Biochimica et biophysica acta. Molecular cell research最新文献

{"title":"Browning of inguinal white adipose tissue by the novel lignan (-)-secoisolariciresinol 4-O-methyl ether attenuates diet-induced obesity through mitochondrial and Peroxisomal activation.","authors":"Wenjun Jiao, Woo Yong Park, Yong-Il Kim, Jin-Hyung Kim, Beomsu Kim, Gahee Song, Ja Yeon Park, Se Jin Jung, Hyun Jeong Kwak, Seong-Kyu Choe, Jong-Hyun Lee, Jae-Young Um","doi":"10.1016/j.bbamcr.2025.119952","DOIUrl":"https://doi.org/10.1016/j.bbamcr.2025.119952","url":null,"abstract":"<p><p>Studies indicate that the induction and activation of brown and beige adipocytes, which can enhance energy expenditure, may be beneficial for managing obesity and its associated diseases. This study investigated whether a novel lignan (-)-secoisolariciresinol 4-O-methyl ether (S4M) obtained from arctigenin inhibited diet-induced obesity by the browning of white adipose tissue (WAT). S4M treatment inhibited adipogenesis and lipid accumulation in white-induced 3 T3-L1 adipocytes and in zebrafish embryonic development. Moreover, S4M treatment promoted browning in white adipocytes by increasing TOM20, UCP1, and PGC1α protein levels and consequently upregulating the mitochondrial content. S4M treatment significantly promoted mitochondrial fission by increasing the expression of DRP1. Furthermore, it enhanced peroxisome biogenesis and function by inducing PEX13, ACOX1, and catalase. Mdivi-1, a mitochondrial dynamics inhibitor, diminished the browning effect of white adipocytes by the S4M treatment. This study found that S4M treatment inhibited weight gain in high-fat diet-induced obese mice, decreased the weight of WAT, and increased the abundance and function of mitochondria and peroxisomes in inguinal WAT, suggesting that S4M treatment could increase energy expenditure. The results suggest that S4M has potential as a therapeutic agent for combating obesity and its associated metabolic disorders.</p>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":" ","pages":"119952"},"PeriodicalIF":4.6,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation and signaling characteristics of the hydroxy-carboxylic acid 3 receptor identified in human neutrophils through a microfluidic flow cell technique.","authors":"Huamei Forsman, Wenyan Li, Neele K Levin, Roger Karlsson, Anders Karlsson, Claes Dahlgren, Martina Sundqvist","doi":"10.1016/j.bbamcr.2025.119950","DOIUrl":"https://doi.org/10.1016/j.bbamcr.2025.119950","url":null,"abstract":"<p><p>Human neutrophils express numerous G protein-coupled receptors (GPCRs) of importance for immune regulation. However, several functionally characterized neutrophil GPCRs, are not included within the human neutrophil proteome. To identify GPCRs not previously demonstrated to be expressed in human neutrophils, we utilized a microfluidic flow cell technique in conjunction with subcellular granule fractionation and liquid chromatography-tandem mass spectrometry (LC-MS/MS). This approach led to the identification of hydroxy-carboxylic acid 3 receptor (HCA₃R, also known as GPR109B) as a novel component of the human neutrophil proteome. The β-oxidation intermediate 3-hydroxy-octanoic acid (3-OH-C8) is the primary endogenous agonist HCA₃R and expressed at high levels in adipocytes where it exerts anti-lipolytic effects. However, literature describing the role and function of HCA₃R in human neutrophils is scarce. We show that 3-OH-C8, as well as the synthetic HCA₃R agonist IBC 293, activate human neutrophils determined as an increase in the intracellular concentration of free calcium ions ([Ca²⁺]_i) and activation of the NADPH oxidase. However, in contrast to the rise in [Ca²⁺]_i, which could be triggered in naïve neutrophils, pre-treatment of neutrophils was required for the HCA₃R agonists to activate the NADPH oxidase. That is, the HCA₃R-mediated NADPH oxidase activation occurred only in neutrophils pre-treated with either an actin cytoskeleton disrupter or an allosteric modulator targeting the GPCR termed free fatty acid receptor 2 (FFA2R). Our findings demonstrate that HCA₃R is not only a new member of the human neutrophil proteome but also exhibits functional activity with complex signaling pathways when stimulated with endogenous and synthetic HCA₃R agonists.