Non-targeted N-glycome profiling reveals multiple layers of organ-specific diversity in mice.

N-glycosylation is one of the most common protein modifications in eukaryotes, with immense importance at the molecular, cellular, and organismal level. Accurate and reliable N-glycan analysis is essential to obtain a systems-wide understanding of fundamental biological processes. Due to the structural complexity of glycans, their analysis is still highly challenging.

Epigenetic regulation by polycomb repressive complex 1 promotes cerebral cavernous malformations.

Cerebral cavernous malformations (CCMs) are anomalies of the cerebral vasculature. Loss of the CCM proteins CCM1/KRIT1, CCM2, or CCM3/PDCD10 trigger a MAPK-Krüppel-like factor 2 (KLF2) signaling cascade, which induces a pathophysiological pattern of gene expression. The downstream target genes that are activated by KLF2 are mostly unknown.

Murine neonatal cardiac regeneration depends on Insulin-like growth factor 1 receptor signaling.

Unlike adult mammals, the hearts of neonatal mice possess the ability to completely regenerate from myocardial infarction (MI). This observation has sparked vast interest in deciphering the potentially lifesaving and morbidity-reducing mechanisms involved in neonatal cardiac regeneration. In mice, the regenerative potential is lost within the first week of life and coincides with a reduction of Insulin-like growth factor 1 receptor (Igf1r) expression in the heart.

Engineering next generation vascularized organoids.

Organoids are self-organizing 3D cell culture models that are valuable for studying the mechanisms underlying both development and disease in multiple species, particularly, in humans. These 3D engineered tissues can mimic the structure and function of human organs in vitro. Methods to generate organoids have substantially improved to better resemble, in various ways, their in vivo counterpart.