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抗Mouse (Murine) MAPKAP Kinase 2 抗体:
抗Human MAPKAP Kinase 2 抗体:
抗Rat (Rattus) MAPKAP Kinase 2 抗体:
Human Polyclonal MAPKAP Kinase 2 Primary Antibody for DB, EIA - ABIN358152
Lukas, Kroe, Wildeson, Peet, Frego, Davidson, Ingraham, Pargellis, Labadia, Werneburg: Catalysis and function of the p38 alpha.MK2a signaling complex. in Biochemistry 2004
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Human Polyclonal MAPKAP Kinase 2 Primary Antibody for IF, WB - ABIN197584
Rouse, Cohen, Trigon, Morange, Alonso-Llamazares, Zamanillo, Hunt, Nebreda: A novel kinase cascade triggered by stress and heat shock that stimulates MAPKAP kinase-2 and phosphorylation of the small heat shock proteins. in Cell 1994
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Human Polyclonal MAPKAP Kinase 2 Primary Antibody for IF, IHC (p) - ABIN197078
Ben-Levy, Leighton, Doza, Attwood, Morrice, Marshall, Cohen: Identification of novel phosphorylation sites required for activation of MAPKAP kinase-2. in The EMBO journal 1996
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Cow (Bovine) Polyclonal MAPKAP Kinase 2 Primary Antibody for IF (p), IHC (p) - ABIN681523
Rosenzweig, Djap, Ou, Quinn: Mechanical injury of bovine cartilage explants induces depth-dependent, transient changes in MAP kinase activity associated with apoptosis. in Osteoarthritis and cartilage / OARS, Osteoarthritis Research Society 2012
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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 抗体)-mediated phosphorylation of RIPK1 (显示 RIPK1 抗体) serves as a checkpoint within the TNF (显示 TNF 抗体) signaling pathway that integrates cell survival and cytokine production.
this study shows that the loss of MK2 (显示 KCNA2 抗体) in mast cells decreases the IL-33 (显示 IL33 抗体)-induced leukocyte recruitment and the resulting skin inflammation
MK2 (显示 KCNA2 抗体) signaling differentially regulated CCL3 (显示 CCL3 抗体) and CCL4 (显示 CCL4 抗体).
In silico analyses and experimental validation demonstrated that the kinase activity of p38(MAPK (显示 MAPK14 抗体)) determines signal amplitude, whereas phosphatase activity affects both signal amplitude and duration. p38(MAPK (显示 MAPK14 抗体)) and MK2 (显示 KCNA2 抗体) concentrations and responsiveness toward IL-1beta (显示 IL1B 抗体) were quantitatively compared between hepatocytes and macrophages
MK2 (显示 KCNA2 抗体)-activating peptide (MK2 (显示 KCNA2 抗体)-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 抗体) regulates postnatal arteriogenesis by controlling vascular recruitment of monocytes/macrophages in dual manner: regulation of endothelial MCP-1 (显示 CPT1B 抗体) expression in response to hemodynamic and inflammatory forces as well as MCP-1 (显示 CPT1B 抗体) dependent monocyte migration
these data suggest there is a sexual dimorphism in MK2 (显示 KCNA2 抗体) signaling of osteoclast progenitor cell subpopulations.
Loss of MK2 (显示 KCNA2 抗体) effectively blocks bone resorption and prevents the development of postmenopausal bone loss.
This study showed that cmpd28, a Mapkapk2/3 inhibitor, represents a potentially new approach to type 2 diabetes therapy.
Deficiency of MK2 (显示 KCNA2 抗体) prevents adverse remodelling and promotes endothelial healing of the arterial wall after injury.
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 抗体), and p38a (显示 MAPK14 抗体)
MK2 (显示 KCNA2 抗体) post-transcriptionally regulates TNF-alpha (显示 TNF 抗体)-induced ICAM-1 (显示 ICAM1 抗体) expression by altering the cytoplasmic localization of HuR (显示 ELAVL1 抗体) in human lung microvascular endothelial cells.
MK2 (显示 KCNA2 抗体) overexpression is associated with primary liver tumors.
CEP131 (显示 AZI1 抗体) is the key regulatory target of MK2 (显示 KCNA2 抗体) and 14-3-3 (显示 YWHAQ 抗体) in centriolar satellite remodeling.
mTOR (显示 FRAP1 抗体) controls the senescence-associated secretory phenotype by differentially regulating the translation of the MK2 (显示 KCNA2 抗体) (also known as MAPKAPK2).
analysis of signaling cooperation between p38-MAPK (显示 MAPK14 抗体)/MAPKAP-2/Hsp27 (显示 HSPB1 抗体) and intracellular calcium release in AA-induced HBEC apoptosis
findings reveal MK2 (显示 KCNA2 抗体)/MK3 (显示 KCNA3 抗体) as crucial stress-responsive kinases that promote autophagy through Beclin 1 (显示 BECN1 抗体) S90 phosphorylation
The protein expression of both HMGB1 (显示 HMGB1 抗体) 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 抗体) or p38 (显示 CRK 抗体) inhibitors blocked human papillomavirus genome amplification, identifying the p38 (显示 CRK 抗体)/MK2 (显示 KCNA2 抗体) 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