c-Jun N-terminal Kinase (JNK) Positively Regulates NFATc2 Transactivation through Phosphorylation within the N-terminal Regulatory Domain

Abstract

The nuclear factor of activated T cells (NFAT) family of transcription factors regulates the transcription of cytokine genes and other genes involved in the regulation and function of the immune system. NFAT activity is regulated by the phosphatase calcineurin, which binds and dephosphorylates the NFAT N-terminal regulatory domain, a critical step required for nuclear translocation and transcriptional activity. Here we show that the mitogen-activated protein kinase (

Nuclear Factor of Activated T Cells c1 Mediates p21-activated Kinase 1 Activation in the Modulation of Chemokine-induced Human Aortic Smooth Muscle Cell F-actin Stress Fiber Formation, Migration, and Proliferation and Injury-induced Vascular Wall Remodeling

“…Activation of NFATc1 requires its dephosphorylation by calcineurin (18). In addition, although the earlier studies have demonstrated a negative role for JNKs in the stimulation of NFATs (44), the later studies have reported that JNKs mediate NFAT activation (45,46). Similarly, the role of Rac1 in the regulation of JNKs has also been reported (47,48).…”

Statistical Model to Analyze Quantitative Proteomics Data Obtained by 18O/16O Labeling and Linear Ion Trap Mass Spectrometry

“…LC-MS/MS Analysis and Peptide Identification-Each SCX fraction was analyzed by LC-MS/MS using a Surveyor LC system coupled to a linear ion trap mass spectrometer (model LTQ, Thermo Finnigan, San Jose, CA) as described previously with minor modifications (43,44). Peptides were concentrated and desalted onto an RP precolumn (0.32 ϫ 30 mm, BioBasic C 18 , Thermo Electron) and eluted on line onto an analytical RP column (0.18 ϫ 150 mm, BioBasic C 18 , Thermo Electron) operating at 2 l/min and using the following gradient: 5% B for 15 min, 5-14% B in 15 min, 14 -30% B in 155 min, 30 -95% B in 7 min, and 95% B for 3 min (solvent A: 0.1% formic acid; solvent B: 0.1% formic acid, 80% CH 3 CN).…”

Effect of Tacrolimus on Myocardial Infarction Is Associated with Inflammation, ROS, MAP Kinase and Akt Pathways in Mini-Pigs

“…Additionally, the MAPK pathway is activated in response to environmental and oxidative stresses, cellular proliferation and apoptosis, as well as inflammation and cytokine stimulation [12][13][14][15][16][17] . Another kinase signaling pathway, the PI-3 kinase/Akt signal pathway, has been shown to participate in the modulation of vascular smooth muscle cell migration and proliferation in response to mechanical stress 18) ; however, whether MAPK and PI-3 kinase/Akt signaling pathways are associated with the inflammatory response, generation of oxidative stress, increased infarct size and cardiac remodeling after AMI is currently unclear.…”

“…Mitogen-activated protein kinase (MAPK) pathways are mediated by extracellular signal-regulated kinases (ERKs), c-Jun amino-terminal kinases (JNKs), and p38 protein kinases that control myriads of physiological processes 12,13) . Additionally, the MAPK pathway is activated in response to environmental and oxidative stresses, cellular proliferation and apoptosis, as well as inflammation and cytokine stimulation [12][13][14][15][16][17] .…”