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学者姓名:刘健康

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LncRNA SAMMSON Mediates Adaptive Resistance to RAF Inhibition in BRAF-Mutant Melanoma Cells SCIE PubMed
期刊论文 | 2021 , 81 (11) , 2918-2929 | CANCER RESEARCH
WoS CC Cited Count: 3
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Abstract :

The long noncoding RNA (lncRNA) SAMMSON is required for human melanoma cell growth and survival. However, whether SAMMSON regulates the response of mutant BRAF melanoma cells to RAF inhibitors remains unknown. In this work, we showed that SAMMSON is rapidly induced upon inhibition of ERK signaling, and SAMMSON overexpression conferred resistance to vemurafenib-induced cytotoxicity in melanoma cells. SOX10 mediated transcriptional induction of SAMMSON by vemurafenib, and SOX10 sumoylation at K55 was essential for this function. In addition, depletion of SAMMSON activated p53 signaling, which is dependent on the SAMMSON-interacting protein CARF. Depletion of SAMMSON sensitized mutant BRAF melanoma cells to RAF inhibitors in vitro and in vivo, while CARF knockdown reversed the enhanced sensitivity. In summary, these findings suggest that SAMMSON may function as a new mediator of adaptive resistance to RAF inhibitors in melanoma by modulating CARF-p53 signaling. Significance: This study highlights the role of a SAMMSON/CARF/p53 signaling axis in modulating the adaptive resistance of mutant BRAF melanoma to RAF inhibitors.

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GB/T 7714 Han, Shujun , Yan, Yuwei , Ren, Yibo et al. LncRNA SAMMSON Mediates Adaptive Resistance to RAF Inhibition in BRAF-Mutant Melanoma Cells [J]. | CANCER RESEARCH , 2021 , 81 (11) : 2918-2929 .
MLA Han, Shujun et al. "LncRNA SAMMSON Mediates Adaptive Resistance to RAF Inhibition in BRAF-Mutant Melanoma Cells" . | CANCER RESEARCH 81 . 11 (2021) : 2918-2929 .
APA Han, Shujun , Yan, Yuwei , Ren, Yibo , Hu, Yiming , Wang, Yan , Chen, Lei et al. LncRNA SAMMSON Mediates Adaptive Resistance to RAF Inhibition in BRAF-Mutant Melanoma Cells . | CANCER RESEARCH , 2021 , 81 (11) , 2918-2929 .
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Regulation of IFN-Is by MEF2D Promotes Inflammatory Homeostasis in Microglia SCIE PubMed
期刊论文 | 2021 , 14 , 2851-2863 | JOURNAL OF INFLAMMATION RESEARCH
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Background: Microglia play an essential role in the central nervous system immune response. The transcription factor myocyte enhancer factor-2 D (MEF2D) is known to participate in stress regulation in various cell types and is easily activated in microglia. MEF2D has been shown to transcriptionally regulate several cytokine genes in immune cells and directly regulates the inflammatory response, suggesting that MEF2D may act as a key stimulus response regulator of microglia and is involved in the regulation of brain micro-homeostasis. To uncover the molecular mechanism of MEF2D in the inflammatory system, in the present study, we investigated the global effect of MEF2D in activated microglia and explored its potential regulatory network. Methods: Experiments with a recombinant lentiviral vector containing either shRNA or overexpressing MEF2D were performed in the murine microglial BV2 cell line. Transcriptome sequencing and global gene expression patterns were analysed in lipopoly-saccharide-stimulated shMEF2D BV2 cells. Pro-and anti-inflammatory factors were assessed by Western blot, qPCR or ELISA, and microglial activity was assessed by phago-cytosis and morphologic analysis. The direct binding of MEF2D to the promoter region of interferon regulatory factor 7 (IRF7) was tested by ChIP-qPCR. The interferon-stimulated genes (ISGs) were tested by qPCR. Results: MEF2D actively participated in the inflammatory response of BV2 microglial cells. Stably expressed RNAi-induced silencing of MEF2D disrupted the microglial immune balance in two ways: (1) the expression of proinflammatory factors, such as NLRP3, IL-1 beta, and iNOS was promoted; and (2) the type-I interferon signalling pathway was markedly inhibited by directly modulating IRF7 transcription. In contrast, overexpression of MEF2D significantly reduced the expression of NLRP3 and iNOS under LPS stimulation and alleviated the level of immune stress in microglia. Conclusion: These findings demonstrate that MEF2D plays an important role in regulating inflammatory homeostasis partly through transcriptional regulation of the type-I interferon signalling pathway.

