Kank2, short for KN motif and ankyrin repeat domains 2, is a gene with multiple functions. It is involved in regulating actin polymerization, microtubule targeting, and cell adhesion [3,6]. It also plays a role in the regulation of focal adhesions (FAs), which are crucial for cell migration. Kank2 binds to talin within FAs, mediating actin-microtubule (MT) crosstalk [1,2,5].

In the MDA-MB-435S melanoma cell line, Kank2 knockdown led to increased sensitivity to MT poisons like paclitaxel and vincristine, as well as reduced cell migration. This indicates that Kank2 is a key molecule enabling the actin-MT crosstalk important for both drug sensitivity and cell migration [1,2]. In nephrotic syndrome, the levels of Kank2 in patients were lower than in healthy controls. Kank2 was found to be positively regulated by E2F1, TFAP2C, and NRF1, and knocking down these transcription factors deformed the cytoskeleton of renal tubular cells [6]. In myocardial infarction rats, overexpression of Kank2 improved cardiac function, decreased myocardial collagen deposition, reduced cardiomyocyte apoptosis, and increased angiogenesis, potentially associated with the reduction of NF-κB p65 expression [4].

In summary, Kank2 is essential for functions related to cell adhesion, migration, and cytoskeletal regulation. Model-based research, such as knockdown experiments in cell lines and in vivo studies in rats, has revealed its significance in diseases like melanoma, nephrotic syndrome, and myocardial infarction. These findings provide insights into potential therapeutic targets for these disease areas.