Product Name: FAK (571-579) pS574+pT575+pY576+pY577
Product Number: PE-04AUA01
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Peptide Name: FAK (571-579) pS574+pT575+pY576+pY577
Product Use: This phosphopeptide may be useful as a substrate for screening the phosphatase activity of protein phosphatases. The peptide sequence is located in the protein kinase catalytic domain activation T-loop between subdomains VII and VIII. Phosphorylation of Y576 and Y577 stimulates phosphotransferase activity. Phosphorylation of S574 and T575 are predicted to be stimulatory for phosphotransferase activity.
Peptide Production Method: Solid-phase peptide synthesis
Peptide Origin: Homo sapiens
Peptide Sequence: MED-pS-pT-pY-pY-KA
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: Amide
Product Use: This phosphopeptide may be useful as a substrate for screening the phosphatase activity of protein phosphatases. The peptide sequence is located in the protein kinase catalytic domain activation T-loop between subdomains VII and VIII. Phosphorylation of Y576 and Y577 stimulates phosphotransferase activity. Phosphorylation of S574 and T575 are predicted to be stimulatory for phosphotransferase activity.
Peptide Production Method: Solid-phase peptide synthesis
Peptide Origin: Homo sapiens
Peptide Sequence: MED-pS-pT-pY-pY-KA
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: Amide
Peptide Modifications Other: Phosphorylated
Storage Conditions: -20°C
Storage Conditions: -20°C
Scientific Background: FAK (PTK2) is a protein-tyrosine kinase of the TK group and Fak family. It is a non-receptor kinase that regulates a variety of cell processes, including cell migration, adhesion, spreading, actin cytoskeletal reorganization, formation/disassembly of focal adhesions, progression through the cell cycle, cell proliferation, and apoptosis. In addition, the FAK protein is required for the proper development of the heart, skeleton, and nervous system. Phosphorylation of T397 increases phosphotransferse activity, induces interaction with FAK and SOCS1, and inhibits interaction with PIK3R2 and Src. Phosphorylation of Y576 and Y577 increases phosphotransferase activity. Phosphorylation of Y861 increases phosphotranserase activity and induces interaction with ITGB5 and p130 Cas. Phosphorylation of Y925 induces interaction with Grb2. Phosphorylation at S722 inhibits FAK binding to the adapter protein p130Cas. FAK appears to be an oncoprotein (OP). A role for FAK in cancer cell migration and motility has been demonstrated for several human cancer types. Knockdown of FAK expression in a human gastric adenocarinoma cell line resulted in the impairment of cancer cell spreading and elongation. In animal studies, deletion of the FAK gene in mice prevented papilloma formation and inhibited the progression of malignancy in pre-formed benign tumours, indicating an oncogenic role for the FAK protein. Additionally, FAK gene deletion was associated with a reduction in keratinocyte migration and increased keratinocyte cell death. Therefore, FAK was concluded to modulate the formation of benign tumours and their subsequent malignant conversion. In 39 hepatocellular carcinoma (HCC) cell lines analyzed for copy number expression, increased copy number was observed at the FAK locus and correlated strongly with expression level of the FAK protein as well as an increased tumour size (>5 cm).
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