Tec, a member of the Tec family of non-receptor tyrosine kinases, is part of a subfamily that also includes Btk, Itk/Emt/Tsk, Etk/Bmx, and Txk/Rlk [1,5,8]. These kinases are crucial in cell signaling and immune regulation, especially in hematopoietic cells, and are involved in pathways like those triggered by T-cell receptor (TCR), B-cell receptor (BCR), and FcεRI [2,3,4,6,7]. They play a role in regulating phospholipase C-γ, actin cytoskeletal reorganization, cellular adhesion, and T-helper-cell differentiation [3,4]. Genetic models, such as KO/CKO mouse models, can be valuable in further elucidating Tec's functions.

In T cells, mutations eliminating Tec family kinases quantitatively reduce proximal signaling and qualitatively alter T cell development and differentiation, indicating their role as signal modulators [3]. In planarians, tec-1 (a conserved tyrosine kinase) was identified as a negative regulator of neuronal regeneration; tec-1RNAi increased the abundance of several neuron subtypes without affecting body patterning or non-neural cells, suggesting it limits the survival of newly differentiated neurons [9]. In the cardiovascular system, Tec kinases are involved in the occurrence and progression of ischemic heart disease, atherosclerosis, and other cardiovascular diseases, although the exact role of Tec specifically within this context is yet to be comprehensively clarified [1].

In conclusion, Tec is an important regulator in cell signaling and immune-related processes. Model-based research, including KO/CKO mouse models in relevant studies, has revealed its role in T-cell development, neuronal regeneration in planarians, and potentially in cardiovascular diseases. Understanding Tec's functions can provide new insights into the mechanisms of these biological processes and diseases, which may contribute to the development of new preventive and treatment strategies.