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Modulating ion current rectification generating high energy output in a single glass conical nanopore channel by concentration gradient

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Chinese Chemical Letters 2015年第1期26卷 43-46页

作者： Li-Xiang Zhang Yu-Bin Zheng sheng-lin cai Xiao-Hong Cao Yao-Qun Li Department of Chemistry and the MOE Key Laboratory of Spectrochemical Analysis & Instrumentation College of Chemistry and Chemical Engineering.Xiamen University Shenzhen Haibin Pharmaceutical Co. Ltd.

Inspired by biological systems that have the inherent skill to generate considerable bioelectricity from the salt content in fluids with highly selective ion channels and pumps on cell membranes, herein, a fully abiotic, single glass conical nanopores energy-harvesting is demonstrated. Ion current rectification （ICR） in negatively charged glass conical nanopores is shown to be controlled by the electrolyte concentration gradient depending on the direction of ion diffusion. The degree of ICR is enhanced with the increasing forward concentration difference. An unusual rectification inversion is observed when the concentration gradient is reversely applied. The maximum power output with the individual nanopore approaches 10^4pW. This facile and cost-efficient energy-harvesting system has the potential to power tiny biomedical devices or construct future clean-energy recovery plants.

关键词： Glass conical nanopore channe Ion current rectification Concentration gradient Energy generation

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Hierarchical inhibition of mTORC1 by glucose starvation-triggered AXIN lysosomal translocation and by AMPK

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Life Metabolism 2023年第3期2卷 19-32页

作者： Mengqi Li Xiaoyan Wei Jinye Xiong Jin-Wei Feng Chen-Song Zhang sheng-cai lin State Key Laboratory of Cellular Stress Biology School of Life SciencesFaculty of Medicine and Life SciencesXiamen UniversityXiamenFujian 361102China

When glucose is replete,mammalian/mechanistic target of rapamycin complex 1(mTORC1)is active and anchored to the lysosomal surface via the two GTPases,Ras-related GTPase(RAG)and Ras homolog enriched in brain(Rheb),which are regulated by Ragulator and tuberous sclerosis complex 2(TSC2),*** glucose is low,aldolase senses low fructose-1,6-bisphosphate level and promotes the translocation of AXIN−liver kinase B1(LKB1)to the lysosomal surface,which leads to the activation of AMP-activated protein kinase(AMPK)and the inhibition of RAGs,sundering mTORC1 from the lysosome and causing its *** can also inactivate mTORC1 by phosphorylating Raptor and ***,the hierarchy of AXIN-and AMPK-mediated inhibition of mTORC1 remains poorly ***,we show that AXIN translocation does not require AMPK expression or *** glucose starvation conditions,knockout of AXIN extended the half-life of mTORC1 inhibition from 15 to 60 min,whereas knockout of AMPK only extended it to 30 ***(constitutively active RAGB)almost entirely blocked the lysosomal dissociation and inhibition of mTORC1 under glucose starvation,but it did not inhibit AMPK,indicating that under these conditions,it is AXIN lysosomal translocation that inhibits mTORC1,and it does so via inhibition of RAGs.5-aminoimidazole-4-carboxamide ribonucleoside(AICAR),a mimetic of AMP,which activates both cytosolic AMPK and lysosomal AMPK,fully inhibited mTORC1 even when it is stably anchored to the lysosome by RAGBGTP,whereas glucose starvation mildly inhibited such anchored ***,we demonstrate that the lysosomal translocation of AXIN plays a primary role in glucose starvation-triggered inhibition of mTORC1 by inhibiting RAGs,and that AMPK activity inhibits mTORC1 through phosphorylating Raptor and TSC2,especially under severe stress.

关键词： mTORC1 glucose sensing AMPK

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Advances on the road map from glucose starvation to AMPK activation

Advances on the road map from glucose starvation to AMPK act...

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中国生物化学与分子生物学会2019年全国学术会议暨学会...

作者： sheng-cai lin School of Life Sciences Xiamen University

AMPK and mTOR are the dichotomy of kinase complexes that plays a pivotal role in maintaining metabolic *** have delineated the pathway that senses falling levels of glucose and activates *** low glucose,v-ATPase-bound aldolase senses the absence of the glycolytic product of fructose-1,6-bisphosphate(FBP)and induces conformational changes in v-ATPase,allowing AXIN in complex with

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Metabolic homeostasis——switch between catabolism and anabolism

Metabolic homeostasis——switch between catabolism and anabo...

