This technology is a transgenic mouse model for studying the nucleus FHOD3 R637P disease-causing allele in cardiac hypertrophy.
Eukaryotic cells’ nuclei actively engage with the actin cytoskeleton through the linker of nucleoplasm and cytoskeleton (LINC) complex. All mechanical interactions with the nucleus require distinct molecular assemblies for transmission. Although current models assume filaments are not altered by their interaction with the LINC complex, there is currently no evidence and no models to study the contribution of the FHOD family to the mechanical behavior of filaments engaged by the nucleus.
This technology is a transgenic mouse model that is based on the FHOD3 R611P disease-causing allele, corresponding to the R637P mutation in humans. Knock-in mice cause dysfunction in nuclear mechanical interaction with the actin cytoskeleton and hypertrophic cardiomyopathy. The dysfunction of FHOD3 can be used to study the mechanism of heart defects caused by mutation and how the function of actin bundling activity regulates the features of formin proteins and actin polymerizing activity.
This technology has been validated in vivo.
IR CU26008
Licensing Contact: Jerry Kokoshka