Keyword :

inflammatory homeostasis microglia MEF2D IRF7 type-I interferons

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GB/T 7714 Lu, Fangfang , Wang, Ronglin , Xia, Li et al. Regulation of IFN-Is by MEF2D Promotes Inflammatory Homeostasis in Microglia [J]. | JOURNAL OF INFLAMMATION RESEARCH , 2021 , 14 : 2851-2863 .
MLA Lu, Fangfang et al. "Regulation of IFN-Is by MEF2D Promotes Inflammatory Homeostasis in Microglia" . | JOURNAL OF INFLAMMATION RESEARCH 14 (2021) : 2851-2863 .
APA Lu, Fangfang , Wang, Ronglin , Xia, Li , Nie, Tiejian , Gao, Fei , Yang, Shaosong et al. Regulation of IFN-Is by MEF2D Promotes Inflammatory Homeostasis in Microglia . | JOURNAL OF INFLAMMATION RESEARCH , 2021 , 14 , 2851-2863 .
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Mitoepigenetics: An intriguing regulatory layer in aging and metabolic-related diseases SCIE PubMed
期刊论文 | 2021 , 177 , 337-346 | FREE RADICAL BIOLOGY AND MEDICINE
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As a key organelle in eukaryotic cells, mitochondria play a central role in maintaining normal cellular functions. Mitochondrial dysfunction is reported to be closely related with aging and various diseases. Epigenetic modifications in nuclear genome provide a substantial layer for the modulation of nuclear-encoded gene expression. However, whether mitochondria could also be subjected to such similar epigenetic alterations and the involved mechanisms remain largely obscure and controversial. Recently, accumulating evidence has suggested that mitochondrial epigenetics, also known as mitoepigenetics may serve as an intriguing regulatory layer in mitochondrial DNA (mtDNA)-encoded gene expression. Given the potential regulatory role of mitoepigenetics, mitochondrial dysfunction derived from mitoepigenetics-induced abnormal gene expression could also be closely associated with aging and disease development. In this review, we summarized the recent advances in mitoepigenetics, with a special focus on mtDNA methylation in aging and metabolic-related diseases as well as the new methods and technologies for the study of mitoepigenetics. Uncovering the regulatory role of mitoepigenetics will help to understand the underlying mechanisms of mitochondrial dysfunction and provide novel strategies for delaying aging and preventing metabolic-related diseases.

Keyword :

Post-translational modifications (PTMs) Mitochondrial epigenetics (mitoepigenetics) mtDNA-associated proteins Mitochondrial DNA (mtDNA) methylation Mitochondrial non-coding RNAs (ncRNAs)

