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王彦青, Yan-Qing Wang, Chong-Bin Zhu, Xiao-Ding Cao, Gen-Cheng Wu*
European Journal of Pharmacology 376(1999)R1-R3,-0001,():
-1年11月30日
[Phe1ψ(CH2-NH) Gly2 nociceptin-(1-13)-NH2, a pseudopeptide analog of nociceptin, was originally seen as an antagonist of nociceptin receptors. In the present study, it was observed that intracerebroventricular (i. c. v.) injection of this pseudopeptide (1, 5, 10μg) significantly decreased the tail-flick latency of rats, indicating a hyperalgesic effect, while intrathecal (i. t.) injection of it (1, 2.5, 10μg) dramatically increased the tail-flick latency, indicating an analgesic effect. This strengthened the in vivo evidence that [Phe1ψ(CH2-NH) Gly2] nociceptin-1-13-NH might be an agonist of nociceptin receptors.
Nociceptin pseudopeptide analog, Hyperalgesia, Analgesia
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王彦青, YANQING WANG, , MIKA SEIMIYA, KIYOKO KAWAMURA, LING YU, TOMOO OGI, KEIZO TAKENAGA, TOMOTANE SHISHIKURA, AKIRA NAKAGAWARA, SHIGERU SAKIYAMA, MASATOSHI TAGAWA and JIYANG O-WANG
INTERNATIONAL JOURNAL OF ONCOLOGY 25: 161-165, 2004,-0001,():
-1年11月30日
DNA polymerase κ (POLκ) is a low fidelity translesional DNA polymerase implicated in spontaneous and DNA damage-induced mutagenesis. We have previously shown that POLκ was frequently overexpressed in human lung cancer tissues as compared with their matched nontumorous tissue counterpart. In the present study, we found a close correlation between elevated POLκ expression and p53 inactivation in lung cancer tissues. To investigate whether POLK expression might be regulated by p53, we have determined the transcriptional initiation site of POLK gene and examined its promoter activity in A549, H358-129, and PC-3 human lung cancer cell lines. Wild-type p53, but not a mutant p53 (R273H) devoid of the DNA-binding activity, strongly inhibited POLK promoter activity in these cells. In addition, POLK promoter exhibited a significantly higher activity in p53-/- murine embryo fibroblasts (MEF) than in p53+√- and p53+√+ MEF. These results link p53 status with POLκ expression and suggest that loss of p53 function may in part contribute to the observed POLκ upregulation in human lung cancers.
DNA polymerase κ,, p53,, trans, c, r, i, p, t, ion,, lung cancer
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【期刊论文】Effects of orphanin FQ on endomorphin-1 induced analgesia
王彦青, Yan-Qing Wanga, Chong-Bin Zhua, Gen-Cheng Wua, *, Xiao-Ding Caoa, Yan Wangb, Da-Fu Cuib
Brain Research 835(1999)241-246,-0001,():
-1年11月30日
Orphanin FQ (also known as nociceptin) is a 17-amino-acid peptide which acts as a potent endogenous agonist of the orphan opioid receptor-like (ORL1) receptor. Endomorphin-1, a 4-amino-acid peptide discovered recently, is a potent and selective endogenous agonist for the m-opiate receptor. In the present study, the effect of OFQ orrand endomorphin-1 on the response to noxious thermal stimuli was observed using the tail-flick test in rats. Intracerebroventricular (i. c. v.) administration of OFQ (1,5μg) could shorten tail-flick latency; In contrast, intrathecal (i. t.) administration of OFQ (1, 2 or 10μg) could increase the latency; i. c. v. (1, 2, 5μg) or i. t. (0.2, 2, 5μg) administration of endomorphin-1 dose-dependently increased the latency, indicating an analgesic effect. Furthermore, OFQ (0.1-5μg) when intraventricularly injected together with endomorphin-1 (5μg), could dose-dependently reverse the analgesia induced by the latter. On the contrary, OFQ (1μg) intrathecally injected together with endomorphin-1 (0.2μg) could further increase the tail-flick latency. The results showed that OFQ at the supraspinal level produces hyperalgesia and is antagonistic to endomorphin-1, while at the spinal level it produces analgesia and is synergic with endomorphin-1. Different interaction mechanism between OFQ and endomorphin-1 in the brain and the spinal cord is thus suggested. © 1999 Elsevier Science B. V. All rights reserved.
Hyperalgesia, Analgesia, Endomorphin-1, m-opiate receptor, Orphanin FQ, ORL1 receptor
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