| Name | p38 |
|---|---|
| Synonyms | AIMP 2; p38; AIMP2; JTV 1; JTV1; JTV1 gene; JTV1 protein; Multisynthetase complex auxiliary component p38… |
| Name | nicotine |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 19247191 | Hu CZ, Cao YL, Huo HY, Zhao WH, Hu J: Inhibitory effect of ghrelin on nicotine-induced VCAM-1 expression in human umbilical vein endothelial cells. J Cardiovasc Pharmacol. 2009 Mar;53(3):241-5. We also found that ghrelin inhibited nicotine-induced PKC, p38 MAPK, and NF-kappaB activation. |
68(0,2,3,3) | Details |
| 19729077 | Jeong GS, Lee SH, Jeong SN, Kim YC, Kim EC: Anti-inflammatory effects of on nicotine- and lipopolysaccharide-stimulated human periodontal ligament cells via heme oxygenase-1. Int Immunopharmacol. 2009 Nov;9(12):1374-80. Epub 2009 Sep 1. Treatment with inhibitors of the phosphoinositide 3-kinase, MAPKs, p38, and JNK, as well as a protein kinase C inhibitor, blocked the anti-inflammatory effects of in nicotine- and LPS-treated cells. |
31(0,1,1,1) | Details |
| 19436652 | Vikman P, Xu CB, Edvinsson L: Lipid-soluble cigarette smoking particles induce expression of inflammatory and extracellular-matrix-related genes in rat cerebral arteries. Vasc Health Risk Manag. 2009;5(1):333-41. Epub 2009 Apr 8. METHODS: (DMSO)-soluble (lipid-soluble) cigarette smoking particles (DSP) were extracted from cigarette smoke (0.8 mg nicotine per cigarette; Marlboro). In addition, the activity of three mitogen-activated protein kinases (p38, ERK 1/2 and SAPK/JNK) and their downstream transcription factors (ATF-2, Elk-1 and c-Jun) were examined. |
3(0,0,0,3) | Details |
| 20211606 | Gubbins EJ, Gopalakrishnan M, Li J: alpha7 nAChR-mediated activation of MAP kinase pathways in PC12 cells. Brain Res. 2010 Mar 6. Robust concentration-dependent increase in ERK1/2 phosphorylation was triggered by structurally diverse alpha7 nAChR agonists such as nicotine, GTS-21, SSR-180711A and PNU-282987 in the presence of the positive allosteric modulator (PAM) PNU-120596. ERK1/2 phosphorylation was also attenuated by inhibitors of calmodulin-dependent protein kinase II (CaMKII), p38 MAP kinase and mitogen-activated protein kinase kinase1/2 (MEK1/2), indicating the involvement of these kinases upstream of ERK1/2. |
3(0,0,0,3) | Details |
| 19139119 | Sun X, Ritzenthaler JD, Zheng Y, Roman J, Han S: inhibits alpha4 nicotinic acetylcholine receptor expression in human lung carcinoma cells through peroxisome proliferator-activated receptor gamma-independent signals. Mol Cancer Ther. 2009 Jan;8(1):110-8. We and others have shown previously that nicotine, a major component of tobacco, stimulates non-small cell lung carcinoma (NSCLC) proliferation through nicotinic acetylcholine receptor (nAChR)-mediated signals. The inhibitory effect of on alpha4 nAChR expression was accompanied by phosphorylation of p38 mitogen-activated protein kinase and extracellular signal-regulated kinase 1/2 and down-regulation of Akt phosphorylation. |
2(0,0,0,2) | Details |
| 19892012 | Lin CC, Lee IT, Yang YL, Lee CW, Kou YR, Yang CM: Induction of COX-2/PGE (2)/IL-6 is crucial for cigarette smoke extract-induced airway inflammation: Role of TLR4-dependent oxidase activation. Free Radic Biol Med. 2010 Jan 15;48(2):240-54. Epub 2009 Nov 3. In addition, treatment with nicotine could induce COX-2, PGE (2), and IL-6 generation in in vivo and in vitro studies. Moreover, CSE-regulated COX-2, PGE (2), and IL-6 generation was inhibited by pretreatment with TLR4 Ab; inhibitors of c-Src (PP1), oxidase (diphenylene iodonium and apocynin), p38 MAPK (SB202190), MEK1/2 (U0126), JNK1/2 (SP600125), and NF-kappaB (helenalin); a ROS scavenger (N-acetyl- and transfection with siRNA of TLR4, MyD88, TRAF6, Src, p47 (phox), p38, p42, JNK2, or p65. |
1(0,0,0,1) | Details |
| 19280689 | Goettsch C, Goettsch W, Muller G, Seebach J, Schnittler HJ, Morawietz H: Nox4 overexpression activates reactive species and p38 MAPK in human endothelial cells. Biochem Biophys Res Commun. 2009 Mar 6;380(2):355-60. Nicotine dinucleotide oxidase (Nox) complexes are the main sources of reactive species (ROS) formation in the vessel wall. |
3(0,0,0,3) | Details |
| 19364472 | Goettsch C, Goettsch W, Muller G, Seebach J, Schnittler HJ, Morawietz H: Nox4 overexpression activates reactive species and p38 MAPK in human endothelial cells. Biochem Biophys Res Commun. 2009 Jan 23. Nicotine dinucleotide oxidase (Nox) complexes are the main sources of reactive species (ROS) formation in the vessel wall. |
3(0,0,0,3) | Details |
| 19358273 | Chipitsyna G, Gong Q, Anandanadesan R, Alnajar A, Batra SK, Wittel UA, Cullen DM, Akhter MP, Denhardt DT, Yeo CJ, Arafat HA: Induction of osteopontin expression by nicotine and cigarette smoke in the pancreas and pancreatic ductal adenocarcinoma cells. Int J Cancer. 2009 Jul 15;125(2):276-85. |
0(0,0,0,0) | Details |
| 19077124 | Welsby PJ, Rowan MJ, Anwyl R: Intracellular mechanisms underlying the nicotinic enhancement of LTP in the rat dentate gyrus. Eur J Neurosci. 2009 Jan;29(1):65-75. Epub 2008 Dec 11. Chronic nicotine enhancement of LTP was found to be dependent on PKA, ERK and Src kinases. |
0(0,0,0,0) | Details |
| 20113502 | Xu Y, Zhang Y, Cardell LO: Nicotine enhances murine airway contractile responses to kinin receptor agonists via activation of JNK- and PDE4-related intracellular pathways. Respir Res. 2010 Jan 29;11:13. |
0(0,0,0,0) | Details |