| Name | peroxisome proliferator activated receptor alpha |
|---|---|
| Synonyms | NR1C1; PPAR; PPAR alpha; PPARA; PPARalpha; Peroxisome proliferator activated receptor; Peroxisome proliferator activated receptor alpha; hPPAR… |
| Name | nicotine |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 19091987 | Melis M, Pillolla G, Luchicchi A, Muntoni AL, Yasar S, Goldberg SR, Pistis M: Endogenous fatty acid ethanolamides suppress nicotine-induced activation of mesolimbic neurons through nuclear receptors. J Neurosci. 2008 Dec 17;28(51):13985-94. They blocked the effects of nicotine by activation of the peroxisome proliferator-activated receptor-alpha (PPAR-alpha), a nuclear receptor transcription factor involved in several aspects of lipid metabolism and energy balance. |
162(2,2,2,2) | Details |
| 20353771 | Hansen HS: Palmitoylethanolamide and other congeners. Exp Neurol. 2010 Mar 27. Inhibitors of the acylethanolamide-degrading enzyme FAAH can increase levels of all acylethanolamides including annandamide, and some of the pharmacological effects caused by these inhibitors may be explained by increased cerebral levels of OEA and PEA, e.g. suppression of nicotine-induced activation of neurons. PPARalpha, vanilloid receptor, K+-channels (Kv4.3, Kv1.5), and OEA can activate GPR119 and inhibit ceramidases. |
3(0,0,0,3) | Details |
| 19654299 | Sun X, Ritzenthaler JD, Zhong X, Zheng Y, Roman J, Han S: Nicotine stimulates PPARbeta/delta expression in human lung carcinoma cells through activation of PI3K/mTOR and suppression of AP-2alpha. Cancer Res. 2009 Aug 15;69(16):6445-53. Epub 2009 Aug 4. Activation of peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) has also been shown to induce NSCLC cell growth. |
1(0,0,0,1) | Details |
| 19641967 | Rehan VK, Asotra K, Torday JS: The effects of smoking on the developing lung: insights from a biologic model for lung development, homeostasis, and repair. Lung. 2009 Sep-Oct;187(5):281-9. Epub 2009 Jul 30. Using a biologic model of lung development, homeostasis, and repair, we have determined that in utero nicotine exposure disrupts specific molecular paracrine communications between epithelium and interstitium that are driven by parathyroid hormone-related protein and peroxisome proliferator-activated receptor (PPAR) gamma, resulting in transdifferentiation of lung lipofibroblasts to myofibroblasts, i.e., the conversion of the lipofibroblast phenotype to a cell type that is not conducive to alveolar homeostasis, and is the cellular hallmark of chronic lung disease, including asthma. |
0(0,0,0,0) | Details |