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a p38 MAPKAPK2 kinase cascade modulates the activity of F-actin at the yolk cell margin circumference allowing the gradual closure of the blastopore as epiboly progresses
MK2 (显示 KCNA2 ELISA试剂盒)-mediated RIPK1 (显示 RIPK1 ELISA试剂盒) phosphorylation is an important molecular mechanism limiting the sensitivity of the cells to the cytotoxic effects of TNF (显示 TNF ELISA试剂盒).
p38MAPK (显示 MAPK14 ELISA试剂盒)/MK2 (显示 KCNA2 ELISA试剂盒) phosphorylation of RIPK1 (显示 RIPK1 ELISA试剂盒) is a crucial checkpoint for cell fate in inflammation and infection that determines the outcome of bacteria-host cell interaction.
MK2 (显示 KCNA2 ELISA试剂盒)-mediated phosphorylation of RIPK1 (显示 RIPK1 ELISA试剂盒) serves as a checkpoint within the TNF (显示 TNF ELISA试剂盒) signaling pathway that integrates cell survival and cytokine production.
this study shows that the loss of MK2 (显示 KCNA2 ELISA试剂盒) in mast cells decreases the IL-33 (显示 IL33 ELISA试剂盒)-induced leukocyte recruitment and the resulting skin inflammation
MK2 (显示 KCNA2 ELISA试剂盒) signaling differentially regulated CCL3 (显示 CCL3 ELISA试剂盒) and CCL4 (显示 CCL4 ELISA试剂盒).
In silico analyses and experimental validation demonstrated that the kinase activity of p38(MAPK (显示 MAPK14 ELISA试剂盒)) determines signal amplitude, whereas phosphatase activity affects both signal amplitude and duration. p38(MAPK (显示 MAPK14 ELISA试剂盒)) and MK2 (显示 KCNA2 ELISA试剂盒) concentrations and responsiveness toward IL-1beta (显示 IL1B ELISA试剂盒) were quantitatively compared between hepatocytes and macrophages
MK2 (显示 KCNA2 ELISA试剂盒)-activating peptide (MK2 (显示 KCNA2 ELISA试剂盒)-AP) blocks the effects of anthrax lethal toxin on endothelial barriers in cultured cells and reduces pulmonary vascular leak in rats.
MK2 (显示 KCNA2 ELISA试剂盒) regulates postnatal arteriogenesis by controlling vascular recruitment of monocytes/macrophages in dual manner: regulation of endothelial MCP-1 (显示 CPT1B ELISA试剂盒) expression in response to hemodynamic and inflammatory forces as well as MCP-1 (显示 CPT1B ELISA试剂盒) dependent monocyte migration
these data suggest there is a sexual dimorphism in MK2 (显示 KCNA2 ELISA试剂盒) signaling of osteoclast progenitor cell subpopulations.
Loss of MK2 (显示 KCNA2 ELISA试剂盒) effectively blocks bone resorption and prevents the development of postmenopausal bone loss.
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 (显示 TNF ELISA试剂盒), and p38a (显示 MAPK14 ELISA试剂盒)
MK2 (显示 KCNA2 ELISA试剂盒) post-transcriptionally regulates TNF-alpha (显示 TNF ELISA试剂盒)-induced ICAM-1 (显示 ICAM1 ELISA试剂盒) expression by altering the cytoplasmic localization of HuR (显示 ELAVL1 ELISA试剂盒) in human lung microvascular endothelial cells.
MK2 (显示 KCNA2 ELISA试剂盒) overexpression is associated with primary liver tumors.
CEP131 is the key regulatory target of MK2 (显示 KCNA2 ELISA试剂盒) and 14-3-3 (显示 YWHAQ ELISA试剂盒) in centriolar satellite remodeling.
mTOR (显示 FRAP1 ELISA试剂盒) controls the senescence-associated secretory phenotype by differentially regulating the translation of the MK2 (显示 KCNA2 ELISA试剂盒) (also known as MAPKAPK2).
analysis of signaling cooperation between p38-MAPK (显示 MAPK14 ELISA试剂盒)/MAPKAP-2/Hsp27 (显示 HSPB1 ELISA试剂盒) and intracellular calcium release in AA-induced HBEC apoptosis
findings reveal MK2 (显示 KCNA2 ELISA试剂盒)/MK3 (显示 KCNA3 ELISA试剂盒) as crucial stress-responsive kinases that promote autophagy through Beclin 1 (显示 BECN1 ELISA试剂盒) S90 phosphorylation
The protein expression of both HMGB1 (显示 HMGB1 ELISA试剂盒) and MAPKAPK2 were increased in KLM1-R cells.
Data indicate the binding mode and molecular mechanism of action of MAPK-activated protein kinase-2 (MK2) and inhibitors.
Treatment with MK2 (显示 KCNA2 ELISA试剂盒) or p38 (显示 CRK ELISA试剂盒) inhibitors blocked human papillomavirus genome amplification, identifying the p38 (显示 CRK ELISA试剂盒)/MK2 (显示 KCNA2 ELISA试剂盒) pathway as a key regulator of the human papillomavirus life cycle.
This gene encodes a member of the Ser/Thr protein kinase family. This kinase is regulated through direct phosphorylation by p38 MAP kinase. In conjunction with p38 MAP kinase, this kinase is known to be involved in many cellular processes including stress and inflammatory responses, nuclear export, gene expression regulation and cell proliferation. Heat shock protein HSP27 was shown to be one of the substrates of this kinase in vivo. Two transcript variants encoding two different isoforms have been found for this gene.
MAP kinase-activated protein kinase 2
, betty boop
, mitogen-activated protein kinase-activated protein kinase 2
, MAPK-activated protein kinase 2
, MAPKAP kinase 2
, map kinase activated protein kinase-2