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CRK — PTGS2

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Arbabi et al., J Surg Res 2001 (Carcinoma...) : Hyperosmolarity induced both p38 and ERK activation within 30 min ; however, only p38 inhibition attenuated osmotic induced COX-2 expression ; inhibition of ERK activation had no effect
Moon et al., Toxicological sciences : an official journal of the Society of Toxicology 2002 : Vomitoxin induced cyclooxygenase-2 gene expression in macrophages mediated by activation of ERK and p38 but not JNK mitogen activated protein kinases
Egger et al., Biochem J 2003 : Activation of COX-2 protein synthesis in LPS stimulated BV-2 cells involved activation of the extracellular-signal regulated kinase 1/2 ( ERK1/2 ) and p38 mitogen activated protein kinase ( MAPK ) pathway and was sensitive to the protein kinase C ( PKC ) inhibitors staurosporine and chelerythrine, and the MAP kinase/ERK kinase 1/2 inhibitors PD98059 and U0126
Lin et al., Cell Signal 2004 : Tumor necrosis factor-alpha induced cyclooxygenase-2 expression in human tracheal smooth muscle cells : involvement of p42/p44 and p38 mitogen activated protein kinases and nuclear factor-kappaB
Mahns et al., Photochem Photobiol Sci 2004 : COX-2 induction by simulated solar light is attenuated in the presence of inhibitors of p38 ( MAPK ) or of c-Jun-N-terminal kinases (JNK), whereas COX-2 induction by UVA is blocked only by inhibition of JNK
Norata et al., Arterioscler Thromb Vasc Biol 2004 (MAP Kinase Signaling System) : Transient transfection experiments showed that CRE is required for HDL induced COX-2 transcription, and we demonstrated that p38 MAPK activation by HDL3 is involved in COX-2 mRNA transcription and stabilization
Lin et al., J Biomed Sci 2004 : Induction of cyclooxygenase-2 expression in human tracheal smooth muscle cells by interleukin-1beta : involvement of p42/p44 and p38 mitogen activated protein kinases and nuclear factor-kappaB
Souza et al., Am J Physiol Gastrointest Liver Physiol 2004 (Adenocarcinoma...) : Acid induced activation of both ERK and p38 causes a significant increase in COX-2 promoter activity, and acid activated ERK stabilizes COX-2 mRNA
Slice et al., J Biol Chem 2005 : Conversely, inhibition of p38MAPK by SB202190 or PD169316 inhibited COX-2 expression by Ang II, but did not block COX-2 induction by EGF ... Luciferase promoter assays showed that Ang II-dependent transcriptional activation of the COX-2 promoter was dependent on activation of small GTPases and p38 ( MAPK ) and on Ca2+ signaling via the cAMP-responsive element/activating transcription factor cis acting element
Wu et al., Am J Physiol Lung Cell Mol Physiol 2005 : These data suggest that p38 and EGFR kinase mediated Akt activation is required for Zn2+ induced COX-2 expression and that the PI3K/Akt signaling pathway plays a central role in this event
Shafer et al., Biochim Biophys Acta 2005 : Anisomycin induces COX-2 mRNA expression through p38 ( MAPK ) and CREB independent of small GTPases in intestinal epithelial cells
Chen et al., Mol Biol Cell 2005 : MG132 induced DNA binding activity of C/EBPdelta, but not C/EBPbeta was regulated by p38 , PI3K, Src, and protein kinase C. Small interfering RNA of C/EBPdelta suppressed COX-2 expression, further strengthening the role of C/EBPdelta in COX-2 gene transcription
Kanda et al., J Allergy Clin Immunol 2005 : The stimulatory effects of IL-17 on COX-2 expression were suppressed by inhibitors of p38 mitogen activated protein kinase ( MAPK ) and extracellular signal regulated kinase ( ERK ) kinase
Schmitz et al., J Clin Pathol 2006 (Breast Neoplasms) : The prognostic effect of COX-2 expression on lymph node negative breast cancer is confirmed-COX-2 is probably not regulated by HER-2, Akt, Erk1/2 or p38
Woo et al., Biochem Biophys Res Commun 2006 : The p38 MAPK inhibitor ( SB 203580 ) prevented MG132 induced COX-2 expression, whereas c-Jun N-terminal kinase (JNK) inhibitor ( SP 600125 ) and MAPK kinase 4 ( MKK4 ) -DN ( dominant negative mutant ) and MKK7-DN significantly enhanced COX-2 expression
Ogunwobi et al., Endocrinology 2006 (Adenocarcinoma...) : We conclude that leptin stimulates cell proliferation and inhibits apoptosis in OAC cells via ERK, p38 MAPK, phosphatidylinositol 3'-kinase/Akt, and JAK2 dependent activation of COX-2 and PGE2 production
