Chondrocytes derived from induced pluripotent stem cells with the dysplasia-causing TRPV4 mutations, V620I and T89I mutation, were resistant to BMP4-induced hypertrophy, suggesting a mechanism underlying the effects of TRPV4 dysfunction on the severity of skeletal dysplasia.

Publicly available gene expression data and proven methodologies for building model Gene Regulatory Networks are applied to successfully construct the IGF1 signaling GRN behind alveologenesis, serving as a pioneer in transforming how lung development and its associated diseases is approached.

Glutamatergic–cholinergic neurons in the postinspiratory complex are critical for swallow motor patterning and the coordination of swallow and breathing, which is disrupted by chronic intermittent hypoxia, a condition seen in many disorders associated with dysphagia and aspiration pneumonia.

Increasing the internal pH of cells can induce dysplasia and enhance oncogene-increased cell growth, while decreasing the internal pH combined with oncogene expression leads to synthetic lethality.

Acute one-hour treatment of Pik3ca mutant mice with a novel anti-epilepsy drug suppresses seizures despite continued developmental brain dysmorphology, promising a new therapeutic strategy for patients with intractable pediatric epilepsy.

Reduced lung myofibroblast proliferation is a unifying feature in multiple models of developmental emphysema and inhibition of myofibroblast proliferation is sufficient to cause this pathology.

XTABLE is the first easy-to-use bioinformatic solution that has been conceived and designed solely to interrogate the transcriptomes of premalignant stages of lung squamous cell carcinoma (LUSC) and enhance the development of LUSC prevention and detection strategies.

Pathogenic mutations in KIF22, which dominantly cause bone dysplasia, improperly activate the motor during anaphase in dividing cells leading to chromosome recongression.

Global, multi-angled genetic analyses identified an age-associated loss of stem cell lineage fidelity that was linked to changes in polycomb regulation in the Drosophila intestinal epithelium.