The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use a concentration of 1 - 2 µg/ml. Predicted molecular weight: 68 kDa.
Acts downstream of various receptor and cytoplasmic protein tyrosine kinases to participate in the signal transduction from the cell surface to the nucleus.
Widely expressed, with highest levels in heart, brain, and skeletal muscle.
Defects 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.
Belongs to the protein-tyrosine phosphatase family. Non-receptor class 2 subfamily. Contains 2 SH2 domains. Contains 1 tyrosine-protein phosphatase domain.
The 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.
Phosphorylated on Tyr-546 and Tyr-584 upon receptor protein tyrosine kinase activation; which creates a binding site for GRB2 and other SH2-containing proteins.
Protein tyrosine phosphatase non receptor type 11 antibody
Protein-tyrosine phosphatase 1D antibody
Protein-tyrosine phosphatase 2C antibody
SH2 domain containing protein tyrosine phosphatase 2 antibody
SHP 2 antibody
Tyrosine-protein phosphatase non-receptor type 11 antibody
Western blot - Anti-SHP2 antibody (ab10555)
Lane 1: Wild-type HAP1 cell lysate (20 µg) Lane 2: SHP2 knockout HAP1 cell lysate (20 µg) Lane 3: A431 cell lysate (20 µg) Lane 4: Jurkat cell lysate (20 µg) Lanes 1 to 4: Merged signal (red and green). Green - ab10555 observed at 70 kDa. Red - loading control, ab8245, observed at 37 kDa. ab10555 was shown to recognize SHP2 when SHP2 knockout samples were used, along with additional cross-reactive bands. Wild-type and SHP2 knockout samples were subjected to SDS-PAGE. ab10555 and ab8245 (loading control to GAPDH) were both diluted at 1 µg/mL and 1/10000 respectively and incubated overnight at 4°C. Blots were developed with Goat anti-Rabbit IgG H&L (IRDye® 800CW) preadsorbed ab216773 and Goat anti-Mouse IgG H&L (IRDye® 680RD) preadsorbed ab216776 secondary antibodies at 1/10000 dilution for 1 h at room temperature before imaging.
Jurkat cell lysates (lanes 1 and 2) were probed with ab10555 at 1/500. This antibody recognises SHP2 at 68 kDa. The lower molecular weight band may represent a variant or differences in the post-translational modification of the protein. M: marker lane 1: ab10555 lane 2: ab10555 + blocking peptide