«Our hope is that, based on the structural data presented in our paper, it may be possible to develop drugs that inhibit cancer progression by blocking the interaction
of focal adhesion kinase with other proteins,» says Dr. Meves.
The protein, known
as focal adhesion kinase, or FAK, activates an enzyme called AKT, which helps islet cells in the pancreas to survive.
The team at Barts Cancer Institute, part of Queen Mary University of London, have found that a molecule,
called focal adhesion kinase (FAK), signals the body to repair itself after chemotherapy or radiotherapy, which kill cancer cells by damaging DNA.
«In our paper, we identify a direct interaction
between focal adhesion kinase and myosin that drives the production of secreted cancer - promoting proteins,» says Alexander Meves, M.D., a dermatologist at Mayo Clinic.
Monika Raab, Yuning Lu, Karsten Kohler, Xin Smith, Klaus Strebhardt & Christopher E. Rudd, «LFA - 1
activates focal adhesion kinases FAK1 / PYK2 to generate LAT - GRB2 - SKAP1 complexes that terminate T - cell conjugate formation», Nature Communications, 2017 July 12.
A Role
for Focal Adhesion Kinase Signaling in Tumor Necrosis Factor - α — Dependent Matrix Metalloproteinase - 9 Production in a Cholangiocarcinoma Cell Line, CCKS1
The stress hormone treatment activated a protein called FAK (
focal adhesion kinase), which is known to protect cells from anoikis.
Other molecular differences between leaders and followers include traction - generating FAK (
focal adhesion kinase) activity in leader cells and growth - promoting Notch signaling in followers — both potential avenues for disrupting the symbiotic relationship between leaders and followers.
He says once
focal adhesion kinase and myosin interact, focal adhesion kinase is shuttled to the cell nucleus to help the cell adapt to its environment through gene transcription.