Chen et al., Eur J Pharmacol 2006 : A p38 MAPK inhibitor, SB 203580, inhibited LPS stimulated COX-2 expression and IKK-beta activation suggesting that LPS may activate the NF-kappaB signaling pathway via upstream p38 MAPK activation
Yoshida et al., J Dermatol 2006 : IL-1beta induced COX-2 expression was regulated by MAPK pathways, especially by p38
Cindrova-Davies et al., Am J Pathol 2007 (Pre-Eclampsia) : Vitamin administration or p38 pathway inhibition also reduced cyclooxygenase-2 expression, tumor necrosis factor-alpha and interleukin-1 beta secretion, and the levels of apoptosis
Ulivi et al., J Cell Biochem 2008 (Inflammation) : In differentiated cells, the treatment with the inflammatory agent neither enhance NF-kB activation, nor synthesis of COX-2 while the addition of SB203580 neither repressed activation of p38 , nor COX-2 synthesis, suggesting a constitutive activation of a p38/NF-kB/COX2 pathway
Subramaniam et al., Gastroenterology 2008 (Adenocarcinoma...) : Gastrin increased the stability of both COX-2 and IL-8 messenger RNA ( mRNA ) in a p38 dependent manner, the half-life increasing from 31 minutes to 8 hours and approximately 4 hours, respectively
Pham et al., Biochim Biophys Acta 2008 (MAP Kinase Signaling System) : COX-2 promoter activation by AT1R-Gq-PAK-p38beta signaling in intestinal epithelial cells
Sun et al., Cell Signal 2008 (MAP Kinase Signaling System) : Corticosterone does not induce p38 MAPK activation or COX2 expression in cardiac fibroblasts or HEK293 cells transfected with glucocorticoid receptor, suggesting that p38 MAPK activation is cell specific and necessary for corticosterone induced COX-2 expression in cardiomyocytes
Amaya et al., Pain 2009 (Disease Models, Animal...) : The COX-2 induction was prevented by ERK and p38 inhibitors
Noguchi et al., J Endod 2009 : After the pretreatment of LPS with O ( 3 ) aq, effects of LPS and O ( 3 ) aq-treated LPS on cell viability ; calcification ability ; expression of cyclooxygenase 2 (COX-2) , interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) ; and activation of p38 of KN-3 cells were examined
Liao et al., Toxicol Lett 2009 : In studying the mechanisms involved in alpha-Triol induced COX-2/PGE ( 2 ) production, inhibitors of NOS, PI3K, p38, and NF-kappaB, effectively attenuated COX-2 protein induction and mRNA expression, suggesting that the PI(3)K-Akt-eNOS pathway, p38MAPK , and NF-kappaB are involved in alpha-Triol induced COX-2 expression, and following increases in p38 and Akt phosphorylation, the concentration dependent inhibition of COX-2 protein expression by L-NAME further suggested their involvement at the translation level
Wei et al., Nan Fang Yi Ke Da Xue Xue Bao 2009 (Parkinson Disease) : To investigate the effect of p38 mitogen activated protein kinase ( p38MAPK ) on the expression of COX-2 and caspase-3 in the substania nigra ( SN ) of mice with MPTP induced Parkinson disease ( PD )
Fitzsimmons et al., Neuroreport 2010 (Disease Models, Animal...) : We investigated whether either the spinal isoform p38alpha or p38beta is involved in peripheral inflammation evoked pain state and increased expression of spinal COX-2
Freudenburg et al., J Gen Virol 2010 : EMCV induced COX-2 expression requires the activation of nuclear factor-kappaB and the mitogen activated protein kinase p38
Pengal et al., American journal of physiology. Renal physiology 2011 (Disease Models, Animal...) : Using cultured podocytes, we analyzed 1 ) the roles of MK-2 and p38 MAPK in puromycin aminonucleoside ( PAN ) -induced podocyte injury ; 2 ) the ability of specific MK-2 and p38 MAPK inhibitors to protect podocytes against injury ; 3 ) the role of serum albumin, known to induce podocyte injury, in activating p38 MAPK/MK-2 signaling ; and 4 ) the role of p38 MAPK/MK-2 signaling in the expression of Cox-2 , an enzyme associated with podocyte injury
Kloesch et al., Immunol Lett 2012 (Arthritis, Rheumatoid...) : H ( 2 ) S-induced expression of IL-6, IL-8 and COX-2 was completely blocked by specific inhibitors of p38 and ERK1/2 MAPK and NF-?B
Zhao et al., Fertil Steril 2012 : In this study, exogenous AA stimulated cPLA ( 2a ) phosphorylation and COX-2 expression, mainly through ERK1/2 in mouse endometrial stromal cells, and p38 inhibitor modestly inhibited cPLA ( 2a ) phosphorylation induced by AA