MK2 is a stress-responsive kinase activated by p38 MAPK, involved in cytokine production, mRNA stability, and cytoskeletal reorganization . It regulates inflammatory responses and cancer progression by phosphorylating substrates like HSP27, TTP, and LIMK1 . MK2 knockout mice exhibit reduced tumor growth and inflammation, highlighting its therapeutic potential .
Multiple monoclonal and polyclonal antibodies against MK2 are used in research:
MK2 inhibition reduced tumor growth in glioblastoma and prostate cancer models by disrupting HSP27-mediated cytoprotection .
In lung cancer, N-acetyl GM2 ganglioside (detected by MK1-16 antibody) correlated with tumor differentiation .
MK2-deficient mice showed resistance to blister formation in pemphigus vulgaris, linking MK2 to keratinocyte cytoskeletal integrity .
Preclinical studies demonstrated that MK2 inhibitors (e.g., CMPD1) synergize with chemotherapy to enhance cytotoxicity .
Specificity: Antibodies like ab32567 and ab63378 distinguish between phosphorylated and total MK2, critical for studying activation states .
Biomarker Potential: MK2 phosphorylation at Thr222/Thr334 serves as a surrogate marker for p38 pathway activity in cancer and inflammation .