Src, a protein-tyrosine kinase encoded by the physiological Src proto-oncogene, plays crucial roles in multiple cell processes such as growth, division, migration, and survival signaling pathways [1]. From N-to C-terminus, it contains unique, SH3, SH2, protein-tyrosine kinase domains, and a regulatory tail. Key phosphorylation sites include activating pTyr419 and inhibitory pTyr530. It is involved in numerous pathways like PI3K-AKT, Ras-MAPK, JAK-STAT3, and FAK/Paxillin, which are vital for carcinogenesis, bone homeostasis, and platelet function [1,2,3,4]. Genetic models, especially knockout (KO) mice, have been instrumental in studying its functions.

Analyses of Src-knockout mice revealed that Src is essential for bone resorption by osteoclasts and suppresses bone formation by osteoblasts. Src-knockout mice exhibit osteopetrosis, indicating its role in bone homeostasis and potential as a target for osteoporosis therapy [3]. In platelets, studies using Src knockout mice showed that Src mediates platelet spreading on fibrinogen, highlighting its role in platelet activation and function [4].

In conclusion, Src is a multifunctional protein-tyrosine kinase. Model-based research, particularly Src KO mouse models, has demonstrated its significance in bone homeostasis, platelet function, and carcinogenesis. Understanding Src's functions through these models provides insights into potential therapeutic strategies for osteoporosis and cancer [2,3,4].