Product nameAnti-SHP2 (phospho S576) antibody
See all SHP2 primary antibodies
DescriptionRabbit polyclonal to SHP2 (phospho S576)
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat
The antiserum was produced against a chemically synthesized phosphopeptide derived from the region of human SHP2 that contains serine 576.
- Hek293 cells treated with PMA.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Storage bufferpH: 7.30
Preservative: 0.05% Sodium azide
Constituents: PBS, 50% Glycerol, 0.1% BSA
PBS is Ca2+ and Mg2+ free
Concentration information loading...
PurityImmunogen affinity purified
Purification notesPurified from rabbit serum by sequential epitope-specific chromatography. The antibody has been negatively preadsorbed using a non-phosphopeptide corresponding to the site of phosphorylation to remove antibody that is reactive with non-phosphorylated SHP2. The final product is generated by affinity chromatography using a SHP2-derived peptide that is phosphorylated at serine 576.
Our Abpromise guarantee covers the use of ab17940 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/1000. Detects a band of approximately 68 kDa (predicted molecular weight: 68 kDa).|
FunctionActs downstream of various receptor and cytoplasmic protein tyrosine kinases to participate in the signal transduction from the cell surface to the nucleus.
Tissue specificityWidely expressed, with highest levels in heart, brain, and skeletal muscle.
Involvement in diseaseDefects in PTPN11 are the cause of LEOPARD syndrome type 1 (LEOPARD1) [MIM:151100]. It is an autosomal dominant disorder allelic with Noonan syndrome. The acronym LEOPARD stands for lentigines, electrocardiographic conduction abnormalities, ocular hypertelorism, pulmonic stenosis, abnormalities of genitalia, retardation of growth, and deafness.
Defects in PTPN11 are the cause of Noonan syndrome type 1 (NS1) [MIM:163950]. Noonan syndrome (NS) is a disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis. Some patients with Noonan syndrome type 1 develop multiple giant cell lesions of the jaw or other bony or soft tissues, which are classified as pigmented villomoduolar synovitis (PVNS) when occurring in the jaw or joints. Note=Mutations in PTPN11 account for more than 50% of the cases. Rarely, NS is associated with juvenile myelomonocytic leukemia (JMML). NS1 inheritance is autosomal dominant.
Defects in PTPN11 are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:607785]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. It is characterized by leukocytosis with tissue infiltration and in vitro hypersensitivity of myeloid progenitors to granulocyte-macrophage colony stimulating factor.
Defects in PTPN11 are a cause of metachondromatosis (MC) [MIM:156250]. It is a skeletal disorder with radiologic fetarures of both multiple exostoses and Ollier disease, characterized by the presence of multiple enchondromas and osteochondroma-like lesions.
Sequence similaritiesBelongs to the protein-tyrosine phosphatase family. Non-receptor class 2 subfamily.
Contains 2 SH2 domains.
Contains 1 tyrosine-protein phosphatase domain.
DomainThe SH2 domains repress phosphatase activity. Binding of these domains to phosphotyrosine-containing proteins relieves this auto-inhibition, possibly by inducing a conformational change in the enzyme.
modificationsPhosphorylated on Tyr-546 and Tyr-584 upon receptor protein tyrosine kinase activation; which creates a binding site for GRB2 and other SH2-containing proteins.
- Information by UniProt
- BPTP3 antibody
- CFC antibody
- JMML antibody
Peptide Competition and Phosphatase Treatment
Lysates prepared from Hek293 treated with PMA were resolved by SDS-PAGE on a 10% polyacrylamide gel and transferred to PVDF. Membranes were either treated with lambda (λ) phosphatase (1) or left untreated (2-7), blocked with a 3% BSA-TBST buffer for one hour at room temperature, and incubated with SHP2 [pS576] antibody for two hours at room temperature in a 3% BSA-TBST buffer, following prior incubation with: no peptide (1, 2), the non-phosphopeptide corresponding to the immunogen (3), a generic phosphoserine-containing peptide (4), the phosphopeptide corresponding to SHP2 [pS585] (5), the phosphopeptide corresponding to SHP2 [pS591] (6), or, the phosphopeptide immunogen (7). After washing, membranes were incubated with goat F(ab’)2 anti-rabbit IgG HRP conjugate and bands were detected using the Pierce SuperSignal™ method.
The data show that only the peptide corresponding to SHP2 [pS576] bl
ab17940 has not yet been referenced specifically in any publications.