P
Peng Huang
Researcher at Temple University
Publications - 57
Citations - 2034
Peng Huang is an academic researcher from Temple University. The author has contributed to research in topics: Receptor & Agonist. The author has an hindex of 21, co-authored 46 publications receiving 1808 citations.
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Journal Article
Comparison of Pharmacological Activities of Buprenorphine and Norbuprenorphine: Norbuprenorphine Is a Potent Opioid Agonist
TL;DR: The binding of norBUP to opioid and nociceptin/orphanin FQ (ORL1) receptors, and its effects on [(35)S]guanosine-5'-O-(gamma-thio)triphosphate ([(35]S]GTP gamma S) binding mediated by opioid or ORL1 receptors are described and highlighted.
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Comparison of pharmacological activities of three distinct kappa ligands (Salvinorin A, TRK-820 and 3FLB) on kappa opioid receptors in vitro and their antipruritic and antinociceptive activities in vivo.
Yulin Wang,Kang Tang,Saadet Inan,Daniel J. Siebert,Ulrike Holzgrabe,David Y.W. Lee,Peng Huang,Jian-Guo Li,Alan Cowan,Lee-Yuan Liu-Chen +9 more
TL;DR: In vitro pharmacological activities on receptors expressed in Chinese hamster ovary cells and in vivo antiscratch and antinociceptive activities in mice are investigated and salvinorin A, TRK-820, and 3FLB caused internalization of the human KOR in a dose-dependent manner.
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Mouse model of OPRM1 (A118G) polymorphism has sex-specific effects on drug-mediated behavior
TL;DR: This work derived a mouse model possessing the equivalent nucleotide/amino acid substitution in the Oprm1 gene and found sex-specific reductions in the rewarding properties of morphine and the aversive components of naloxone-precipitated morphine withdrawal.
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A common single nucleotide polymorphism A118G of the μ opioid receptor alters its N-glycosylation and protein stability.
TL;DR: The A118G SNP reduces MOPR N-glycosylation and protein stability using a knockin mouse model and Pulse-chase studies revealed that the half-life of the mature form of 118G/Asp40-hMOPR was shorter than that of 118A/Asn40-mOPR (~28 h).
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Cholesterol reduction by methyl-β-cyclodextrin attenuates the delta opioid receptor-mediated signaling in neuronal cells but enhances it in non-neuronal cells
TL;DR: It is found that caveolin-1 level was very low in rat brain and undetectable in NG108-15 cells, which endogenously express delta opioid receptors (DOR), and lipid rafts sustain DOR-mediated signaling in Caveolin-deficient neuronal cells, but appear to inhibit it in cavesolin-enriched non-neuronal cells.