Ignacy Czajewski, Bijayalaxmi Swain ... Daan MF van Aalten
Modelling O-GlcNAc transferase intellectual disability reveals the roles of this post-translational modification in regulating normal axonal terminal morphology and maintaining appropriate sleep homeostasis, pharmacological and genetic rescues of O-GlcNAcylation highlight the complexities of addressing this disorder.
A single-nucleus atlas of bone repair uncovers the trajectories of periosteal skeletal stem/progenitor cells in response to fracture and identifies injury-induced fibrogenic cells as intermediate osteochondroprogenitors and key paracrine regulators.
Maternal obesity mouse model reveal that melatonin deficiency causes the genomic hyper-methylation of oocytes via increasing the expression of DNA methyltransferases.
In metastatic NSCLC patients, CHIP showed minimal impact on immunotherapy response but was more prevalent and associated with inflammatory pathways in myeloid cells, particularly in lung squamous cell carcinoma.