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PBS, 40% Glycerol, 0.05% BSA, 0.03% Proclin 300





ELISA
Sandwich ELISA
CLIA
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WB
1:1000-1:2000IP
IHC-P
ICC
IF
ICFCM
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mIHC
ChIP

MAPKAPK-2 (commonly referred to as MK2) is a serine/threonine protein kinase encoded by the MAPKAPK2 gene and serves as the most pivotal direct substrate of p38 MAPK, acting as a signaling hub in inflammation, tumorigenesis, the DNA damage response, and cellular senescence. In its resting state, MK2 remains inactive due to an autoinhibitory conformation formed between its C-terminal regulatory domain and its kinase domain. Upon exposure to cellular stress, inflammatory cytokines, or pathogen stimulation, p38α phosphorylates MK2 at Thr334, triggering a conformational switch that simultaneously exposes a nuclear export signal (NES) —promoting p38-bound MK2 translocation to the cytoplasm—and masks its C-terminal nuclear localization signal (NLS) , thereby directing p38 signaling precisely toward cytoplasmic targets. Activated MK2 executes pleiotropic functions via phosphorylation of a diverse substrate repertoire: in the cytoplasm, it phosphorylates HSP27 to remodel the actin cytoskeleton and facilitate cell migration; in RNA metabolism, it phosphorylates ARE-binding proteins such as Tristetraprolin (TTP) and hnRNP A0, causing their 14-3-3-mediated sequestration and inactivation, thereby stabilizing the mRNAs of pro-inflammatory cytokines including TNF-α, IL-6, and IL-1β—a core mechanism driving chronic inflammation. Within the nucleus, MK2 phosphorylates transcription factors such as CREB and SRF, and contributes to maintaining the G2/M checkpoint by regulating the stability of GADD45A mRNA following DNA damage. Recent studies have expanded the functional landscape of MK2 far beyond the classical inflammatory axis: within the tumor microenvironment, MK2 promotes cell survival, drives epithelial-mesenchymal transition (EMT), and confers chemoresistance (e.g., desensitizing pancreatic cancer to gemcitabine and tongue squamous cell carcinoma to paclitaxel), positioning it as a promising target for overcoming drug resistance. In senescent cells, the mTOR pathway selectively upregulates MK2 translation via 4EBP1; the accumulated MK2 then phosphorylates ZFP36L1, relieving its degradation of SASP component mRNAs and thereby establishing the senescence-associated secretory phenotype (SASP).


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