MPK2 Antibody

Overview of MAPKAPK2 (MK2) Antibodies

MAPKAPK2 antibodies are immunochemical reagents designed to detect and quantify mitogen-activated protein kinase-activated protein kinase 2 (MAPKAPK2 or MK2), a serine/threonine kinase downstream of p38 MAPK. These antibodies enable researchers to study MK2's involvement in:

• Post-transcriptional regulation of inflammatory cytokines (e.g., TNF-α, VEGF)

• Cellular stress responses and DNA damage repair

• Cancer progression, metastasis, and therapeutic resistance

Key epitopes targeted include phosphorylation sites (e.g., Thr222, Ser272) critical for MK2 activation .

Cancer Biology

• Head and Neck Squamous Cell Carcinoma (HNSCC): MK2 knockdown stabilizes p27 and destabilizes TNF-α/VEGF transcripts, reducing tumor growth in xenograft models .

• Triple-Negative Breast Cancer (TNBC): MK2 sustains AP1 transcriptional activity, driving tumorigenesis. MK2 inhibition suppresses AP1 activity comparably to p38 inhibitors .

Autoimmune Diseases

• Pemphigus Vulgaris (PV): Pathogenic autoantibodies activate MK2, causing cytoplasmic translocation and desmoglein-3 endocytosis. MK2 inhibition blocks blister formation in murine models .

Inflammatory Pathways

• MK2 regulates cytokine mRNA stability via phosphorylation of RNA-binding proteins (e.g., tristetraprolin) .

• Genetic MK2 deletion reduces TNF-α production without causing embryonic lethality, unlike p38 knockout .

Technical Considerations

• Subcellular Localization: Unstimulated MK2 resides in the nucleus; stress signals (e.g., oxidative stress, cytokines) trigger cytoplasmic translocation .

• Phosphorylation Status: Antibodies specific to phospho-Thr222 (e.g., Cell Signaling #3042) are critical for detecting activated MK2 .

• Isoforms: Two splice variants exist (~42–60 kDa), requiring antibody validation across isoforms .

Clinical Implications

MK2 inhibitors are under investigation as adjunct therapies for:

• Cancer: Synergizes with chemotherapy/radiotherapy by reducing pro-survival cytokine production .

• Autoimmunity: Topical MK2 inhibitors may mitigate blistering in pemphigus without systemic immunosuppression .