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SAPKStress-Activated Protein Kinase
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Whilst, the Ser/Thre residues on Glu-rich region on NF tail domain; are phosphorylated by casein kinases, (18,36) c--Jun N--terminal kinase (JNK)/stress activated protein kinase (SAPK) has also been associated with aberrant phosphorylation of NFs seen in diabetes.
The p38 SAPK pathway is required for Ha-ras induced in vitro invasion of NIH3T3 cells.
In particular, they investigated the role of stress-activated protein kinases (SAPK, also known as JNK).
BBMD3 also increased phosphorylation of the cJun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK), resulting in increased expression of phosphorylated cJun and total c-Fos [56].
Antibodies against human phospho-p-38 (Thrl80/Tyrl82, rabbit polyclonal, phospho ERK1/2 (Thr202/Tyr204, rabbit polyclonal), phospho- SAPK /JNK (Thrl83/yrl85, mouse monoclonal, clone G8), phospho-c-Jun (Ser73, rabbit, monoclonal, clone D47G9) and the horseradish peroxidase (HRP)-labeled secondary antibodies, anti-mouse and anti-rabbit were from Cell Signaling Technology (Boston, USA), anti-human COX-2 was from R&D System (Wiesbaden, Germany), anti-human COX-1 and anti-human 5-LO (mouse monoclonal, clone 33) from SantaCruz Biotechnology (Heidelberg, Germany).
Prolactin-induced VEGF expression after dexamethasone treatment was significantly reduced by PD98059, an inhibitor of upstream kinase that activates p44/p42 MAP kinase (MEK) (Alessi et al., 1995), but not by SB203580, an inhibitor of p38 MAP kinase (Cuenda et al., 1995), or SP600125, a specific inhibitor of stressactivated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK) (Bennett et al., 2001) (Figure 3A).
These include second-messenger-regulated kinases such as PKA, PKC, and CAMKII (Sihag et al., 1988; Sihag and Nixon, 1989; Dosemeci et al., 1990; Dosemeci and Pant, 1992), preferentially phosphorylating head domain sites; second messenger independent kinases, CKI, CKII (Floyd et al., 1991); GSK3 (Guidato et al., 1996) and proline-directed kinases Erk1/2, JNK, SAPK, cdc-2, cdk5, among others (Sun et al., 1996; Giasson and Mushynski, 1997; Veeranna et al., 1998; Li et al., 1999).
The Stress-activated Protein Kinase (SAPK)/-c-jun N-terminal kinases (JNK1/2/3) are important signaling kinases that are elevated in neurodegenerative diseases including glaucoma [58].
TEXs with TGF-[beta] upregulate Treg-related genes through TGF-[beta]/Smad signaling activation and SAPK signaling devitalization in colorectal cancer [24].
Jun-amino-terminal kinase (JNK) (also named as stress-activated protein kinase, SAPK) is activated by various stimuli such as UV damage, inflammatory cytokines, and ceramides [57-59].