Render Target: SSR
Render Timestamp: 2024-12-19T21:42:32.355Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-11-19 18:01:10.976
Product last modified at: 2024-12-04T12:45:10.318Z
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PDP - Template Name: Antibody Sampler Kit
PDP - Template ID: *******4a3ef3a

SHP-2 Antibody Sampler Kit #9793

    Product Information

    Product Description

    The SHP-2 Antibody Sampler Kit provides an economical means to evaluate levels of SHP-2 protein phosphorylated at the specified sites, as well as total SHP-2 levels. The kit contains enough primary and secondary antibody to perform two western blot experiments per antibody.

    Specificity / Sensitivity

    SHP-2 (D50F2) Rabbit mAb detects endogenous levels of total SHP-2 protein. Phospho- (Tyr542) SHP-2 Antibody detects endogenous SHP-2 only when phosphorylated at the specified at Tyr542. Phospho- SHP-2 (Tyr580) Antibody detects endogenous level of SHP2 only when phosphorylated at Tyr580. Some cross-reactivity with phosphorylated RTKs may occur. See individual product webpages for more information.

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to the carboxy-terminal sequence of human SHP-2. Polyclonal antibodies are produced by immunizing animals with synthetic phosphopeptides corresponding to residues surrounding Tyr542 and Tyr580 of human SHP-2 protein. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    SHP-2 (PTPN11) is a ubiquitously expressed, nonreceptor protein tyrosine phosphatase (PTP). It participates in signaling events downstream of receptors for growth factors, cytokines, hormones, antigens, and extracellular matrices in the control of cell growth, differentiation, migration, and death (1). Activation of SHP-2 and its association with Gab1 is critical for sustained Erk activation downstream of several growth factor receptors and cytokines (2). In addition to its role in Gab1-mediated Erk activation, SHP-2 attenuates EGF-dependent PI3 kinase activation by dephosphorylating Gab1 at p85 binding sites (3). SHP-2 becomes phosphorylated at Tyr542 and Tyr580 in its carboxy terminus in response to growth factor receptor activation (4). These phosphorylation events are thought to relieve basal inhibition and stimulate SHP-2 tyrosine phosphatase activity (5). Mutations in the corresponding gene result in a pair of clinically similar disorders (Noonan syndrome and LEOPARD syndrome) that may result from abnormal MAPK regulation (6).
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