This technology is a mouse model engineered to conditionally delete the autophagy-linked FYVE protein WDFY3, creating an effective research tool for studying autophagy, mitophagy, efferocytosis, and diseases impacted by these pathways, including neurodevelopmental and neurodegenerative disorders.
The autophagy-linked FYVE protein WDFY3 is a large multidomain scaffolding protein required for autophagy and clearance of damaged mitochondria (mitophagy). Loss of WDFY3 can result in neurodevelopmental delays and intellectual disabilities and has been linked to autism spectrum disorder and Huntington’s disease. The gene has also been shown to be required for macrophage efferocytosis, suggesting a role in resolving inflammation and chronic inflammatory diseases. Currently, there are no commercially available WDFY3-depleted mouse models, making it challenging to conduct in vivo analyses of this gene for research or therapeutic purposes.
This technology describes a mouse model generated to conditionally knock out the murine WDFY3 gene. In this model, the 5th exon of WDFY3 is flanked by loxP sites, which lead to the production of a truncated 66-amino-acid peptide after Cre-mediated recombination, thereby silencing the effect of the full-length 3,508-amino-acid Wdfy3 protein.
This technology has been experimentally validated in both the context of neurodevelopmental disorders and macrophage-dependent inflammation.
IR CU26114
Licensing Contact: Kristin Neuman
