Description
Key facts
Species or organism:Human,
Form:LiquidSee storage information
Product details:
ab94321 is a 293T cell transfected lysate in which Human FAK has been transiently over-expressed using a pCMV-FAK plasmid. The lysate is provided in 1X Sample Buffer.
Properties and Storage Information:
Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Focal Adhesion Kinase (FAK) also known as Protein Tyrosine Kinase 2 (PTK2) is a non-receptor tyrosine kinase. This protein has a molecular weight of approximately 125 kDa. FAK is expressed at high levels in brain muscle and liver tissues. Mechanically FAK plays a role in cellular adhesion and migration by regulating integrin signaling and cell-extracellular matrix interactions. FAK auto-phosphorylates at tyrosine residue 397 creating a binding site for Src family kinases and promoting downstream signaling pathways.
Biological function summary
Focal Adhesion Kinase participates in the formation of focal adhesions which are complexes that connect the cytoskeleton to the extracellular matrix. The FAK protein functions as an important signaling node in these structures allowing for the assembly of multiprotein signal transduction complexes. FAK also controls cellular processes such as spreading motility and survival. The interaction with proteins such as Src kinases paxillin and talin facilitates its biological roles in cell signaling.
Pathways
Focal Adhesion Kinase engages in the regulation of the MAPK/ERK signaling pathway and the PI3K/AKT pathway. These pathways are instrumental for cell proliferation survival and migration. In these pathways FAK interacts with proteins such as PI3K Grb2 and Sos linking integrin-mediated signals with downstream effects that influence cell behavior and survival.
Altered FAK signaling has ties to cancer progression and metastasis as well as cardiovascular diseases. In cancer the overexpression of FAK and its interaction with proteins like Src and VEGFR can drive tumor growth and angiogenesis. In cardiovascular diseases improper FAK activation can lead to aberrant heart tissue remodeling and associated pathologies. Abnormalities in FAK signaling pathways can therefore contribute significantly to the development and progression of these diseases.