</p>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":" ","pages":"119950"},"PeriodicalIF":4.6,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced store operated calcium entry contributes to autophagy mediated escape of prostate cancer to oxaliplatin treatment.","authors":"Dheeraj Kannancheri Puthooru, Maya Yassine, Dmitri Gordienko, Nathalie Ziental-Gelus, Emilie Desruelles, Valerio Farfariello, Loïc Lemonnier, Natalia Prevarskaya","doi":"10.1016/j.bbamcr.2025.119953","DOIUrl":"https://doi.org/10.1016/j.bbamcr.2025.119953","url":null,"abstract":"<p><p>Oxaliplatin, a third-generation platinum-based chemotherapeutic drug, induces cell cycle arrest and apoptosis in prostate cancer treatment. However, both intrinsic and acquired resistance mechanisms limit its therapeutic efficacy. Notably, chemotherapeutic agents often induce autophagy-a cellular recycling process-that can contribute to drug resistance. Calcium (Ca²⁺) signalling plays a pivotal role in regulating cell fate. However, the involvement of Ca²⁺ and Ca²⁺ channels in oxaliplatin resistance within prostate cancer cells remains controversial and poorly understood. In this study, we demonstrate that oxaliplatin treatment enhances autophagy in prostate cancer cells. Concurrently, oxaliplatin modulates the expression of key proteins involved in store-operated calcium entry (SOCE): it upregulates Orai3 channels while downregulating Orai1 and Stim1. These alterations result in diminished SOCE activity, contributing to an apoptosis-resistant phenotype. Importantly, we found that targeting Orai3 expression and inhibiting autophagy sensitizes prostate cancer cells to oxaliplatin-induced apoptosis. Our findings suggest that combining Orai3 downregulation with autophagy inhibition may enhance the efficacy of oxaliplatin in treating prostate cancer. This combinatorial approach could hold potential for overcoming resistance and improving therapeutic outcomes.</p>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":" ","pages":"119953"},"PeriodicalIF":4.6,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apurinic/apyrimidinic endonuclease 1 (APE1) prevents alopecia by promoting regeneration of hair follicles.","authors":"Han Gao, Zhaoqian Dang, Lin'ang Wang, Chaofan Li, Xueling Tong, He Xiao, Xunjie Kuang, Lin Cao, Yuxin Yang, Lei Zhang, Yi Cheng, Tianyi Chen, Xiao Yang, Mengxia Li","doi":"10.1016/j.bbamcr.2025.119951","DOIUrl":"https://doi.org/10.1016/j.bbamcr.2025.119951","url":null,"abstract":"<p><p>Hair follicle (HF) regeneration, which relies on the self-renewal and differentiation capacity of bulge cells, involves multiple molecular mechanisms. In this study, we found that Apurinic/apyrimidinic endonuclease 1 (APE1) acts as a positive regulator of spontaneous and depilation-induced HF regeneration. Loss of APE1 leads to hair thinning and delayed HF transition from telogen to anagen. As shown in our systematic conditional Apex1 knockout (Apex1^flox/floxCre-ER⁺) mouse model, Apex1^-/- mice gradually lost hair coat over time and eventually became hairless after 10 months. Histological analyses revealed that Apex1 knockout caused the retarded growth of HF and the reduction of hair density, as a result of repressed proliferation of bulge cells by downregulating the β-catenin pathway. Moreover, APE1 is indispensable in the depilation-induced HF regeneration, and its deficiency contributes to the depletion of bulge cells, which in turn causes failure of hair growth. These findings highlight the indispensable role of APE1 for HF activation, maintenance, and growth.</p>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":" ","pages":"119951"},"PeriodicalIF":4.6,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"VRK2 kinase pathogenic pathways in cancer and neurological diseases","authors":"Pedro A. Lazo","doi":"10.1016/j.bbamcr.2025.119949","DOIUrl":"10.1016/j.bbamcr.2025.119949","url":null,"abstract":"<div><div>The VRK2 ser-thr kinase, belonging to the dark kinome, is implicated in the pathogenesis of cancer progression, neurological and psychiatric diseases. The <em>VRK2</em> gene codes for two isoforms. The main isoform (VRK2A) is mainly located in the cytoplasm, and anchored to different types of membranes, such as the endoplasmic reticulum, mitochondria and nuclear envelope. The VRK2A isoform interacts with signaling modules assembled on scaffold proteins such as JIP1 or KSR1, forming stable complexes and blocking the activation of regulatory signaling pathways by altering their intracellular localization and the balance among them. VRK2 regulates apoptosis, nuclear membrane organization, immune responses, and Cajal bodies. Wild-type VRK2 is overexpressed in tumors and contributes to cancer development. In cells and tumors with low levels of nuclear VRK1, <em>VRK2</em> generates by alternative splicing a shorter isoform (VRK2B) that lacks the C-terminal hydrophobic tail and permits its relocation to nuclei. Furthermore, rare <em>VRK2</em> gene variants are associated with different neurological or psychiatric diseases such as schizophrenia, epilepsy, bipolar disorder, depression, autism, circadian clock alterations and insomnia, but their pathogenic mechanism is unknown. These diseases are a likely consequence of an altered balance among different signaling pathways that are regulated by VRK2.