Biochemistry (Moscow)最新文献

{"title":"MAPK/ERK Signaling Pathway in Schizophrenia: Expression Levels of Regulatory Proteins in Peripheral Blood Mononuclear Cells","authors":"Anastasiia S. Boiko,&nbsp;Ivan S. Kopnov,&nbsp;Elena V. Epimakhova,&nbsp;Elena G. Kornetova,&nbsp;Svetlana A. Ivanova","doi":"10.1134/S0006297925603466","DOIUrl":"10.1134/S0006297925603466","url":null,"abstract":"<p>Schizophrenia is a severe mental disorder whose molecular mechanisms remain poorly understood. Investigating brain-derived neurotrophic factor (BDNF)-dependent signaling pathways and their contribution to schizophrenia pathogenesis is a promising research direction in schizophrenia research. BDNF activates multiple intracellular cascades, among which the MAPK/ERK pathway plays a central role. In this study, expression levels of key regulatory proteins of the MAPK/ERK signaling pathway (ERK1/2, STAT3, STAT5, NF-κB, IGF1R, IRS1, IR, TSC2, and CREB1) were examined in lysates of peripheral blood mononuclear cells (PBMCs) from schizophrenia patients using multiplex analysis. The study group included 58 patients diagnosed with schizophrenia (F20); the control group included 60 healthy individuals. The results revealed significantly increased expression of ERK1/2 and STAT3, along with decreased NF-κB levels, in PBMCs from schizophrenia patients compared to controls. Moreover, patients with leading positive symptoms exhibited elevated expression of CREB1 and ERK1/2. These findings suggest that dysregulation of the MAPK/ERK signaling may play a significant role in the pathogenesis schizophrenia. BDNF-dependent signaling pathways may therefore represent promising targets for diagnostics and therapy of this disorder.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 2","pages":"299 - 308"},"PeriodicalIF":2.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147441588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Teichuronic Acid-Like Polymer in the Cell Wall of Rathayibacter sp. VKM Ac-2856 – A New Type of Acidic Glycopolymer for Representatives of the Genus","authors":"Maksim S. Kokoulin,&nbsp;Natalia V. Potekhina,&nbsp;Elena M. Tulskaya,&nbsp;Yury V. Ospennikov,&nbsp;Lyudmila I. Evtushenko","doi":"10.1134/S0006297925604186","DOIUrl":"10.1134/S0006297925604186","url":null,"abstract":"<p>Using chemical methods and methods of NMR spectroscopy, the structures of three cell wall glycopolymers of <i>Rathayibacter</i> sp. VKM Ac-2856 (family Microbacteriaceae, class Actinomycetes), isolated from <i>Brachypodium distachyon</i> (family Poaceae), were determined. The first polymer, an unsubstituted mannan with a repeating unit, →2)-α-<span>d</span>-Man<i>p</i>-(1→, was discovered in the cell walls of <i>Rathayibacter</i> for the first time. The second, a rhamnomannan, consists of regularly alternating residues of α-<span>d</span>-rhamnose and α-<span>d</span>-mannose and has non-stoichiometric substitution with β-<span>d</span>-Xyl<i>p</i> residues in a 3 : 1 ratio, →2)-α-<span>d</span>-Rha<i>p</i>-(1→3)-[β-<span>d</span>-Xyl<i>p</i>-(1→2)]-α-<span>d</span>-Man<i>p</i>-(1→. The third, a minor, teichuronic acid-like polymer with a trisaccharide repeating unit and <i>R</i>-pyruvic acid, bears side residues of β-<span>d</span>-glucuronic acid, →3)-α-<span>d</span>-[4,6-<i>R</i>-Pyr]-Gal<i>p</i>-(1→3)-β-<span>d</span>-Glc<i>p</i>-(1→6)-[β-<span>d</span>-Glc<i>p</i>A-(1→3)]-α-<span>d</span>-Man<i>p</i>-(1→. The latter distinguishes this polymer from teichuronic acids, which contain uronic acid residues in the main chain. Structure of the teichuronic acid-like polymer is novel for both <i>Rathayibacter</i> and prokaryotes in general. The results of this study demonstrate structural diversity of microbial glycopolymers and are consistent with the previously reported data on the species-specific composition of glycopolymers in the representatives of the genus <i>Rathayibacter</i>.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 2","pages":"369 - 379"},"PeriodicalIF":2.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147441674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CYP9E Expression and Repertoire in Lasius Ants: Making the Ecological Connection","authors":"Svetlana S. Zhukova,&nbsp;Vitaly D. Djabrailov,&nbsp;Mikhail Belenky,&nbsp;Victoria A. Scobeyeva","doi":"10.1134/S0006297926600146","DOIUrl":"10.1134/S0006297926600146","url":null,"abstract":"<p>Ecological adaptations of a species can be shaped by its repertoire of gene variants. The black garden ant <i>Lasius niger</i> shows high level of <i>CYP9E</i> duplication. In contrast to its congener, the jet ant <i>L. fuliginosus</i>, it exhibits tolerance toward fungus-infected aphids. In these two species, we compared expression of a subset of <i>CYP9E</i> genes, potentially involved in mycotoxin metabolism. No significant differences in expression were found. Similarly to <i>L. niger</i>, the jet ant has six copies of these genes, grouping pairwise on the phylogenetic tree with their <i>L. niger</i> counterparts. Beyond the gene subset targeted in the expression study, we found multiple <i>CYP9E</i> genes in the genomes of <i>L. niger</i>, <i>L. fuliginosus</i>, and – fewer by a third – in the outgroup <i>Formica rufa</i>, suggesting <i>CYP9E</i> amplification as an ancestral trait of the genus Lasius or a more basal clade.