bs-70156R

DATASHEET

Host: Rabbit

Target Protein: MerTK Tyr749/753/754

Specificity: Specific for the ~160 kDa MerTK protein phosphorylated at Tyr749/753/754. The immunolabeling is completely eliminated by treatment with λ-phosphatase. Due to post-translational modifications of the Mer protein, a significant shift in molecular weight is seen from the predicted molecular weight of 110 kDa. For optimal results immunoprecipitation is recommended due to the 91% homology of the related receptor tyrosine kinase, Axl, that runs at ~140 kDa.

Modification Site: Tyr749,753,754

Clonality: Polyclonal

Isotype: IgG

Entrez Gene: 10461

Swiss Prot: Q12866

Source: Synthetic phospho-peptide corresponding to amino acid residues surrounding Tyr749/753/754 of human MerTK, conjugated to keyhole limpet hemocyanin (KLH).

Purification: Antigen Affinity purification from Pooled whole antiserum

Storage Buffer: 10 mM HEPES (pH 7.5), 150 mM NaCl, 100 µg per ml BSA and 50% glycerol.

Storage: Storage at -20°C is recommended, as aliquots may be taken without freeze/thawing due to presence of 50% glycerol. Stable for at least 1 year at -20°C.

Background:

Along with Tyro-3 and Axl, Mer is a member of the TAM family of receptor tyrosine kinases (RTKs). The TAM family of RTKs regulates cell proliferation/survival, cell adhesion and migration, and blood clot stabilization processes, along with the regulation of inflammatory cytokine release (Linger et al, 2008). Additionally, the TAM family has been linked to coagulopathy and cancer when altered experimentally or genetically (Linger et al, 2008). Tri-phosphorylation of MerTK at tyr749, tyr753 and tyr754 has been identified as a key target in platelet aggregation for developing a new anti-platelet drug that decreases bleeding complications, which are current side effects of similar drugs on the market today (Zhang et al, 2013). MerTK is also seen as a therapeutic target for treating lymphoblastic leukemias, melanoma, breast, lung, colon, liver, gastric, kidney, ovarian, uterine and brain cancers (Graham et al, 1994). There has recently been increased interest in synthesizing novel ATP-competitive small molecule tyrosine kinase inhibitors to decrease tri-phosphorylation of MerTK at tyr749, tyr753, and tyr754 as a therapeutic target to treat AML (Lee-Sherick et al, 2013).