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GB/T 7714 Cao, Ke , Feng, Zhihui , Gao, Feng et al. Mitoepigenetics: An intriguing regulatory layer in aging and metabolic-related diseases [J]. | FREE RADICAL BIOLOGY AND MEDICINE , 2021 , 177 : 337-346 .
MLA Cao, Ke et al. "Mitoepigenetics: An intriguing regulatory layer in aging and metabolic-related diseases" . | FREE RADICAL BIOLOGY AND MEDICINE 177 (2021) : 337-346 .
APA Cao, Ke , Feng, Zhihui , Gao, Feng , Zang, Weijin , Liu, Jiankang . Mitoepigenetics: An intriguing regulatory layer in aging and metabolic-related diseases . | FREE RADICAL BIOLOGY AND MEDICINE , 2021 , 177 , 337-346 .
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Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status SCIE PubMed
期刊论文 | 2021 , 10 (11) | ANTIOXIDANTS
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NF-E2-related factor 2 (Nrf2), the key transcription regulator of phase II enzymes, has been considered beneficial for neuronal protection. We previously designed a novel chalcone analog, 1-(2,3,4-trimethoxyphenyl)-2-(3,4,5-trimethoxyphenyl)-acrylketone (Tak), that could specifically activate Nrf2 in vitro. Here, we report that Tak confers significant hippocampal neuronal protection both in vitro and in vivo. Treatment with Tak has no significant toxicity on cultured neuronal cells. Instead, Tak increases cellular ATP production by increasing mitochondrial function and decreases the levels of reactive oxygen species by activating Nrf2-mediated phase II enzyme expression. Tak pretreatment prevents glutamate-induced excitotoxic neuronal death accompanied by suppressed mitochondrial respiration, increased superoxide production, and activation of apoptosis. Further investigation indicates that the protective effect of Tak is mediated by the Akt signaling pathway. Meanwhile, Tak administration in mice can sufficiently abrogate scopolamine-induced cognitive impairment via decreasing hippocampal oxidative stress. In addition, consistent benefits are also observed in an energy stress mouse model under a high-fat diet, as the administration of Tak remarkably increases Akt signaling-mediated antioxidative enzyme expression and prevents hippocampal neuronal apoptosis without significant effect on the mouse metabolic status. Overall, our study demonstrates that Tak protects cognitive function by Akt-mediated Nrf2 activation to maintain redox status both vivo and in vitro, suggesting that Tak is a promising pharmacological candidate for the treatment of oxidative neuronal diseases.

Keyword :

mitochondrial function phase II enzymes Nrf2 hippocampus Akt

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GB/T 7714 Cui, Yuting , Xiong, Yue , Li, Hua et al. Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status [J]. | ANTIOXIDANTS , 2021 , 10 (11) .
MLA Cui, Yuting et al. "Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status" . | ANTIOXIDANTS 10 . 11 (2021) .
APA Cui, Yuting , Xiong, Yue , Li, Hua , Zeng, Mengqi , Wang, Yan , Li, Yuan et al. Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status . | ANTIOXIDANTS , 2021 , 10 (11) .
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Integrative Analyses Reveal Tstd1 as a Potential Modulator of HDL Cholesterol and Mitochondrial Function in Mice SCIE PubMed
期刊论文 | 2021 , 10 (11) | CELLS
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High-density lipoprotein (HDL) cholesterol levels are closely associated with human health and diseases. To identify genes modulating plasma HDL levels, we integrated HDL measurements and multi-omics data collected from diverse mouse cohorts and combined a list of systems genetics methods, including quantitative trait loci (QTL) mapping analysis, mediation analysis, transcriptome-wide association analysis (TWAS), and correlation analysis. We confirmed a significant and conserved QTL for plasma HDL on chromosome 1 and identified that Tstd1 liver transcript correlates with plasma HDL in several independent mouse cohorts, suggesting Tstd1 may be a potential modulator of plasma HDL levels. Correlation analysis using over 70 transcriptomics datasets in humans and mice revealed consistent correlations between Tstd1 and genes known to be involved in cholesterol and HDL regulation. Consistent with strong enrichment in gene sets related to cholesterol and lipoproteins in the liver, mouse strains with high Tstd1 exhibited higher plasma levels of HDL, total cholesterol and other lipid markers. GeneBridge using large-scale expression datasets identified conserved and positive associations between TSTD1/Tstd1 and mitochondrial pathways, as well as cholesterol and lipid pathways in human, mouse and rat. In summary, we identified Tstd1 as a new modulator of plasma HDL and mitochondrial function through integrative systems analyses, and proposed a new mechanism of HDL modulation and a potential therapeutic target for relevant diseases. This study highlights the value of such integrative approaches in revealing molecular mechanisms of complex traits or diseases.

