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This purified ABfinity™ recombinant rabbit anti-MNK [pT197/202] monoclonal antibody is specific to human MNK [pT197/202] and it does not recognize non-phosphorylated MNK. MNK [pT197/pT202] is encoded by the 17346 gene, also known as MAP kinase-interacting serine/theronine kinase 1, Mnk1, 2410048M24Rik, and Mknk1. Rabbit anti-MNK [pT197/202] monoclonal antibody is used in flow cytometry, immunofluorescence, and immunohistochemistry.
• Applications: Validated applications for monoclonal antibody are flow cytometry, immunofluorescence, and immunohistochemistry. • Host Species and Isotype: The host species and isotype of the antibody is rabbit IgG. • Clone ID of Monoclonal Antibody (mAb): The rabbit anti-MNK [pT197/202] monoclonal antibody clone is 18H4L11. • Reactivity: Reacts with human MNK [pT197/202]. • Product Size: Rabbit anti-MNK [pT197/202] monoclonal antibody is available in a 100 µg size.
MAP kinase-interacting serine/threonine kinases (Mnk) function in signal transduction pathways through phosphorylation of eIF4E and are directly phosphorylated by ERK or p38 MAP kinases. In human and mouse there are two Mnk genes (Mnk1 and Mnk2). Alternative splicing gives rise to at least two protein products for each gene in human, but not mouse, which differ in their C-termini which affect their subcellular localization and binding affinities. Mnk1 is activated by phosphorylation at Thr197 and Thr202. Mnk1 and Mnk2 are essential for the phosphorylation of eIF4E at Ser209 however they differ markedly in their activity and regulatory patterns. Mnk1 is responsible for inducible phosphorylation of eIF4E while Mnk2 is responsible for basal levels of phosphorylation. Additionally, Mnk2 binds phosphorylated ERK while Mnk2 cannot. Mnk1 has been implicated in signaling in response to oxidative stress by increasing eIF4E phosphorylation upon H2O2 treatment in mice. Oxidative stress induced Mnk1 activity has also been linked to hyperproliferative diseases through the over-activation of eIF4E. Reactivity with Mnk2 has not been tested.
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