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. Author manuscript; available in PMC: 2024 Aug 18.
Published in final edited form as: Circ Res. 2023 Jul 26;133(5):400–411. doi: 10.1161/CIRCRESAHA.123.322750

Fig. 1. F93A/L98E mutations impairs the interaction between FLNC ABD and actin.

Fig. 1

(A) Filamin ABD (green) binds to F-actin at a junction between adjacent actin monomers (orange and blue) in F-actin (pdb: 6d8c). The residues corresponding to F93 and L98 of mouse FLNC (F99 and L104 in human FLNC) are highlighted in magenta. F99 contacts in actin are in red and L104 contacts are in cyan. Inset: Selection of close contacts to F99 and L104 are highlighted. The double mutant F93A and L99E in mouse FLNC was hypothesized to substantially disrupt FLNC ABD interaction to F-actin. (B) Co-immunoprecipitation (Co-IP) and reverse Co-IP of Human influenza hemagglutinin (HA) tagged full length cardiac α-actin (ACTC1) with 3 x FLAG tagged wild type (WT) or F93A/L98E mutant FLNC actin binding domain (ABD). The cDNA sequences encoding all fusion proteins were inserted into pcDNA3 vector and co-transfected into HEK 293 cells for overexpression. n = 3 independently repeated experiments.