CRK Human

The CRKL gene was first identified as an oncogene product of the avian sarcoma virus CT10 . The protein encoded by this gene is structurally similar to the v-Crk protein, which consists of a viral Gag portion fused with a Src homology domain . The human recombinant version of CRKL retains these critical domains, enabling it to interact with various signaling molecules within the cell.

CRKL is involved in multiple cellular signaling pathways. It acts as an adaptor protein, facilitating the interaction between different signaling molecules. This protein is known to be upregulated in several types of human cancers, including leukemia, cervical cancer, and hepatocellular carcinoma . Its role in cancer progression is attributed to its ability to regulate alternative splicing of cancer-related genes and its involvement in key signaling pathways such as DNA repair, G2/M mitotic cell cycle, and GnRH signaling .

CRKL exerts its effects through its SH2 and SH3 domains, which allow it to bind to phosphorylated tyrosine residues on other proteins. This binding facilitates the formation of protein complexes that are essential for signal transduction. In cancer cells, CRKL has been shown to regulate the expression of genes involved in cell proliferation and invasion, contributing to tumor growth and metastasis .

The overexpression of CRKL in various cancers makes it a potential target for therapeutic interventions. Understanding the regulatory mechanisms of CRKL and its role in cancer progression can provide insights into developing targeted therapies for cancer treatment. Additionally, the identification of the ETV6-miR-429-CRKL regulatory circuitry in hepatocellular carcinoma highlights the complex interactions between different signaling molecules and their impact on cancer aggressiveness .