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phosphorylation of PDE4A5 by MAPKAPK2 enhances PDE4A5 interaction with p75NTR and that this, in turn, serves to attenuate fibrin degradation
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The MK2 phosphorylates a cytoplasmic pool of RIPK1 that presumably subsequently integrates complex I, while IKKalpha/beta phosphorylate RIPK1 directly in complex I.
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Altogether, MAPKAPK2 is responsible for regulating the transcript stability and is functionally important to modulate Head and neck squamous-cell carcinoma pathogenesis.
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In this review, we have highlighted in detail the importance of MK2(MAPKAPK2) as the master regulator of RBPs and its role in the regulation of transcript stability, tumor progression, as well as the possibility of use of MK2 as a therapeutic target in tumor management
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These results reveal a novel mechanism by which miR-296-3p negatively regulated by nicotine directly targets MK2-induced Ras/Braf/Erk/Mek/c-Myc or PI3K/AKT/c-Myc signaling to stimulate its own expression and suppress NPC cell proliferation and metastasis.
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Platelets drive a p38-MK2-RTN4-Bcl-xl pathway associated with the regulation of the endoplasmic reticulum and platelet phosphatidylserine exposure, modulating procoagulant phenotype.
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Study found an elevated expression level of MK2 in serum specimens of patients with spinal cord injury. MiR-137 targets MK2 and inhibits its mediated inflammatory response and apoptosis after spinal cord injury.
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The novel MK2 substrates have emerged in the DNA damage response, autophagy, and obesity, making MK2 a multifunctional kinase at the crossroads of stress response and cell death.
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According to the information mentioned above, we now report the design and synthesis of some series of new urea derivatives that were then evaluated for their inhibitory activities against MAPKAPK2, TNF-a, and p38a
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MK2 post-transcriptionally regulates TNF-alpha-induced ICAM-1 expression by altering the cytoplasmic localization of HuR in human lung microvascular endothelial cells.
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MK2 overexpression is associated with primary liver tumors.
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CEP131 is the key regulatory target of MK2 and 14-3-3 in centriolar satellite remodeling.
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mTOR controls the senescence-associated secretory phenotype by differentially regulating the translation of the MK2 (also known as MAPKAPK2).
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analysis of signaling cooperation between p38-MAPK/MAPKAP-2/Hsp27 and intracellular calcium release in AA-induced HBEC apoptosis
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findings reveal MK2/MK3 as crucial stress-responsive kinases that promote autophagy through Beclin 1 S90 phosphorylation
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Low pMK2 expression was found to correlate significantly with overall survival after induction plus chemoradiation therapy in head and neck squamous cell carcinoma patients.
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The protein expression of both HMGB1 and MAPKAPK2 were increased in KLM1-R cells.
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Data indicate the binding mode and molecular mechanism of action of MAPK-activated protein kinase-2 (MK2) and inhibitors.
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Treatment with MK2 or p38 inhibitors blocked human papillomavirus genome amplification, identifying the p38/MK2 pathway as a key regulator of the human papillomavirus life cycle.
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a key role of MK2 and FasR in the regulation and limitation of the immune response in the CNS