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中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议

作者： sheng-cai lin School of Life Sciences Xiamen University

Metabolic homeostasis is maintained by various cellular sensors,including the master kinases AMPK(AMP-activated protein kinase)and *** response to low energy status,AMPK is activated to enhance catabolic activities with concurrent inhibition of anabolic processes such as fatty acid *** contrast,mTORC1 is activated when nutrients and growth factors are *** have recently discovered the mechanism by which AMP,as a low energy-charge signal,can autonomously initiate the assembly of an activating complex for AMPK in response to *** binding causes a higher affinity of AMPK for the scaffold protein AXIN that also binds to LKB1,thereby promoting phosphorylation and activation of *** recently,we found most surprisingly that the late

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Mechanism for glucose sensing

Mechanism for glucose sensing

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： sheng-cai lin School of Life Sciences Xiamen University

Glucose is not only the main source for energy, but also a precursor for the synthesis of many *** entering glycolysis, glucose is converted in three steps to fructose-1,6-bisphosphate (FBP), which is then split into triose phosphates by FBP aldolases. Glucose deprivation activates AMP-activated protein kinase (AMPK), a sensor known to play a pivotal role in adaptive responses to energy stress, but it had been unclear how glucose deprivation is sensed and signals to activate AMPK and inactivate mTORC1.

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Signaling pathways for response to nutritional stress

Signaling pathways for response to nutritional stress

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中国生物化学与分子生物学会2016年全国学术会议

作者： sheng-cai lin School of Life Sciences Xiamen University

Metabolic homeostasis is maintained by various cellular sensors,including the master kinases AMPK(AMPactivated protein kinase)and mT *** response to low energy status,AMPK is activated to enhance catabolic activities with concurrent inhibition of anabolic processes such as fatty acid *** contrast,mT ORC1 is activated when nutrients and growth factors are *** mechanism for AMPK activation

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Metformin signaling intersects the glucose sensing-AMPK pathway

Metformin signaling intersects the glucose sensing-AMPK path...

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第四届中国生物物理学会代谢生物学分会学术研讨会

作者： sheng-cai lin

＜正＞We have elucidated a glucose sensing pathway, in that fructose-1,6-bisphosphate（FBP）-unoccupied aldolase renders v-ATPase inactive, triggering translocation of Axin/LKB1 to the lysosomal surface to activate AMPK. In 2016, we showed that metformin activates AMPK through this lysosomal AMPK pathway. We later synthesized a photoactive metformin probe to profile binding partners of the drug in lysates of purified lysosomes.

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Axin bridges Daxx to p53

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Cell Research 2007年第4期17卷 301-302页

作者： sheng-cai lin~1 Qinxi Li ~1Key Laboratory of Ministry of Education for Cell Biology and Tumor Cell Engineering,Xiamen University,Xiamen 361005,China Key Laboratory of Ministry of Education for Cell Biology and Tumor Cell Engineering Xiamen University Xiamen China

The death domain-associated protein Daxx exerts manyreported functions that include mediating the signaling fromFasL to apoptosis via activating the c-Jun N-terminal kinase(JNK)[1],induction and inhibition of apoptosis[2-5],and regulation of chromatin *** was originallycloned from a yeast two-hybrid screen using the intracel-lular tail of the Fas receptor as the bait[1].Whereas manyof the initial reports remain controversial,it is clear thatDaxx plays important roles in the regulation of apoptosistriggered by a series of stress signals including UV irradia-tion,hydrogen peroxide treatment and TGF-βtreatment[2,3].In this Commentary,we focus on Axin being a tetheringfactor linking Daxx to p53.A possible functional linkage of Daxx to p53 was firstreported by Ohiro et al.[6].In that study,it was shown thatsome tumorigenic mutants of p53,but not wild-type p53,interact with Daxx and inhibit Daxx-induced cell death byblocking Daxx-dependent activation of the JNK kinase,suggesting that mutant p53 in tumor cells may contrib-ute to tumorigenesis by inhibiting stress-induced kinase

关键词： Daxx Axin bridges Daxx to p53

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To die or not to die upon DNA damage

To die or not to die upon DNA damage

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2008年中国病理生理学会第十一届肿瘤和第十二届免疫专业委员会学术会议

作者： sheng-cai lin School of Life Sciences Xiamen University

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To Die or Not to Die Upon DNA Damage

To Die or Not to Die Upon DNA Damage

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2008年全国生物化学与分子生物学学术大会

作者： sheng-cai lin (School of Life Sciences,Xiamen University,Xiamen 361005)

Many factors exert roles in cellular commitment to undergo cell arrest or apoptosis following genotoxic stresses;how they are orchestrated to selectively reach respective thresholds remains *** have found that Axin scaffolds with HIPK2,p53 and Pirh2,forming distinct complexes in cellular commitment to cell-cycle arrest or ***2 strongly abrogates Axin-based genotoxic induction of p53 Set-46 phosphorylation by

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