated Integration of Multi-Slice Spatial Transcriptomics Data in 2D and 3D

VR-Omics automates integration of multi-slice spatial transcriptomics data in 2D and 3D, revealing dysregulated metabolic networks in paediatric cardiac rhabdomyomas.

Proteome-wide systems genetics identifies UFMylation as a regulator of skeletal muscle function

The paper identifies UFMylation as a negative regulator of skeletal muscle function through proteome-wide systems genetics in mice and validates it in a disease model.

Detailed metabolic phenotyping of four tissue specific Cas9 transgenic mouse lines

This study demonstrates that long-term tissue-specific Cas9 expression in mice does not cause detrimental health effects or metabolic changes, supporting its use for gene-specific studies.