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NECAB family of neuronal calcium-binding proteins in health and disease

Neural Regeneration Research 2025年第5期20卷 1236-1243页

作者： Diones Bueno Michael K.E.Schafer Sudena Wang Michael J.Schmeisser Axel Methner Institute for Molecular Medicine University Medical Center of the Johannes Gutenberg-UniversityMainzGermany Department of Anesthesiology University Medical Center of the Johannes Gutenberg-UniversityMainzGermany Institute of Anatomy University Medical Center of the Johannes Gutenberg-UniversityMainzGermany

The N-terminal EF-hand calcium-binding proteins 1–3(NECAB1–3) constitute a family of predominantly neuronal proteins characterized by the presence of at least one EF-hand calcium-binding domain and a functionally less well characterized C-terminal antibiotic biosynthesis monooxygenase domain. All three family members were initially discovered due to their interactions with other proteins. NECAB1 associates with synaptotagmin-1, a critical neuronal protein involved in membrane trafficking and synaptic vesicle exocytosis. NECAB2 interacts with predominantly striatal G-protein-coupled receptors, while NECAB3 partners with amyloid-β A4 precursor protein-binding family A members 2 and 3, key regulators of amyloid-β production. This demonstrates the capacity of the family for interactions with various classes of proteins. NECAB proteins exhibit distinct subcellular localizations: NECAB1 is found in the nucleus and cytosol, NECAB2 resides in endosomes and the plasma membrane, and NECAB3 is present in the endoplasmic reticulum and Golgi apparatus. The antibiotic biosynthesis monooxygenase domain, an evolutionarily ancient component, is akin to atypical heme oxygenases in prokaryotes but is not wellcharacterized in vertebrates. Prokaryotic antibiotic biosynthesis monooxygenase domains typically form dimers, suggesting that calcium-mediated conformational changes in NECAB proteins may induce antibiotic biosynthesis monooxygenase domain dimerization, potentially activating some enzymatic properties. However, the substrate for this enzymatic activity remains uncertain. Alternatively, calcium-mediated conformational changes might influence protein interactions or the subcellular localization of NECAB proteins by controlling the availability of protein–protein interaction domains situated between the EF hands and the antibiotic biosynthesis monooxygenase domain. This review summarizes what is known about genomic organization, tissue expression, intracellular localization, interac

关键词： calcium EF hand mitochondria nervous system signal transduction

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Two paths, one goal: mechanism of calcium homeostasis to balance plant growth and immunity

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Science China Life Sciences 2025年第1期68卷 306-308页

作者： Aziz Ul Ikram Yanping Jing Huan Chen Jian Chen International Genome center Jiangsu University Joint center for Single Cell Biology School of Agriculture and BiologyShanghai Jiao Tong University

Calcium(Ca2+) is an essential nutrient and a cellular signal in plants. The level of free Ca2+in the apoplast is ～10,000-fold higher than that in the cytoplasm at the resting state. This large Ca2+level gradient across the membrane between the interior and exterior can cause Ca2+overload and toxicity. Plants have evolved mechanisms to export Ca2+out of the cytoplasm or store it in intracellular organelles, such as endoplasmic reticulum（ER）, mitochondria, and vacuole.

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Decision making module based on stochastic magnetic tunnel junctions

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Science China(Physics,Mechanics & Astronomy) 2025年第1期Mechanics & Astronomy) .卷 202-209页

作者： Yifan Miao Li Zhao Yajun Zhang Zhe Yuan center for Advanced Quantum Studies and Department of Physics Beijing Normal University Institute for Nanoelectric Devices and Quantum Computing Fudan University Interdisciplinary center for Theoretical Physics and Information Sciences Fudan University

In biological neural systems, noise is ubiquitous but does not affect the correct decisions made in the complex cognitive ***-making in biological neural system is typically achieved by accumulating input information over a period of *** by recent developments in neurosciences, we design a decision-making module based on spintronic devices, utilizing superparamagnetic tunnel junctions as artificial neurons. The feasibility of this decision-making module is verified through circuit simulations. Taking a multi-layer perceptron as an example, the module significantly improves the accuracy of the perceptron in the handwritten digit recognition task. Furthermore, the spintronic decision-making module offers advantages over the conventional pooling methods, such as adaptive decision time, high performance and the absence of analog-to-digital conversion. The decision-making module is flexible to be integrated into artificial neural networks and provides a general yet effective solution to enhance performance against device noise.

