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| 1 | Primary structure of helix C to helix G of a new retinal protein in H.sp.xz515显示文摘The gene fragment encoding the retinal protein from helix C to helix G in a new strain of halobacteria, H.sp.xz515 has been amplified by PCR method. The nucleotide sequence of this fragment has been determined. The deduced amino acid sequence has been compared with halobium br and other two br-like proteins, ar-1 and ar-2. Results show that those amino acid residues in br, essential for proton pumping and binding to retinal, are conserved. The residue M145 in br may be important for isomerization reaction of retinal. | Hui Wang Shuxuan Zhan Qingan Sun Deqiang Xu Wei Zhao Weida Huang Qingguo Li | 2000 | Chinese Science Bulletin2000，45，12： | 5 |
| 2 | Peripheral Lymphocyte Subsets as a Marker of Parkinson's Disease in a Chinese Population显示文摘In this study, we conducted a clinical analysis of lymphocyte subtypes in 268 patients with Parkinson's disease(PD) to assess their clinical impact as a potential marker of advanced PD in Chinese patients. The participants comprised 268 sporadic PD patients and 268 healthy controls. The numbers of natural killer(NK) cells and CD3+, CD3+CD4+, CD3+CD8+, and CD19+ lymphocytes from peripheral blood were determined by immunostaining and flow cytometric analysis and the percentages of these CD+ T cells were calculated. The ratio of regulatory T(Treg)/helper T 17(Th17) lymphocytes from 64 PD patients and 46 controls was determined by flow cytometric analysis.The results showed that the percentage of NK cells was higher in advanced PD patients than in controls(22.92% ±10.08% versus 19.76% ± 10.09%, P = 0.006), while CD3+ T cells are decreased(62.93% ± 9.27% versus65.75% ± 9.13%, P = 0.005). The percentage of CD19+B cells in male patients was lower(P = 0.021) than in female patients, whereas NK cells were increased(P \ 0.0001). The scores on the Unified Parkinson's Disease Rating Scale(UPDRS) and the Non-Motor Symptoms Scale in late-onset PD patients were significantly higher than those in earlyonset patients(P = 0.024 and P = 0.007, respectively). The percentage of CD19+ B cells in patients with UPDRS scores[24 was lower than in those with scores \24(10.17% ±4.19% versus 12.22% ± 5.39%, P = 0.009). In addition, the Treg/Th17 ratio in female patients was higher than that in female controls(13.88 ± 6.32 versus 9.94 ± 4.06, P =0.042). These results suggest that the percentages of NK cells,CD3+ T cells, and CD19+ B cells along with the Treg/Th17 ratio in peripheral blood may be used to predict the risk of PD in Chinese individuals and provide fresh avenues for novel diagnostic biomarkers and therapeutic designs. | Luan Cen Chaohao Yang Shuxuan Huang Miaomiao Zhou Xiaolu Tang Kaiping Li Wenyuan Guo Zhuohua Wu Mingshu Mo Yousheng Xiao Xiang Chen Xinling Yang Qinhui Huang Chaojun Chen Shaogang Qu Pingyi Xu | 2017 | Neuroscience Bulletin2017，33，5： | 5 |
| 3 | CHCHD2 Thr61Ile mutation impairs F1F0-ATPase assembly in in vitro and in vivo models of Parkinson's disease显示文摘Mitochondrial dysfunction is a significant pathological alte ration that occurs in Parkinson's disease(PD),and the Thr61lle(T61I)mutation in coiled-coil helix coiled-coil helix domain containing 2(CHCHD2),a crucial mitochondrial protein,has been reported to cause Parkinson's disease.FIFO-ATPase participates in the synthesis of cellular adenosine triphosphate(ATP)and plays a central role in mitochondrial energy metabolism.However,the specific roles of wild-type(WT)CHCHD2 and T611-mutant CHCHD2 in regulating F1FO-ATPase activity in Parkinson's disease,as well as whether CHCHD2 or CHCHD2 T61I affects mitochondrial function through regulating F1FO-ATPase activity,remain unclea r.Therefore,in this study,we expressed WT CHCHD2 and T61l-mutant CHCHD2 in an MPP^(+)-induced SH-SY5Y cell model of PD.We found that CHCHD2 protected mitochondria from developing MPP^(+)-induced dysfunction.Under normal conditions,ove rexpression of WT CHCHD2 promoted F1FO-ATPase assembly,while T61I-mutant CHCHD2 appeared to have lost the ability to regulate F1FO-ATPase assembly.In addition,mass spectrometry and immunoprecipitation showed that there was an interaction between CHCHD2 and F1FO-ATPase.Three weeks after transfection with AAV-CHCHD2 T61I,we intraperitoneally injected 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine into mice to establish an animal model of chronic Parkinson's disease and found that exogenous expression of the mutant protein worsened the behavioral deficits and dopaminergic neurodegeneration seen in this model.These findings suggest that WT CHCHD2 can alleviate mitochondrial dysfunction in PD by maintaining F1F0-ATPase structure and function. | Xiang Chen Yuwan Lin Zhiling Zhang Yuting Tang Panghai Ye Wei Dai Wenlong Zhang Hanqun Liu Guoyou Peng Shuxuan Huang Jiewen Qiu Wenyuan Guo Xiaoqin Zhu Zhuohua Wu Yaoyun Kuang Pingyi Xu Miaomiao Zhou | 2024 | Neural Regeneration Research2024，19，1： | 0 |
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