Keyword :

integrative analysis mitochondria systems genetics HDL correlation analysis mediation analysis transcriptome-wide association analysis (TWAS) quantitative trait loci (QTL)

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GB/T 7714 Zheng, Adi , Li, Hao , Feng, Zhihui et al. Integrative Analyses Reveal Tstd1 as a Potential Modulator of HDL Cholesterol and Mitochondrial Function in Mice [J]. | CELLS , 2021 , 10 (11) .
MLA Zheng, Adi et al. "Integrative Analyses Reveal Tstd1 as a Potential Modulator of HDL Cholesterol and Mitochondrial Function in Mice" . | CELLS 10 . 11 (2021) .
APA Zheng, Adi , Li, Hao , Feng, Zhihui , Liu, Jiankang . Integrative Analyses Reveal Tstd1 as a Potential Modulator of HDL Cholesterol and Mitochondrial Function in Mice . | CELLS , 2021 , 10 (11) .
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Hypermethylation of Hepatic Mitochondrial ND6 Provokes Systemic Insulin Resistance EI SCIE PubMed
期刊论文 | 2021 , 8 (11) | ADVANCED SCIENCE
WoS CC Cited Count: 3
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Mitochondrial epigenetics is rising as intriguing notion for its potential involvement in aging and diseases, while the details remain largely unexplored. Here it is shown that among the 13 mitochondrial DNA (mtDNA) encoded genes, NADH-dehydrogenase 6 (ND6) transcript is primarily decreased in obese and type 2 diabetes populations, which negatively correlates with its distinctive hypermethylation. Hepatic mtDNA sequencing in mice unveils that ND6 presents the highest methylation level, which dramatically increases under diabetic condition due to enhanced mitochondrial translocation of DNA methyltransferase 1 (DNMT1) promoted by free fatty acid through adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) activation. Hepatic knockdown of ND6 or overexpression of Dnmt1 similarly impairs mitochondrial function and induces systemic insulin resistance both in vivo and in vitro. Genetic or chemical targeting hepatic DNMT1 shows significant benefits against insulin resistance associated metabolic disorders. These findings highlight the pivotal role of ND6 epigenetic network in regulating mitochondrial function and onset of insulin resistance, shedding light on potential preventive and therapeutic strategies of insulin resistance and related metabolic disorders from a perspective of mitochondrial epigenetics.

Keyword :

mitochondrial dysfunction mitochondrial NADH&#8208 obesity and type 2 diabetes mellitus (T2DM) dehydrogenase 6 (ND6) insulin resistance DNA methyltransferase 1 (DNMT1)

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GB/T 7714 Cao, Ke , Lv, Weiqiang , Wang, Xueqiang et al. Hypermethylation of Hepatic Mitochondrial ND6 Provokes Systemic Insulin Resistance [J]. | ADVANCED SCIENCE , 2021 , 8 (11) .
MLA Cao, Ke et al. "Hypermethylation of Hepatic Mitochondrial ND6 Provokes Systemic Insulin Resistance" . | ADVANCED SCIENCE 8 . 11 (2021) .
APA Cao, Ke , Lv, Weiqiang , Wang, Xueqiang , Dong, Shanshan , Liu, Xuyun , Yang, Tielin et al. Hypermethylation of Hepatic Mitochondrial ND6 Provokes Systemic Insulin Resistance . | ADVANCED SCIENCE , 2021 , 8 (11) .
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Dynamic motions and architectural changes in DNA supramolecular aggregates visualized via transmission electron microscopy without liquid cells EI SCIE PubMed
期刊论文 | 2021 , 13 (37) , 15928-15936 | NANOSCALE
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In the last decade, breakthroughs in liquid-phase transmission electron microscopy (TEM) have enabled in situ visualization of the motion dynamics of nanostructures in liquid media with unprecedented detail. However, it remains a significant challenge to perform liquid-phase TEM due to the intricate preparation procedure of liquid cells to keep liquid from evaporating under ultrahigh vacuum conditions in TEM columns. In the present study, the nonvolatility and remarkable solvation property of ionic liquids (ILs) is exploited to image the dynamic processes of DNA supramolecular aggregates and Au nanoparticle (NP) aggregates encompassing Brownian motions, interactions among individual nanoobjects and changes in architecture at nanometer resolution. Significant differences in motion behaviors are observed between DNA supramolecular aggregates and Au NP aggregates. Moreover, the temperature and dose dependence of dynamic motions are also investigated. The findings provide insights into the dynamics of DNA supramolecular aggregates and Au NP aggregates in ILs and present an easily accessible approach for probing the dynamic processes of biomacromolecular and other soft matter aggregates with various kinds of ILs at the nanoscale level.