关键词： neuromorphic computing spintronics magnetic tunnel junction neural networks

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Cellular models of stress resistance may pave ways to fight neurodegenerative diseases

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Neural Regeneration Research 2025年第9期20卷 2579-2580页

作者： Thu Nguyen Minh Pham Christian Behl Institute of Pathobiochemistry University Medical Center of the Johannes Gutenberg UniversityMainzGermany

Alzheimer's disease(AD),the most common form of neurodegeneration,is characterized by selective neuronal vulnerability and brain regionselective neuron *** entorhinal cortex and hippoc,ampal CA1 projection neurons are at greater risk in AD whereas other regions display resistance to ***,the cerebellum,a phylogenetically very old region,is affected only very late in the disease progression.

关键词： cortex resistance Alzheimer

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Potential role and therapeutic implications of glutathione peroxidase 4 in the treatment of Alzheimer's disease

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Neural Regeneration Research 2025年第3期20卷 613-631页

作者： Yanxin Shen Guimei Zhang Chunxiao Wei Panpan Zhao Yongchun Wang Mingxi Li Li Sun Department of Neurology and Neuroscience center The First Hospital of Jilin UniversityJilin UniversityChangchunJilin ProvinceChina Cognitive Impairment center Department of NeurologyThe First Hospital of Jilin UniversityJilin UniversityChangchunJilin ProvinceChina

Alzheimer's disease is an age-related neurodegenerative disorder with a complex and incompletely understood pathogenesis. Despite extensive research, a cure for Alzheimer's disease has not yet been found. Oxidative stress mediates excessive oxidative responses, and its involvement in Alzheimer's disease pathogenesis as a primary or secondary pathological event is widely accepted. As a member of the selenium-containing antioxidant enzyme family, glutathione peroxidase 4 reduces esterified phospholipid hydroperoxides to maintain cellular redox homeostasis. With the discovery of ferroptosis, the central role of glutathione peroxidase 4 in anti-lipid peroxidation in several diseases, including Alzheimer's disease, has received widespread attention. Increasing evidence suggests that glutathione peroxidase 4 expression is inhibited in the Alzheimer's disease brain, resulting in oxidative stress, inflammation, ferroptosis, and apoptosis, which are closely associated with pathological damage in Alzheimer's disease. Several therapeutic approaches, such as small molecule drugs, natural plant products, and non-pharmacological treatments, ameliorate pathological damage and cognitive function in Alzheimer's disease by promoting glutathione peroxidase 4 expression and enhancing glutathione peroxidase 4 activity. Therefore, glutathione peroxidase 4 upregulation may be a promising strategy for the treatment of Alzheimer's disease. This review provides an overview of the gene structure, biological functions, and regulatory mechanisms of glutathione peroxidase 4, a discussion on the important role of glutathione peroxidase 4 in pathological events closely related to Alzheimer's disease, and a summary of the advances in small-molecule drugs, natural plant products, and non-pharmacological therapies targeting glutathione peroxidase 4 for the treatment of Alzheimer's disease. Most prior studies on this subject used animal models, and relevant clinical studies are lacking. Future clinica

关键词： apoptosis ferroptosis inflammation lipid peroxidation natural plant products neurodegenerative disorder neuroprotection oxidative stress small-molecule drugs

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Boosting cationic and anionic redox activity of Li-rich layered oxide cathodes via Li/Ni disordered regulation

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Journal of Energy Chemistry 2025年第1期100卷 533-543页

作者： Zewen Liu Zhen Wu Hao Wang Xudong Zhang Yuanzhen Chen Yongning Liu Shengwu Guo Shenghua Chen Yanli Nan Yan Liu State Key Laboratory for Mechanical Behavior of Materials Xi'an Jiaotong University School of Materials Science and Engineering Xi'an University of Architecture and Technology Hefei Advanced Computing center Operation Management Corp Ltd Network Information center Xi'an Jiaotong University

Lithium-rich layered oxides （LLOs） are increasingly recognized as promising cathode materials for nextgeneration high-energy-density lithium-ion batteries （LIBs）.However,they suffer from voltage decay and low initial Coulombic efficiency （ICE） due to severe structural degradation caused by irreversible O ***,we introduce a three-in-one strategy of increasing Ni and Mn content,along with Li/Ni disordering and TM–O covalency regulation to boost cationic and anionic redox activity simultaneously and thus enhance the electrochemical activity of *** target material,Li1.2Ni0.168Mn0.558Co0.074O2（L1）,exhibits an improved ICE of 87.2%and specific capacity of 293.2 mA h g-1and minimal voltage decay of less than 0.53 m V cycle-1over 300 cycles at 1C,compared to Li1.2Ni0.13Mn0.54Co0.13O2（Ls）(274.4 mA h g-1for initial capacity,73.8%for ICE and voltage decay of 0.84 mV/cycle over 300 cycles at 1C).Theoretical calculations reveal that the density of states （DOS） area near the Fermi energy level for L1 is larger than that of Ls,indicating higher anionic and cationic redox reactivity than ***,L1 exhibits increased O-vacancy formation energy due to higher Li/Ni disordering of 4.76%（quantified by X-ray diffraction Rietveld refinement） and enhanced TM–O covalency,making lattice O release more difficult and thus improving electrochemical *** increased Li/Ni disordering also leads to more Ni2+presence in the Li layer,which acts as a pillar during Li+de-embedding,improving structural *** research not only presents a viable approach to designing low-Co LLOs with enhanced capacity and ICE but also contributes significantly to the fundamental understanding of structural regulation in high-performance LIB cathodes.