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 5","pages":"Article 119949"},"PeriodicalIF":4.6,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143783137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The multifaceted role of Sestrin 3 (SESN3) in oxidative stress, inflammation and tumorigenesis","authors":"Qiusan Chen ,&nbsp;Guoqiang Zhong ,&nbsp;Xianmei Fang ,&nbsp;Chuangzhen Lin ,&nbsp;Shanping Wang ,&nbsp;Mingsong Li","doi":"10.1016/j.bbamcr.2025.119938","DOIUrl":"10.1016/j.bbamcr.2025.119938","url":null,"abstract":"<div><div>The pathogenesis of inflammation and tumors is a focal point of scientific inquiry, with oxidative stress often serving as the primary initiator. Within the human genome, the SESN3 gene encodes the SESN3 protein, a crucial antioxidant stress protein. Acting as a regulatory factor, SESN3 intricately modulates cellular oxidative stress, actively participating in cellular protection and repair mechanisms. Its functions span antioxidative, anti-aging, and anti-tumor properties. The expression of SESN3 is closely linked to cellular and oxidative stress, metabolic status, and specific signaling pathways. This review aims to delve into the origins and functions of SESN3, its role within signaling pathways, and its contributions to inflammation and tumorigenesis.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 5","pages":"Article 119938"},"PeriodicalIF":4.6,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143767511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beneficial effects of Glc-1,6-P2 modulation on mutant phosphomannomutase-2","authors":"Maria Monticelli ,&nbsp;Debora Paris ,&nbsp;Maria Chiara Monti ,&nbsp;Elva Morretta ,&nbsp;Zuzana Pakanova ,&nbsp;Marek Nemcovic ,&nbsp;Rebeka Kodrikova ,&nbsp;Maria Vittoria Cubellis ,&nbsp;Giuseppina Andreotti","doi":"10.1016/j.bbamcr.2025.119948","DOIUrl":"10.1016/j.bbamcr.2025.119948","url":null,"abstract":"<div><div>The metabolite Glucose-1,6-bisphosphate (Glc-1,6-P₂) plays a vital role in human metabolism, and is a crucial activator and stabilizer for phosphomannomutase-2 (PMM2) - mutations within this protein propagate the most common congenital disorder of glycosylation (PMM2-CDG). <em>In vivo</em>, Glc-1,6-P₂ is hydrolysed by phosphomannomutase-1 (PMM1), predominantly in the brain, under the influence of inosine monophosphate (IMP). In the present study, we employed knock-out <em>PMM1</em> in ^{Arg141His/Phe119Leu}PMM2 patient-derived fibroblasts and investigated the phenotypic improvement. Increased Glc-1,6-P₂ was associated with glycosylation enhancement, confirmed by glycan profiling. Previously identified PMM2-CDG biomarkers, such as LAMP1, PTX3 and lysosomal enzymes showed empirical imrovement- these findings were corroborated by metabolomic and proteomic analysis. Moreover, our results support the potential of Glc-1,6-P₂ modulation for PMM2-CDG, potentiating novel perspectives in drug discovery.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 5","pages":"Article 119948"},"PeriodicalIF":4.6,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143760950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of non-muscle myosin II Zipper leads to apoptosis-induced compensatory proliferation in Drosophila","authors":"Dipti Verma,&nbsp;Bappi Sarkar,&nbsp;Jyoti Singh,&nbsp;Ankita Singh,&nbsp;Mousumi Mutsuddi,&nbsp;Ashim Mukherjee","doi":"10.1016/j.bbamcr.2025.119939","DOIUrl":"10.1016/j.bbamcr.2025.119939","url":null,"abstract":"<div><div><em>Drosophila</em> Non-muscle myosin II Zipper (Zip) belongs to a functionally divergent class of molecular motors that play a vital role in various cellular processes including cell adhesion, cell migration, cell protrusion, and maintenance of polarity via its cross-linking property with actin. To further determine its role in cell proliferation and apoptosis, we carried out Zip loss of function studies that led to compromised epithelial integrity in <em>Drosophila</em> wing imaginal discs as evident from the perturbed expression pattern of cell-cell junction proteins Cadherin, Actin, and Armadillo. Disruption of these adhesion proteins resulted in the cells undergoing apoptosis as evident from the increased level of effector caspase, cDcp-1. The induction of cell death due to the loss of function of Zip was accompanied by proliferation as apparent from increased PH3 staining. The control of apoptosis-induced compensatory proliferation lies under the caspase cascade. We carried out experiments that suggested that the apical caspase Dronc is responsible for the apoptosis-induced compensatory proliferation due to the loss of Zip function and not the effector caspase Drice/Dcp-1. Further, it was observed that Dronc leads to the subsequent activation of Jun N-terminal kinase pathway (JNK) pathway and Wingless (Wg) mitogen that diffuse to the neighboring cells and prompt them to undergo cell division. Taken together, our results suggest that loss of function of Zip leads to apoptosis-induced compensatory proliferation.