FAK Signaling Pathway and Interaction Networks in Diseases

Dear Colleagues,

Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase of 126 kDa, which localizes at sites of cell adhesion to the extracellular matrix (ECM) and mediates downstream events from integrins and other signals by acting as a signaling integrator. Therefore, FAK has been implicated in diverse signaling pathways and molecular networks that impact on cell growth, migration and survival, as well as, more recently, immune-escape of tumor cells through kinase-independent scaffolding functions. Moreover, FAK has multiple roles in the control of several process in human embryonic stem cells, such as in survival, proliferation, anchorage, contractility, and support or inhibition of self-renewal.

This multi-faced FAK roles indicate that this protein is a potential relevant pathogenic trigger in several complex diseases, mainly cancers, suggesting that FAK is a promising target for therapeutic use.

Along these lines, this Special Issue welcomes submissions of research articles and reviews covering molecular aspects of the FAK role in several diseases (cancer, cardiovascular and kidney diseases, etc.) and its interaction with other molecular networks and dynamic cell processes, such as cell differentiation and pluripotency, in both humans and experimental models. Pilot studies on the use of novel FAK inhibitors are also appreciated.

Dr. Anna Alisi
Dr. Rossella Rota
Guest Editor

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