|Other Names||Tyrosine-protein phosphatase non-receptor type 11, Protein-tyrosine phosphatase 1D, PTP-1D, Protein-tyrosine phosphatase 2C, PTP-2C, SH-PTP2, SHP-2, Shp2, SH-PTP3, PTPN11, PTP2C, SHPTP2|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP8471d was selected from the Y584 region of human SHP2. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Acts downstream of various receptor and cytoplasmic protein tyrosine kinases to participate in the signal transduction from the cell surface to the nucleus. Dephosphorylates ROCK2 at Tyr-722 resulting in stimulatation of its RhoA binding activity. Dephosphorylates CDC73 (PubMed:26742426).|
|Cellular Location||Cytoplasm. Nucleus|
|Tissue Location||Widely expressed, with highest levels in heart, brain, and skeletal muscle.|
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Provided below are standard protocols that you may find useful for product applications.
SHP2, also known as PTPN11, is a member of the protein tyrosine phosphatase (PTP) family. PTPs are known to be signaling molecules that regulate a variety of cellular processes including cell growth, differentiation, mitotic cycle, and oncogenic transformation. This PTP contains two tandem Src homology-2 domains, which function as phospho-tyrosine binding domains and mediate the interaction of this PTP with its substrates. This PTP is widely expressed in most tissues and plays a regulatory role in various cell signaling events that are important for a diversity of cell functions, such as mitogenic activation, metabolic control, transcription regulation, and cell migration. Mutations in the gene are a cause of Noonan syndrome as well as acute myeloid leukemia.
Chan, R.J., et al., Blood 105(9):3737-3742 (2005).Sturla, L.M., et al., J. Biol. Chem. 280(15):14597-14604 (2005).Loh, M.L., et al., Leuk. Res. 29(4):459-462 (2005).Wang, Q., et al., J. Biol. Chem. 280(9):8397-8406 (2005).Niihori, T., et al., J. Hum. Genet. 50(4):192-202 (2005).
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