EMAP II Antibody | 33-049

EMAP II Antibody | 33-049 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse, Rat

Homology: N/A

Immunogen: A recombinant protein fragment from the C-terminal region of human EMAP II was used as the immunogen for this antibody.

Research Area: Immunology

Tested Application: WB

Application: Western blot: 2-5 ug/ml
Provided assay concentrations are suggestions only, antibody titration may be required for optimal results.

Specificiy: N/A

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: N/A

Validation: N/A

Isoform: N/A

Purification: Protein A purified antibody

Clonality: Polyclonal

Clone: N/A

Isotype: IgG

Conjugate: Unconjugated

Physical State: Liquid

Buffer: PBS with 0.1 mg/ml BSA and 0.05% sodium azide

Concentration: 0.5 mg/mL

Storage Condition: Aliquot and Store at -20˚C. Avoid freez-thaw cycles.

Alternate Name: AIMP1 Antibody: p43, HLD3, EMAP2, SCYE1, EMAPII, Aminoacyl tRNA synthase complex-interacting multifunctional protein 1, Multisynthase complex auxiliary component p43, EMAP-2

User Note: Optimal dilutions for each application to be determined by the researcher

BACKGROUND: EMAP II (Endothelial monocyte-activating polypeptide 2) is a pro-inflammatory cytokine and participant in apoptotic cell death. It is synthesized as a precursor (pro-EMAP II) , lacking a secretion signal peptide. In apoptotic cells, the ~34 kDa pro-form of EMAP II is cleaved by Caspase-7 (and Caspase-3 to a lesser extent) at aspartate 144 to its mature, ~20 kDa form. The mature form of EMAP II has been found to have many different functions. In vivo, it recruits leukocytes to the site of apoptotic cell death. In vitro it has been shown to activate endothelial cells (and the release of von Willebrand factor, E-selectin and P-selectin) , neutrophils, and induces macrophage expression of TNFa and TF (tissue factor) . EMAP II is also a possible biomarker for brain injury, having been found to be differentially expressed in two types: traumatic injury shows an increase and ischemic injury shows a decrease in EMAP II expression (Dave, et al, 2014) .