This study investigates the role of NLRC5 in metabolic regulation. Female Nlrc5<sup>−/−</sup> mice subjected to a high-fat diet exhibited increased weight gain and adiposity compared to wild-type controls. Mechanistically, NLRC5 enhances the expression of PPARγ target genes, such as FABP4, through interaction with co-regulators like Sin3A and NELFB, highlighting its role in adipogenesis and lipid metabolism.
NLRC5 deficiency leads to increased adiposity in female mice on a high-fat diet, associated with impaired regulation of PPARγ target genes. NLRC5 interacts with transcriptional co-regulators Sin3A and NELFB, influencing adipocyte differentiation and lipid metabolism.
Nlrc5(−/−) (NLRC5 Knockout) mouse model developed by genOway, featuring a targeted deletion of the Nlrc5 gene to study its function in metabolic processes.
Obesity, Adipogenesis, PPARγ signaling, Metabolic regulation, Transcriptional co-regulation
Constitutive Knockout model, Targeted gene deletion, High-fat diet-induced obesity model, Transcriptional regulation studies, Adipocyte differentiation assays
From model design to experimental results
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