The study investigates the role of Alms1 in mesenchymal lineage cells. Mesenchymal-specific deletion of Alms1 induces metabolic dysfunction resembling Alström syndrome, including obesity, insulin resistance, and fatty liver. The findings demonstrate that loss of Alms1 in adipose lineage cells is sufficient to drive systemic metabolic alterations and organ dysfunction.
Mesenchymal deletion of Alms1 recapitulates key metabolic features of Alström syndrome including fatty liver and systemic metabolic dysregulation, confirming a central role of adipose lineage dysfunction in disease pathogenesis
Alms1 conditional Knockout mouse (mesenchymal-specific deletion using Pdgfra-Cre) — genOway-developed
Alström syndrome, obesity, insulin resistance, lipodystrophy-like phenotype, metabolic disease modeling
Conditional Knockout of Alms1 using Pdgfra-Cre, mesenchymal lineage targeting, metabolic phenotyping, glucose homeostasis assays, liver steatosis analysis, adipose tissue characterization
From model design to experimental results
Featured in 600+ scientific articles
Collaboration with 17 Top Pharmas,
170+ Biotechs and 380+ Academic Institutions
Generated with biopharma partners and in-house
and guaranteed freedom to operate
Models with certified health status from professional breeders in US and Europe
