Flna, encoding an actin-binding protein, is involved in multiple biological processes. It has been associated with pathways like RAC1-Cofilin activity modulation and is crucial for maintaining normal cellular functions, with implications in various diseases [1].

In conditional Flna flox/flox mice, depletion of Flna from cortical pyramidal neurons via in-utero electroporation of Cre recombinase showed that Flna regulates dendritogenesis and spinogenesis, promoting an appropriate excitatory/inhibitory inputs balance. It modulates RAC1 and cofilin activity through interaction with ARHGAP24, suggesting its role in neural circuit development [1]. Conditional knockout mouse models also indicated that the skeletal dysplasia phenotype associated with pathogenic variants in FLNA is not caused by a cell-autonomous loss-of-function in the osteoblast-osteocyte lineage, adding evidence to the gain-of-function hypothesis [2].

In conclusion, Flna is essential for functions such as neuronal maturation and potentially for normal skeletal development. The use of gene knockout and conditional knockout mouse models has been instrumental in revealing its role in neural and skeletal-related disease conditions, enhancing our understanding of these biological processes and associated pathologies.