|1.||Xia, Ying: 4 articles (08/2014 - 01/2012)|
|2.||Chao, Dongman: 4 articles (08/2014 - 01/2012)|
|3.||Chen, Tao: 2 articles (08/2014 - 05/2014)|
|4.||Sandhu, Harleen K: 2 articles (05/2014 - 01/2013)|
|5.||He, Xiaozhou: 2 articles (01/2013 - 01/2012)|
|6.||Salvadori, S: 2 articles (12/2009 - 12/2007)|
|7.||Sandhu, Harleen: 1 article (08/2014)|
|8.||Wang, Qinyu: 1 article (08/2014)|
|9.||Wen, Guoqiang: 1 article (05/2014)|
|10.||Zhao, Jianlong: 1 article (05/2014)|
12/01/2007 - "Studies were performed in the human neuroblastoma SK-N-BE cells to establish i) binding parameters for UFP-512 ii) signalling pathways activated after acute and chronic treatment iii) regulation (phosphorylation and trafficking) of human DOP (hDOP) receptors after sustained activation by UFP-512. "
08/01/2014 - "We found that hypoxia reduced cell viability in both astrocytes and PC-12 cells, and DOR activation with UFP-512 (5 μM) effectively protected both the cells against hypoxic insult. "
01/01/2013 - "The results showed that: (1) 1-day hypoxia had no appreciable effect on BDNF expression, while 3- and 10-day hypoxia progressively decreased BDNF expression, resulting in 37.3% reduction (p < 0.05) after 10-day exposure; (2) DOR activation with UFP-512 (1 mg/kg, i.p., daily) partially reversed the hypoxia-induced reduction of BDNF expression in the 3- or 10-day exposed cortex; (3) DOR activation partially reversed the hypoxia-induced reduction in functional TrkB (140-kDa) and attenuated hypoxia-induced increase in truncated TrkB (90-kDa) in the 3- or 10-day hypoxic cortex; and (4) prolonged hypoxia (10 days) significantly increased TNF-α level and decreased CD11b expression in the cortex, which was completely reversed following DOR activation; and (5) there was no significant change in pCREB and pATF-1 levels in the hypoxic cortex. "
01/01/2012 - "To determine if the miRNAs expressed in the cortex mediated DOR neuroprotection, we examined 19 miRNAs that were previously identified as hypoxia- and DOR-regulated miRNAs in the kidney, in the rat cortex treated with UFP-512, a potent and specific DOR agonist under hypoxic condition. "
05/01/2014 - "We found that in HEK293 cells 1) MPP(+) in normoxia enhanced ɑ-synuclein expression and the formation of ɑ-synuclein oligomers thereby causing cytotoxic injury; 2) hypoxia at 1% O2 for 48h or at 0.5% O2 for 24h also induced ɑ-synuclein overexpression and its oligomer formation with cell injury; 3) however, hypoxia at 1% O2 for 24h, though increasing ɑ-synuclein expression, did not cause ɑ-synuclein oligomer formation and cell injury; 4) UFP-512 mediated DOR activation markedly attenuated the hypoxic cell injury and ɑ-synuclein overexpression, which was largely attenuated by DOR antagonism with naltrindole or siRNA "knock-down" of the DOR; and 5) DOR activation enhanced CREB phosphorylation and prevented the collapse of mitochondrial membrane potential (△ψm). "
|3.||Parkinsonian Disorders (Parkinsonism)
|3.||Small Interfering RNA (siRNA)
|4.||Brain-Derived Neurotrophic Factor (BDNF)