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GB/T 7714 Lu, Zhuoyang , Liu, Xiangyang , He, Maogang et al. Dynamic motions and architectural changes in DNA supramolecular aggregates visualized via transmission electron microscopy without liquid cells [J]. | NANOSCALE , 2021 , 13 (37) : 15928-15936 .
MLA Lu, Zhuoyang et al. "Dynamic motions and architectural changes in DNA supramolecular aggregates visualized via transmission electron microscopy without liquid cells" . | NANOSCALE 13 . 37 (2021) : 15928-15936 .
APA Lu, Zhuoyang , Liu, Xiangyang , He, Maogang , Long, Jiangang , Liu, Jiankang . Dynamic motions and architectural changes in DNA supramolecular aggregates visualized via transmission electron microscopy without liquid cells . | NANOSCALE , 2021 , 13 (37) , 15928-15936 .
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Htd2 deficiency-associated suppression of a-lipoic acid production provokes mitochondrial dysfunction and insulin resistance in adipocytes SCIE PubMed
期刊论文 | 2021 , 41 | REDOX BIOLOGY
WoS CC Cited Count: 2
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Mitochondria harbor a unique fatty acid synthesis pathway (mtFAS) with mysterious functions gaining increasing interest, while its involvement in metabolic regulation is essentially unknown. Here we show that 3-Hydroxyacyl-ACP dehydratase (HTD2), a key enzyme in mtFAS pathway was primarily downregulated in adipocytes of mice under metabolic disorders, accompanied by decreased de novo production of lipoic acid, which is the byproduct of mtFAS pathway. Knockdown of Htd2 in 3T3-L1 preadipocytes or differentiated 3T3-L1 mature adipocytes impaired mitochondrial function via suppression of complex I activity, resulting in enhanced oxidative stress and impaired insulin sensitivity, which were all attenuated by supplement of lipoic acid. Moreover, lipidomic study revealed limited lipid alterations in mtFAS deficient cells which primarily presenting accumulation of triglycerides, attributed to mitochondrial dysfunction. Collectively, the present study highlighted the pivotal role of mtFAS pathway in regulating mitochondrial function and adipocytes insulin sensitivity, demonstrating supportive evidence for lipoic acid being potential effective nutrient for improving insulin resistance and related metabolic disorders.

Keyword :

3-Hydroxyacyl-ACP dehydratase (HTD2) Insulin resistance Lipoic acid Mitochondrial dysfunction Mitochondrial fatty acid synthesis (mtFAS) Oxidative stress

