Slk, also known as STE20-like kinase or STK2, is a kinase belonging to the Sterile 20 family. Its enzymatic activity is linked to the regulation of ezrin, radixin, and moesin function, as well as lymphocyte migration and the cell cycle [2]. It is essential for embryonic development and is involved in processes like wound healing, muscle homeostasis, cell migration, and tumor growth [3].

Studies using gene-knockout mouse models have provided significant insights into Slk's functions. Blastocysts homozygous for the kinase-dead allele SLKK63R do not develop into viable mice, suggesting that at least 50% kinase activity is sufficient for embryonic development [1]. Podocyte-specific deletion of Slk in mice leads to albuminuria, loss of podocytes, and exacerbates glomerular injury in adriamycin nephrosis, indicating its importance in maintaining podocyte integrity [3,5]. In cultured podocytes, deletion of Slk increased adhesion to collagen, though focal adhesion complex proteins were not major substrates of Slk [4].

In conclusion, Slk plays a crucial role in embryonic development and maintaining podocyte integrity. Gene-knockout mouse models have been instrumental in revealing its functions in these processes and in understanding its potential implications in diseases related to podocyte injury and embryonic development [1,3,4,5].