Product nameAnti-Met (c-Met) (phospho Y1234) antibody
See all Met (c-Met) primary antibodies
DescriptionRabbit polyclonal to Met (c-Met) (phospho Y1234)
SpecificityThis antibody is specific for Met (c-Met), only when phosphorylated at tyrosine 1234.
Tested applicationsSuitable for: WB, ELISAmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat
A synthesized phosphopeptide derived from human Met (c-Met) around the phosphorylation site of tyrosine 1234 (K-E-YP-Y-S)
- WB: Extract from HepG2 cells
Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: PBS, 50% Glycerol, 0.87% Sodium chloride
Concentration information loading...
PurityImmunogen affinity purified
Purification notesThe antibody was affinity purified from rabbit antiserum by affinity chromatography using epitope specific phosphopeptide. The antibody against non phosphopeptide was removed by chromatography using non phosphopeptide corresponding to the phosphorylation site.
Our Abpromise guarantee covers the use of ab47402 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/500 - 1/1000. Detects a band of approximately 135 kDa (predicted molecular weight: 156 kDa).|
FunctionReceptor for hepatocyte growth factor and scatter factor. Has a tyrosine-protein kinase activity. Functions in cell proliferation, scattering, morphogenesis and survival.
Involvement in diseaseNote=Activation of MET after rearrangement with the TPR gene produces an oncogenic protein.
Note=Defects in MET may be associated with gastric cancer.
Defects in MET are a cause of hepatocellular carcinoma (HCC) [MIM:114550].
Defects in MET are a cause of renal cell carcinoma papillary (RCCP) [MIM:605074]. It is a subtype of renal cell carcinoma tending to show a tubulo-papillary architecture formed by numerous, irregular, finger-like projections of connective tissue. Renal cell carcinoma is a heterogeneous group of sporadic or hereditary carcinoma derived from cells of the proximal renal tubular epithelium. It is subclassified into common renal cell carcinoma (clear cell, non-papillary carcinoma), papillary renal cell carcinoma, chromophobe renal cell carcinoma, collecting duct carcinoma with medullary carcinoma of the kidney, and unclassified renal cell carcinoma.
Note=A common allele in the promoter region of the MET shows genetic association with susceptibility to autism in some families. Functional assays indicate a decrease in MET promoter activity and altered binding of specific transcription factor complexes.
Note=MET activating mutations may be involved in the development of a highly malignant, metastatic syndrome known as cancer of unknown primary origin (CUP) or primary occult malignancy. Systemic neoplastic spread is generally a late event in cancer progression. However, in some instances, distant dissemination arises at a very early stage, so that metastases reach clinical relevance before primary lesions. Sometimes, the primary lesions cannot be identified in spite of the progresses in the diagnosis of malignancies.
Sequence similaritiesBelongs to the protein kinase superfamily. Tyr protein kinase family.
Contains 3 IPT/TIG domains.
Contains 1 protein kinase domain.
Contains 1 Sema domain.
DomainThe kinase domain is involved in SPSB1 binding.
modificationsDephosphorylated by PTPRJ at Tyr-1349 and Tyr-1365.
- Information by UniProt
- AUTS9 antibody
- c met antibody
- D249 antibody
All lanes : Anti-Met (c-Met) (phospho Y1234) antibody (ab47402)
Lane 1 : HUVEC cell lysates
Lane 2 : COS7 cell lysates
Lane 3 : COS7 cell lysates with phosphopeptide
Predicted band size: 156 kDa
All lanes : Anti-Met (c-Met) (phospho Y1234) antibody (ab47402) at 1/500 dilution
Lane 1 : Extracts from HepG2 cells, untreated
Lane 2 : Extracts from HepG2 cells, treated with phosphopeptide
Predicted band size: 156 kDa
ab47402 has not yet been referenced specifically in any publications.