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GB/T 7714 Zeng, Mengqi , Xu, Jie , Zhang, Zhengyi et al. Htd2 deficiency-associated suppression of a-lipoic acid production provokes mitochondrial dysfunction and insulin resistance in adipocytes [J]. | REDOX BIOLOGY , 2021 , 41 .
MLA Zeng, Mengqi et al. "Htd2 deficiency-associated suppression of a-lipoic acid production provokes mitochondrial dysfunction and insulin resistance in adipocytes" . | REDOX BIOLOGY 41 (2021) .
APA Zeng, Mengqi , Xu, Jie , Zhang, Zhengyi , Zou, Xuan , Wang, Xueqiang , Cao, Ke et al. Htd2 deficiency-associated suppression of a-lipoic acid production provokes mitochondrial dysfunction and insulin resistance in adipocytes . | REDOX BIOLOGY , 2021 , 41 .
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Central and Peripheral Metabolic Defects Contribute to the Pathogenesis of Alzheimer's Disease: Targeting Mitochondria for Diagnosis and Prevention. PubMed SCIE
期刊论文 | 2020 , 32 (16) , 1188-1236 | Antioxidants & redox signaling | IF: 8.401
WoS CC Cited Count: 23
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<b> <i>Significance:</i> </b> Epidemiological studies indicate that metabolic disorders are associated with an increased risk for Alzheimer's disease (AD). Metabolic remodeling occurs in the central nervous system (CNS) and periphery, even in the early stages of AD. Mitochondrial dysfunction has been widely accepted as a molecular mechanism underlying metabolic disorders. Therefore, focusing on early metabolic changes, especially from the perspective of mitochondria, could be of interest for early AD diagnosis and intervention. <b> <i>Recent Advances:</i> </b> We and others have identified that the levels of several metabolites are fluctuated in the periphery before their accumulation in the CNS, which plays an important role in the pathogenesis of AD. Mitochondrial remodeling is likely one of the earliest signs of AD, linking nutritional imbalance to cognitive deficits. Notably, by improving mitochondrial function, mitochondrial nutrients efficiently rescue cellular metabolic dysfunction in the CNS and periphery in individuals with AD. <b> <i>Critical Issues:</i> </b> Peripheral metabolic disorders should be intensively explored and evaluated for the early diagnosis of AD. The circulating metabolites derived from mitochondrial remodeling represent novel potential diagnostic biomarkers for AD that are more readily detected than CNS-oriented biomarkers. Moreover, mitochondrial nutrients provide a promising approach to preventing and delaying AD progression. <b> <i>Future Directions:</i> </b> Abnormal mitochondrial metabolism in the CNS and periphery is involved in AD pathogenesis. More clinical studies provide evidence for the suitability and reliability of circulating metabolites and cytokines for the early diagnosis of AD. Targeting mitochondria to rewire cellular metabolism is a promising approach to preventing AD and ameliorating AD-related metabolic disorders.

Keyword :

biomarkers ketogenesis glucose lipogenesis mitochondrial nutrients

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GB/T 7714 Peng Yunhua , Gao Peipei , Shi Le et al. Central and Peripheral Metabolic Defects Contribute to the Pathogenesis of Alzheimer's Disease: Targeting Mitochondria for Diagnosis and Prevention. [J]. | Antioxidants & redox signaling , 2020 , 32 (16) : 1188-1236 .
MLA Peng Yunhua et al. "Central and Peripheral Metabolic Defects Contribute to the Pathogenesis of Alzheimer's Disease: Targeting Mitochondria for Diagnosis and Prevention." . | Antioxidants & redox signaling 32 . 16 (2020) : 1188-1236 .
APA Peng Yunhua , Gao Peipei , Shi Le , Chen Lei , Liu Jiankang , Long Jiangang . Central and Peripheral Metabolic Defects Contribute to the Pathogenesis of Alzheimer's Disease: Targeting Mitochondria for Diagnosis and Prevention. . | Antioxidants & redox signaling , 2020 , 32 (16) , 1188-1236 .
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Skp2 dictates cell cycle-dependent metabolic oscillation between glycolysis and TCA cycle (Jul, 10.1038/s41422-0200372-z, 2020) SCIE CSCD PubMed
期刊论文 | 2020 , 31 (1) , 104-104 | CELL RESEARCH | IF: 25.617
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An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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GB/T 7714 Liu, Jing , Peng, Yunhua , Shi, Le et al. Skp2 dictates cell cycle-dependent metabolic oscillation between glycolysis and TCA cycle (Jul, 10.1038/s41422-0200372-z, 2020) [J]. | CELL RESEARCH , 2020 , 31 (1) : 104-104 .
MLA Liu, Jing et al. "Skp2 dictates cell cycle-dependent metabolic oscillation between glycolysis and TCA cycle (Jul, 10.1038/s41422-0200372-z, 2020)" . | CELL RESEARCH 31 . 1 (2020) : 104-104 .
APA Liu, Jing , Peng, Yunhua , Shi, Le , Wan, Lixin , Inuzuka, Hiroyuki , Long, Jiangang et al. Skp2 dictates cell cycle-dependent metabolic oscillation between glycolysis and TCA cycle (Jul, 10.1038/s41422-0200372-z, 2020) . | CELL RESEARCH , 2020 , 31 (1) , 104-104 .
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