关键词： Ice

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Three-dimensional models:from cell culture to Patient-Derived Organoid and its application to future liposarcoma research

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Oncology Research 2025年第1期33卷 1-13页

作者： SAYUMI TAHARA SYDNEY RENTSCH FERNANDA COSTAS CASAL DE FARIA PATRICIA SARCHET ROMA KARNA FEDERICA CALORE RAPHAEL E.POLLOCK Department of Surgery Division of Surgical OncologyThe James Comprehensive Cancer CenterThe Ohio State University Wexner Medical CenterColumbusOH 43210USA Department of Cancer Biology and Genetics The James Comprehensive Cancer CenterThe Ohio State University Wexner Medical CenterColumbusOH 43210USA

Liposarcoma is one of the most common soft tissue sarcomas,however,its occurrence rate is still rare compared to other *** to its rarity,in vitro experiments are an essential approach to elucidate liposarcoma *** cell culture-based research(2D cell culture)is still playing a pivotal role,while several shortcomings have been recently under *** vivo,mouse models are usually adopted for pre-clinical analyses with expectations to overcome the issues of 2D cell ***,they do not fully recapitulate human dedifferentiated liposarcoma(DDLPS)***,three-dimensional(3D)culture systems have been the recent research focus in the cell biology field with the expectation to overcome at the same time the disadvantages of 2D cell culture and in vivo animal models and fill in the gap between *** the liposarcoma rarity,we believe that 3D cell culture techniques,including 3D cell cultures/co-cultures,and Patient-Derived tumor Organoids(PDOs),represent a promising approach to facilitate liposarcoma investigation and elucidate its molecular mechanisms and effective therapy *** this review,we first provide a general overview of 3D cell cultures compared to 2D cell *** then focus on one of the recent 3D cell culture applications,Patient-Derived Organoids(PDOs),summarizing and discussing several PDO ***,we discuss the current and future applications of PDOs to sarcoma,particularly in the field of liposarcoma.

关键词： Cell culture Liposarcoma Patient-Derived Organoid(PDO) Spheroid Three-dimensional(3D)cell culture

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Effects of P301L-TAU on post-translational modifications of microtubules in human iPSC-derived cortical neurons and TAU transgenic mice

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Neural Regeneration Research 2025年第8期20卷 2348-2360页

作者： Mohamed Aghyad Al Kabbani Christoph Köhler Hans Zempel Institute of Human Genetics Faculty of Medicine and University Hospital CologneUniversity of CologneCologneGermany center for Molecular Medicine Cologne(CMMC) University of CologneCologneGermany center Anatomy Department ⅡMedical FacultyUniversity of CologneCologneGermany

TAU is a microtubule-associated protein that promotes microtubule assembly and stability in the *** is missorted and aggregated in an array of diseases known as *** are essential for neuronal function and regulated via a complex set of post-translational modifications,changes of which affect microtubule stability and dynamics,microtubule interaction with other proteins and cellular structures,and mediate recruitment of microtubule-severing *** impairment of microtubule dynamics causes neuronal dysfunction,we hypothesize cognitive impairment in human disease to be impacted by impairment of microtubule *** therefore aimed to study the effects of a disease-causing mutation of TAU(P301L)on the levels and localization of microtubule post-translational modifications indicative of microtubule stability and dynamics,to assess whether P301L-TAU causes stability-changing modifications to *** investigate TAU localization,phosphorylation,and effects on tubulin post-translational modifications,we expressed wild-type or P301L-TAU in human MAPT-KO induced pluripotent stem cell-derived neurons(i Neurons)and studied TAU in neurons in the hippocampus of mice transgenic for human P301L-TAU(p R5 mice).Human neurons expressing the longest TAU isoform(2N4R)with the P301L mutation showed increased TAU phosphorylation at the AT8,but not the p-Ser-262 epitope,and increased polyglutamylation and acetylation of microtubules compared with endogenous TAU-expressing neurons.P301L-TAU showed pronounced somatodendritic presence,but also successful axonal enrichment and a similar axodendritic distribution comparable to exogenously expressed 2N4R-wildtype-TAU.P301L-TAU-expressing hippocampal neurons in transgenic mice showed prominent missorting and tauopathy-typical AT8-phosphorylation of TAU and increased polyglutamylation,but reduced acetylation,of microtubules compared with non-transgenic *** sum,P301L-TAU results in changes in micr

