Product nameAnti-MEK2 antibody [Y78] (Phycoerythrin)
See all MEK2 primary antibodies
DescriptionRabbit monoclonal [Y78] to MEK2 (Phycoerythrin)
ConjugationPhycoerythrin. Ex: 488nm, Em: 575nm
Tested applicationsSuitable for: Flow Cytmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse
Synthetic peptide. within Human MEK2 aa 1-100 (N terminal). The exact sequence is proprietary.
Database link: P36507
- Flow Cyt: HeLa cells.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents
This product is a recombinant rabbit monoclonal antibody.
Storage instructionsShipped at 4°C. Store at 4°C (stable for up to 12 months). Upon delivery aliquot. Store at +4°C. Do Not Freeze. Store In the Dark.
Storage bufferpH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 1% BSA, PBS
Concentration information loading...
PurityProtein A purified
- Anti-MEK2 antibody [Y78] (Alexa Fluor® 647) (ab200519)
- Anti-MEK2 antibody [Y78] (Alexa Fluor® 488) (ab200606)
- Anti-MEK2 antibody [Y78] (HRP) (ab200607)
- Anti-MEK2 antibody [Y78] (Alexa Fluor® 555) (ab214633)
- Anti-MEK2 antibody [Y78] (Alexa Fluor® 594) (ab214845)
- Anti-MEK2 antibody [Y78] - BSA and Azide free (ab233731)
- Anti-MEK2 antibody [Y78] (ab32517)
Our Abpromise guarantee covers the use of ab213661 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
The cellular localisation of this product has been verified in ICC/IF.
FunctionCatalyzes the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in MAP kinases. Activates the ERK1 and ERK2 MAP kinases.
Involvement in diseaseDefects in MAP2K2 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.
Sequence similaritiesBelongs to the protein kinase superfamily. STE Ser/Thr protein kinase family. MAP kinase kinase subfamily.
Contains 1 protein kinase domain.
modificationsMAPKK is itself dependent on Ser/Thr phosphorylation for activity catalyzed by MAP kinase kinase kinases (RAF or MEKK1).
Acetylation of Ser-222 and Ser-226 by Yersinia yopJ prevents phosphorylation and activation, thus blocking the MAPK signaling pathway.
- Information by UniProt
- Cardiofaciocutaneous syndrome antibody
- CFC syndrome antibody
- CFC4 antibody
Overlay histogram showing HeLa cells stained with ab213661 (red line). The cells were fixed with 4% formaldehyde (10 min) and then permeabilized with 0.1% PBS-Triton X-100 for 15 min. The cells were then incubated in 1x PBS / 10% normal goat serum to block non-specific protein-protein interactions followed by the antibody (ab213661, 1/2500 dilution) for 30 min at 22°C.
Isotype control antibody (black line) was rabbit IgG (monoclonal) Phycoerythrin (ab209478) used at the same concentration and conditions as the primary antibody. Unlabelled sample (blue line) was also used as a control.
Acquisition of >5,000 events were collected using a 50mW Yellow/Green laser (561nm) and 586/15 bandpass filter.
This antibody gave a positive signal in HeLa cells fixed with 80% methanol (5 min)/permeabilized with 0.1% PBS-Triton X-100 for 15 min used under the same conditions.
ab213661 has not yet been referenced specifically in any publications.