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 5","pages":"Article 119939"},"PeriodicalIF":4.6,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A dynamin-like protein in Plasmodium falciparum plays an essential role in parasite growth, mitochondrial development and homeostasis during asexual blood stages","authors":"Vandana Thakur ,&nbsp;Md. Muzahidul Islam ,&nbsp;Shweta Singh ,&nbsp;Sumit Rathore ,&nbsp;Azhar Muneer ,&nbsp;Gaurav Dutta ,&nbsp;Mudassir M. Banday ,&nbsp;Priya Arora ,&nbsp;Mohammad E. Hossain ,&nbsp;Shaifali Jain ,&nbsp;Shakir Ali ,&nbsp;Asif Mohmmed","doi":"10.1016/j.bbamcr.2025.119940","DOIUrl":"10.1016/j.bbamcr.2025.119940","url":null,"abstract":"<div><div>Malaria parasites harbour a single mitochondrion, and its proper segregation during parasite multiplication is crucial for the propagation of the parasite within the host. Mitochondrial division machinery consists of several proteins that associate with the mitochondrial membrane during segregation. Here, we have identified a dynamin-like protein in <em>P. falciparum</em>, <em>Pf</em>Dyn2, and deciphered its role in mitochondrial growth and homeostasis. A GFP targeting approach combined with high-resolution microscopy studies showed that the <em>Pf</em>Dyn2 associates with the mitochondrial membrane at specific sites during mitochondrial division. The C-terminal degradation tag mediated inducible knock-down (iKD) of <em>Pf</em>Dyn2 significantly inhibited parasite growth. <em>Pf</em>Dyn2-iKD hindered mitochondrial development and functioning, decreased mtDNA replication, and induced mitochondrial oxidative stress, ultimately causing parasite death. Regulated overexpression of a phosphorylation mutant of <em>Pf</em>Dyn2 (Ser-612-Ala) did not affect the recruitment of <em>Pf</em>Dyn2 on the mitochondria; normal mitochondrial division and parasite growth showed that phosphorylation/dephosphorylation of this conserved serine residue (Ser612) may not be responsible for regulating recruitment of <em>Pf</em>Dyn2 to the mitochondrion. Overall, we show the essential role of <em>Pf</em>Dyn2 in mitochondrial development and maintaining its homeostasis during the asexual cycle of the parasite.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 5","pages":"Article 119940"},"PeriodicalIF":4.6,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of CDC45 mutations on DNA replication and genome stability.","authors":"Milena Denkiewicz-Kruk, Deepali Chaudhry, Alina Krasilia, Malgorzata Jedrychowska, Iwona J Fijalkowska, Michal Dmowski","doi":"10.1016/j.bbamcr.2025.119936","DOIUrl":"https://doi.org/10.1016/j.bbamcr.2025.119936","url":null,"abstract":"<p><p>Cdc45 is a non-catalytic subunit of the CMG helicase complex that is recruited to the autonomously replicating sequence at the onset of DNA replication. The Cdc45 protein is required for the initiation of DNA replication as well as for nascent DNA strand synthesis. It interacts with Mcm2 and Psf1 elements of CMG helicase, as well as with Sld3, an initiation factor, and Pol2, the catalytic subunit of DNA polymerase epsilon (Pol ε). In this study, we analyzed the effects of amino acid substitutions in the Cdc45 region involved in the interaction of this protein with Mcm2-7 (Cdc45-1), Psf1 (Cdc45-26), and Sld3 (Cdc45-25, Cdc45-35). We found that mutations in CDC45 resulted in defective DNA replication. Under permissive conditions, delayed DNA synthesis was observed. At restrictive temperatures, the mutant cells were unable to efficiently replicate DNA. However, after the initiation of DNA replication under permissive conditions, the four analyzed CDC45 mutants exhibited DNA synthesis under the restrictive conditions. Moreover, we observed increased mutation rates, mainly dependent on DNA polymerase zeta (Pol ζ), as well as increased incidence of replication errors. These findings confirm the essential function of Cdc45 in DNA replication initiation and demonstrate that impaired Cdc45 subunit has an impact on the fidelity of the nascent DNA strand synthesis. The changes in cell function observed in this study, related to defects in Cdc45 function, may help understand some diseases associated with CDC45.</p>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":" ","pages":"119936"},"PeriodicalIF":4.6,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143727932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}