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Overview
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Product nameAnti-MEK1 (phospho T292) antibody
See all MEK1 primary antibodies -
DescriptionRabbit polyclonal to MEK1 (phospho T292)
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Host speciesRabbit
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Tested applicationsSuitable for: WBmore details
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Species reactivityReacts with: Mouse, Rat, Human
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Immunogen
The antiserum was produced against a chemically synthesized phosphopeptide derived from a region of human MEK 1 that contains threonine 292.
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Positive control
- NIH3T3 cells +/- PDGF.
Properties
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FormLiquid
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Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
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Storage bufferpH: 7.30
Preservative: 0.05% Sodium azide
Constituents: PBS, 50% Glycerol, 0.1% BSA -
Concentration information loading... -
PurityImmunogen affinity purified
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Purification notesThe antibody has been negatively preadsorbed using a non-phosphopeptide corresponding to the site of phosphorylation to remove antibody that is reactive with non-phosphorylated MEK 1. The final product is generated by affinity chromatography using a MEK 1 derived peptide that is phosphorylated at threonine 292.
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ClonalityPolyclonal
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IsotypeIgG
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Research areas
Associated products
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Compatible Secondaries
Applications
Our Abpromise guarantee covers the use of ab5612 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
| Application | Abreviews | Notes |
|---|---|---|
| WB | 1/1000. Predicted molecular weight: 50 kDa. |
Target
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FunctionCatalyzes the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in MAP kinases. Activates ERK1 and ERK2 MAP kinases.
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Tissue specificityWidely expressed, with extremely low levels in brain.
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Involvement in diseaseDefects in MAP2K1 are a cause of cardiofaciocutaneous syndrome (CFC syndrome) [MIM:115150]; also known as cardio-facio-cutaneous syndrome. CFC syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. Heart defects include pulmonic stenosis, atrial septal defects and hypertrophic cardiomyopathy. Some affected individuals present with ectodermal abnormalities such as sparse, friable hair, hyperkeratotic skin lesions and a generalized ichthyosis-like condition. Typical facial features are similar to Noonan syndrome. They include high forehead with bitemporal constriction, hypoplastic supraorbital ridges, downslanting palpebral fissures, a depressed nasal bridge, and posteriorly angulated ears with prominent helices. The inheritance of CFC syndrome is autosomal dominant.
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Sequence similaritiesBelongs to the protein kinase superfamily. STE Ser/Thr protein kinase family. MAP kinase kinase subfamily.
Contains 1 protein kinase domain. -
Post-translational
modificationsPhosphorylation on Ser/Thr by MAP kinase kinase kinases (RAF or MEKK1) regulates positively the kinase activity.
Acetylation by Yersinia yopJ prevents phosphorylation and activation, thus blocking the MAPK signaling pathway. - Information by UniProt
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Database links
- Entrez Gene: 5604 Human
- Entrez Gene: 26395 Mouse
- Entrez Gene: 170851 Rat
- Omim: 176872 Human
- SwissProt: Q02750 Human
- SwissProt: P31938 Mouse
- SwissProt: Q01986 Rat
- Unigene: 145442 Human
see all -
Alternative names
- Dual specificity mitogen activated protein kinase kinase 1 antibody
- Dual specificity mitogen-activated protein kinase kinase 1 antibody
- ERK activator kinase 1 antibody
see all
Images
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Western blot - Anti-MEK1 (phospho T292) antibody (ab5612)Peptide Competition and Mutant Analysis: Recombinant wild-type (lanes 1 4) and mutant (T292A) MEK1 (lane 5) treated with ERK to induce phosphorylation was added to background extracts and resolved by SDS PAGE on a 10% Tris-glycine gel and transferred to PVDF. Membranes were blocked with a 5% BSA-TBST buffer overnight at 4oC, then were incubated with 0.50µ g/mL ab5612 antibody for two hours at room temperature, following prior incubation with: no peptide (1, 5), the nonphosphopeptide corresponding to the immunogen (2), a generic phosphothreonine containing peptide (3), or, the phosphopeptide immunogen (4). After washing, membranes were incubated with goat F(ab’ 2 anti-rabbit IgG alkaline phosphatase and signals were detected using the Tropix WesternStar method. The data show that only the peptide corresponding to ab5612 blocks the antibody signal, and the T292A mutant is not reactive, demonstrating the specificity of the antibody. The recombinant wild-type and mutant MEK1 were kindly provided by Dr. Natalie Ahn, University of Colorado.
Peptide Competition and Mutant Analysis: Recombinant wild-type (lanes 1 4) and mutant (T292A) MEK1 (lane 5) treated with ERK to induce phosphorylation was added to background extracts and resolved by SDS PAGE on a 10% Tris-glycine gel and transferred to PVDF. Membranes were blocked with a 5% BSA-TBST buffer overnight at 4oC, then were incubated with 0.50 µg/mL ab5612 antibody for two hours at room temperature, following prior incubation with: no peptide (1, 5), the nonphosphopeptide corresponding to the immunogen (2), a generic phosphothreonine containing peptide (3), or, the phosphopeptide immunogen (4). After washing, membranes were incubated with goat F(ab’ 2 anti-rabbit IgG alkaline phosphatase and signals were detected using the Tropix WesternStar method. The data show that only the peptide corresponding to ab5612 blocks the antibody signal, and the T292A mutant is not reactive, demonstrating the specificity of the antibody. The recombinant wild-type and mutant MEK1 were kindly provided by Dr. Natalie Ahn, University of Colorado.
References
ab5612 has not yet been referenced specifically in any publications.
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