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Forcing FAK into Transcriptional Activity
1Cell Signalling and Adhesion Group, Structural Biology and Biocomputing Programme, Spanish National Cancer Research Centre (CNIO), Calle Melchor Fernández Almagro 3, Madrid 28029, Spain.
Structure (London, England : 1993)
|August 4, 2016
Summary
Mechanical forces move focal adhesion kinase (FAK) into the nucleus of heart cells. There, FAK and MEF2 interaction offers structural insights into controlling cardiac hypertrophy.
Area of Science:
- Molecular biology
- Cell biology
- Biochemistry
Background:
- Focal adhesion kinase (FAK) traditionally signals in cytoplasmic adhesion structures.
- Recent findings indicate FAK also functions as a nuclear transcriptional regulator.
Purpose of the Study:
- To investigate the translocation of FAK to the nucleus in cardiomyocytes under mechanical stress.
- To elucidate the structural basis of FAK interaction with the MEF2 transcription factor.
- To understand FAK's role in controlling cardiac hypertrophy.
Main Methods:
- Studies involving cardiomyocytes subjected to mechanical forces.
- Structural biology techniques to analyze protein interactions.
- Molecular assays to assess transcriptional regulation and cardiac hypertrophy markers.
Main Results:
- Mechanical forces were shown to translocate FAK from the cytoplasm to the nucleus of cardiomyocytes.
- Structural insights were provided into the interaction between FAK and the MEF2 transcription factor.
- The FAK-MEF2 interaction was linked to the regulation of cardiac hypertrophy.
Conclusions:
- FAK plays a dual role, functioning both in cytoplasmic signaling and nuclear transcriptional regulation.
- Mechanical cues can alter FAK localization, impacting its nuclear function.
- Understanding the FAK-MEF2 interaction mechanism is crucial for targeting cardiac hypertrophy.