Cell Signaling Technology

Product Pathways - Phosphatases

Phospho-SHP-2 (Tyr580) Antibody #3703

Applications Reactivity Sensitivity MW (kDa) Source
W IP H M R (C) Endogenous 72 Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  R=Rat  C=Chicken
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

Phospho-SHP-2 (Tyr580) Antibody detects endogenous levels of SHP-2 only when phosphorylated at Tyr580.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Tyr580 of human SHP-2. Antibodies are purified by peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of total cell lysates from NIH/3T3 cells, serum-starved overnight and treated with PDGF (#9909) for 5 minutes, using Phospho-SHP-2 (Tyr580) Antibody (upper) or control SHP-2 Antibody #3752 (lower).

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).

  1. Qu, C.K. (2000) Cell Res 10, 279-88.
  2. Maroun, C.R. et al. (2000) Mol Cell Biol 20, 8513-25.
  3. Zhang, S.Q. et al. (2002) Mol Cell Biol 22, 4062-72.
  4. Bennett, A.M. et al. (1994) Proc Natl Acad Sci USA 91, 7335-9.
  5. Lu, W. et al. (2001) Mol Cell 8, 759-69.
  6. Edouard, T. et al. (2007) Cell Mol Life Sci 64, 1585-90.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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