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| 1 | 3D numeri-cal simulation of transient temperature field for lens mold embedded with heaters显示文摘 | LIN YUWAN LI HAIMEI CHEN S C | | 0，，09： | 1 |
| 2 | 3D humeri- cal simulation of transient temperature field for lens mold embedded with heaters显示文摘 | LIN YUWAN LI HAIMEI CHEN S C | 2005 | International Journal of Heat and Mass Transfer2005，32，9： | 1 |
| 3 | Variable mold temperature to improve surface quality of mieroeellular injection molded parts using induction heating technology 显示文摘 | CHEN Shiachung LIN Yuwan CHIEN Reander | 2008 | Advances in Polymer Technology2008，27，4： | 1 |
| 4 | 3D numerical simulation of transient temperature field for lens mold embedded with heaters 显示文摘 | LIN Yuwan LI Haimei CHEN S C | 2005 | International Journal of Heat and Mass Transfer2005，32，9： | 1 |
| 5 | Chaperone-mediated Autophagy Regulates Cell Growth by Targeting SMAD3 in Glioma显示文摘Previous studies suggest that the reduction of SMAD3(mothers against decapentaplegic homolog 3)has a great impact on tumor development,but its exact pathological function remains unclear.In this study,we found that the protein level of SMAD3 was greatly reduced in human-grade IV glioblastoma tissues,in which LAMP2A(lysosome-associated membrane protein type 2A)was significantly up-regulated.LAMP2A is a key ratelimiting protein of chaperone-mediated autophagy(CMA),a lysosome pathway of protein degradation that is activated in glioma.We carefully analyzed the amino-acid sequence of SMAD3 and found that it contained a pentapeptide motif biochemically related to KFERQ,which has been proposed to be a targeting sequence for CMA.In vitro,we confirmed that SMAD3 was degraded in either serum-free or KFERQ motif deleted condition,which was regulated by LAMP2A and interacted with HSC70(heat shock cognate 71 kDa protein).Using isolated lysosomes,amino-acid residues 75 and 128 of SMAD3 were found to be of importance for this process,which affected the CMA pathway in which SMAD3 was involved.Similarly,down-regulating SMAD3 or up-regulating LAMP2A in cultured glioma cells enhanced their proliferation and invasion.Taken together,these results suggest that excessive activation of CMA regulates glioma cell growth by promoting the degradation of SMAD3.Therefore,targeting the SMAD3-LAMP2Amediated CMA-lysosome pathway may be a promising approach in anti-cancer therapy. | Hanqun Liu Yuxuan Yong Xingjian Li Panghai Ye Kai Tao Guoyou Peng Mingshu Mo Wenyuan Guo Xiang Chen Yangfu Luo Yuwan Lin Jiewen Qiu Ziling Zhang Liuyan Ding Miaomiao Zhou Xinling Yang Lin Lu Qian Yang Pingyi Xu | 2022 | Neuroscience Bulletin2022，38，6： | 0 |
| 6 | CHCHD2 maintains mitochondrial contact site and cristae organizing system stability and protects against mitochondrial dysfunction in an experimental model of Parkinson’s disease显示文摘Background:Parkinson’s disease(PD)is the second most common neurodegenerative disease after Alzheimer’s dementia.Mitochondrial dysfunction is involved in the pathology of PD.Coiled-coil-helix-coiled-coil-helix domain-containing 2(CHCHD2)was identified as associated with autosomal dominant PD.However,the mechanism of CHCHD2 in PD remains unclear.Methods:Short hairpin RNA(ShRNA)-mediated CHCHD2 knockdown or lentivirus-mediated CHCHD2 overexpression was performed to investigate the impact of CHCHD2 on mitochondrial morphology and function in neuronal tumor cell lines represented with human neuroblastoma(SHSY5Y)and HeLa cells.Blue-native polyacrylamide gel electrophoresis(PAGE)and two-dimensional sodium dodecyl sulfate-PAGE analysis were used to illustrate the role of CHCHD2 in mitochondrial contact site and cristae organizing system(MICOS).Co-immunoprecipitation and immunoblotting were used to address the interaction between CHCHD2 and Mic10.Serotype injection of adeno-associated vector-mediated CHCHD2 and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)administration were used to examine the influence of CHCHD2 in vivo.Results:We found that the overexpression of CHCHD2 can protect against methyl-4-phenylpyridinium(MPP+)-induced mitochondrial dysfunction and inhibit the loss of dopaminergic neurons in the MPTP-induced mouse model.Furthermore,we identified that CHCHD2 interacted with Mic10,and overexpression of CHCHD2 can protect against MPP+-induced MICOS impairment,while knockdown of CHCHD2 impaired the stability of MICOS.Conclusion:This study indicated that CHCHD2 could interact with Mic10 and maintain the stability of the MICOS complex,which contributes to protecting mitochondrial function in PD. | Lin Lu Hengxu Mao Miaomiao Zhou Yuwan Lin Wei Dai Jiewen Qiu Yousheng Xiao Mingshu Mo Xiaoqin Zhu Zhuohua Wu Zhong Pei Wenyuan Guo Pingyi Xu Xiang Chen | 2022 | Chinese Medical Journal2022，，13： | 0 |
| 7 | 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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