关键词： human induced pluripotent stem cell microtubules P301L pR5 mice TAU tauopathy tubulin code

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Exploring the role of N-acetyltransferases in diseases:a focus on N-acetyltransferase 9 in neurodegeneration

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Neural Regeneration Research 2025年第10期20卷 2862-2871页

作者： Prajakta Deshpande Anuradha Venkatakrishnan Chimata Amit Singh Department of Biology University of DaytonDaytonOHUSA Premedical Program University of DaytonDaytonOHUSA center for Tissue Regeneration and Engineering at Dayton(TREND) University of DaytonDaytonOHUSA Integrative Science and Engineering center University of DaytonDaytonOHUSA center for Genomic Advocacy(TCGA) Indiana State UniversityTerre HauteINUSA

Acetyltransferases,required to transfer an acetyl group on protein are highly conserved proteins that play a crucial role in development and *** acetylation is a common post-translational modification pivotal to basic cellular *** to 80%-90%of proteins are acetylated during translation,which is an irreversible process that affects protein structure,function,life,and *** this review,we have discussed the various N-acetyltransferases present in humans,their function,and how they might play a role in ***,we have focused on N-acetyltransferase 9 and its role in microtubule *** have shed light on how N-acetyltransferase 9 and acetylation of proteins can potentially play a role in neurodegenerative *** have specifically discussed the N-acetyltransferase 9-acetylation independent function and regulation of c-Jun N-terminal kinase signaling and microtubule stability during development and neurodegeneration.

关键词： acetyl-coenzyme A Alzheimer’s disease animal models cell death drosophila eye human disease c-Jun N-terminal kinase signaling N-Acetyltransferases N-acetyltransferase 9 neurodegeneration

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AZD1775 synergizes with SLC7A11 inhibition to promote ferroptosis

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Science China Life Sciences 2025年第1期68卷 204-218页

作者： Chen Xiong Hong Ling Yingdan Huang Hanzhi Dong Bangxiang Xie Qian Hao Xiang Zhou Fudan university Shanghai Cancer center and Institutes of Biomedical Sciences Fudan University Department of Oncology Shanghai Medical CollegeFudan University Department of Breast Surgery Fudan University Shanghai Cancer CenterFudan University Department of Oncology First Affiliated Hospital of Nanchang University Beijing Institute of Hepatology Beijing Youan HospitalCapital Medical University Beijing Engineering Research center for Precision Medicine and Transformation of Hepatitis and Liver Cancer Key Laboratory of Breast Cancer in Shanghai Fudan University Shanghai Cancer CenterFudan University Shanghai Key Laboratory of Medical Epigenetics International Co-laboratory of Medical Epigenetics and Metabolism (Ministry of Science and Technology)Institutes of Biomedical SciencesFudan University

Tumor suppressor p53-mediated cell cycle arrest and DNA damage repair may exert cytoprotective effects against cancer therapies, including WEE1 inhibition. Considering that p53 activation can also lead to multiple types of cell death, the role of this tumor suppressor in WEE1 inhibitor-based therapies remains disputed. In this study, we reported that nucleolar stress-mediated p53 activation enhanced the WEE1 inhibitor AZD1775-induced ferroptosis to suppress lung cancer growth. Our findings showed that AZD1775 promoted ferroptosis by blocking cystine uptake, an action similar to that of Erastin. Meanwhile, inhibition of WEE1 by the WEE1 inhibitors or si RNAs induced compensatory upregulation of SLC7A11, which conferred resistance to ferroptosis. Mechanistically, AZD1775 prevented the enrichment of H3K9me3, a histone marker of transcriptional repression, on the SLC7A11 promoter by repressing the expression of the histone methyltransferase SETDB1, thereby enhancing NRF2-mediated SLC7A11 transcription. This finding was also validated using the H3K9me3 inhibitor BRD4770. Remarkably, we found that the nucleolar stress-inducing agent Actinomycin D(Act. D) inhibited SLC7A11 expression by activating p53, thus augmenting AZD1775-induced ferroptosis. Moreover, the combination of AZD1775 and Act. D synergistically suppressed wild-type p53-harboring lung cancer cell growth both in vitro and in vivo. Altogether, our study demonstrates that AZD1775 promotes ferroptosis by targeting cystine uptake but also mediates the adaptive activation of SLC7A11 through the WEE1-SETDB1 cascade and NRF2-induced transcription, and inhibition of SLC7A11 by Act. D boosts the anti-tumor efficacy of AZD1775 by enhancing ferroptosis in cancers with wild-type p53.

关键词： p53 NRF2 SLC7A11 WEE1 AZD1775 ferroptosis nucleolar stress

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