Mitogen-activated protein kinase-activated protein kinase 2 (MAPKAPK2, or MK2) is a kinase belonging to the MAPKAPK family, a group of kinases activated by MAPK signaling. MK2 is activated by p38α and regulates the production of inflammatory cytokines, such as TNF-α.

Literature (1)
Gene Data

MK2 Inhibitors

Cat. No. Product Name / Activity
4279 PF 3644022
Potent MK2 inhibitor
3140 PHA 767491 hydrochloride
MK2 inhibitor; also cdk inhibitor; potently inhibits cdk9


Cat. No. Product Name / Activity
2186 CMPD-1
Selective inhibitor of p38α-mediated MK2a phosphorylation; also tubulin polymerization inhibitor

Mitogen-activated protein kinase-activated protein kinase 2 (MK2; MAPKAPK2), EC, is a member of the MAPKAPK family of kinases, which also consists of MK3 and MK5 (PRAK). The MAPKAPK family are activated by MAPK signaling, with MK2 being a downstream substrate of p38.

MK2 is ubiquitously expressed, with its highest expression in the heart, kidney and skeletal muscle. In quiescent cells MK2 is predominantly localized to the nucleus. In response to stress stimuli (such as UV irradiation, heat shock and oxidative stress), as well as LPS and Toll-like receptor signaling, p38 is activated and subsequently phosphorylates MK2, which is exported from the nucleus into the cells cytoplasm. Substrates for MK2 include AU-rich element-binding (ARE) proteins; the chaperone Hsp27; the cell cycle phosphatase cdc25; the transcription factor AATF; and LIMK. MK2 has a role in a number of physiological processes including, inflammation, actin remodeling, cell cycle arrest and apoptosis.

Activation of ARE proteins by MK2 results in the stabilization and translation of mRNA, including that of TNF-α, IL-6 and IL-8, therefore increasing proinflammatory cytokine production and secretion. MK2 has been shown to be essential for LPS-induced TNF-α production, so may be of therapeutic interest for the treatment of chronic inflammatory diseases, such as rheumatoid arthritis. MK2 may also have a role in the neuroinflammation exhibited in neurodegenerative disorders such as Alzheimer's and Parkinson's disease. For example MK2-deficient mice have been shown to exhibit attenuated neuroinflammation in a mouse model of Parkinson's disease.

MK2 is also a potential therapeutic target for the treatment of cancer. It is activated by DNA damage, before phosphorylating cdc25, causing cell cycle arrest at G2/M phase. This gives the cell time to repair the damage to its DNA. MK2 depletion has been shown to enhance the effectiveness of chemotherapeutics against cancer cells in vitro. MK2 also phosphorylates the transcription factor AATF, which suppresses the expression of p53 pro-apoptotic target genes. Furthermore the phosphorylation of Hsp27 by MK2, inhibits its chaperone activity, resulting in actin polymerization and enhanced cell motility.

External sources of pharmacological information for MK2 :

Literature for MK2

Tocris offers the following scientific literature for MK2 to showcase our products. We invite you to request* your copy today!

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Cell Cycle & DNA Damage Repair Poster

Cell Cycle & DNA Damage Repair Poster

In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. This poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.

MK2 Gene Data

Gene Species Gene Symbol Gene Accession No. Protein Accession No.
MAPKAPK2 Human MAPKAPK2 NM_004759 P49137
Mouse Mapkapk2 NM_008551 P49138
Rat Mapkapk2 NM_178102 NP_835203