Abcam, ab4794, Anti-FAK (phospho S910) antibody

Size: 50µL
Rabbit Polyclonal FAK phospho S910 antibody. Suitable for WB and reacts with Human samples. Cited in 1 publication. Immunogen corresponding to Synthetic Peptide within Human PTK2 phospho S910.
Key facts
Host species:Rabbit,
Clonality:Polyclonal,
Isotype:IgG,
Carrier free:No,
Reacts with:Human,
Applications:WBSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Immunogen:Synthetic Peptide within Human PTK2 phospho S910. The exact immunogen used to generate this antibody is proprietary information.Q05397

Product details:
FAK is a non-receptor protein tyrosine kinase discovered as a substrate for Src and it is a key protein in integrin, growth factor and bioactive peptide signaling. FAK plays a central role in cell spreading, differentiation, migration, cell death and acceleration of the G1 to S phase transition of the cell cycle. FAK regulation includes phosphorylation at multiple tyrosine and serine residues. Phosphorylation of tyrosine generally is associated with positive regulation and growth promotion, however, dephosphorylation at these sites occurs as cells enter mitosis (M-Phase of the cell cycle). In contrast, serine phosphorylation either remains high or is increased as cells enter mitosis and may play a role in focal adhesion disassembly.

Properties and Storage Information:
Form-Liquid, Purification technique-Affinity purification Immunogen, Purification notes-Purified from rabbit serum by sequential epitope-specific chromatography. The antibody has been negatively preadsorbed using (i) a non-phosphopeptide corresponding to the site of phosphorylation to remove antibody that is reactive with non-phosphorylated Focal Adhesion Kinase enzyme and (ii) a generic serine phosphorylated peptide to remove antibody that is reactive with phospho-serine, irrespective of the sequence. The final product is generated by affinity chromatography using a Focal Adhesion Kinase-derived peptide that is phosphorylated at serine 910., Storage buffer-pH: 7.3Preservative: 0.05% Sodium azideConstituents: PBS, 50% Glycerol (glycerin, glycerine), 0.1% BSA, Shipped at conditions-Blue Ice, Appropriate short-term storage conditions-+4°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.