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 2","pages":"216 - 229"},"PeriodicalIF":2.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147441549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beta-Amyloid Suppresses Mitochondrial ATP Production in Human Neuroblastoma Cells","authors":"Yuliya A. Zagryadskaya,&nbsp;Semen V. Nesterov,&nbsp;Vladimir A. Mitkevich,&nbsp;Sergey A. Kozin,&nbsp;Anastasia K. Kryuchkova,&nbsp;Galina Yu. Lomakina,&nbsp;Mikhail S. Karbyshev,&nbsp;Eduard V. Bocharov,&nbsp;Alexander A. Makarov,&nbsp;Ivan S. Okhrimenko","doi":"10.1134/S0006297925602060","DOIUrl":"10.1134/S0006297925602060","url":null,"abstract":"<p>β-Amyloid peptides (Aβ), which play a crucial role in the pathogenesis of Alzheimer’s disease by forming toxic oligomeric species, are known to affect mitochondrial function. In this study, luciferin-luciferase assay was used to assess changes in ATP production by mitochondria isolated from human neuroblastoma SH-SY5Y cells cultured in the presence of monomeric Aβ at a nanomolar concentration. ATP synthesis rates were measured in the presence of substrates specific for respiratory chain complexes I, II, and IV alongside inhibitors targeting the other complexes. Aβ significantly reduced both the rate of ATP generation and amount of ATP synthesized by mitochondria. This effect of Aβ on ATP synthesis did not result from a direct influence on the respiratory chain complexes I, II, and IV. Our findings provide insights into possible causes of mitochondrial dysfunction in neurons in Alzheimer’s disease.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 2","pages":"230 - 244"},"PeriodicalIF":2.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147441570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antiviral and Mutagenic Effects of APOBEC Deaminases A3C, A3D, and A3H in a Hepatitis B Virus Model","authors":"Ivan V. Karandashov,&nbsp;Sergey A. Brezgin,&nbsp;Natalia I. Ponomareva,&nbsp;Andrey S. Tikhonov,&nbsp;Vladimir P. Chulanov,&nbsp;Dmitry S. Kostyushev,&nbsp;Anastasiya P. Kostyusheva","doi":"10.1134/S0006297925603326","DOIUrl":"10.1134/S0006297925603326","url":null,"abstract":"<p>Hepatitis B virus (HBV) infects human hepatocytes, causing acute or chronic liver infection. Chronic HBV infection leads to progressive liver damage, potentially resulting in cirrhosis or hepatocellular carcinoma. One promising antiviral strategy involves activating cytidine deaminases of the APOBEC/AID family, which could induce mutational degradation of HBV. Using a CRISPRa-based transcriptional activation system with modified sgRNAs, we investigated antiviral and oncogenic effects of the activating genes encoding APOBEC3C, APOBEC3D, and APOBEC3H.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 2","pages":"289 - 298"},"PeriodicalIF":2.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147441572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Features of Mitochondrial Dynamics Changes in Large Pyramidal Neurons of the Human Motor Cortex during Aging","authors":"Tatiana I. Baranich,&nbsp;Dmitry N. Voronkov,&nbsp;Kseniia M. Okulova,&nbsp;Ekaterina V. Shcherbak,&nbsp;Anna V. Egorova,&nbsp;Olga V. Velts,&nbsp;Maria S. Ryabova,&nbsp;Kristina A. Skvortsova,&nbsp;Zainab M. Omarova,&nbsp;Dmitry A. Kharlamov,&nbsp;Valeria V. Glinkina,&nbsp;Vladimir S. Sukhorukov","doi":"10.1134/S0006297925604447","DOIUrl":"10.1134/S0006297925604447","url":null,"abstract":"<p>Brain aging is a physiological process characterized by various neurodegenerative manifestations, largely driven by mitochondrial dysfunctions, including changes in mitochondrial metabolism and dynamics. Conflicting reports in the literature regarding mitochondrial fusion and fission in the human cerebral cortex during aging underscore the need to elucidate the mechanisms of this dysfunction. The aim of this study was to assess features of mitochondrial dynamics in the large pyramidal neurons of the human motor cortex during aging. The study was conducted on autopsy material from the motor cortex of individuals aged 75 years and older. The control group consisted of similar material from individuals aged 35-44 years who died from sudden cardiac death. Intensity of immunohistochemical staining for TOMM20, Drp1, Mfn1, Mfn2, and Opa1 proteins in the large pyramidal neurons of the human motor cortex was evaluated. Decrease in the staining intensity of TOMM20 and Opa1 markers and increase in the staining intensity of the Drp1 marker were observed, indicating enhanced mitochondrial fragmentation in the pyramidal neurons of layer V of the motor cortex, possibly associated with reduction in the mitochondrial pool volume due to dysfunction in the mitochondrial fusion process, which impedes organelle growth.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 2","pages":"380 - 387"},"PeriodicalIF":2.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147441587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urban Dust Nanoparticles Induce Proinflammatory Activation of Human Bronchial Epithelial Cells","authors":"Anna A. Dashkevich,&nbsp;Lyudmila A. Zinovkina,&nbsp;Alexander I. Ivaneev,&nbsp;Mikhail S. Ermolin,&nbsp;Petr S. Fedotov,&nbsp;Boris V. Chernyak,&nbsp;Roman A. Zinovkin","doi":"10.1134/S0006297925602448","DOIUrl":"10.1134/S0006297925602448","url":null,"abstract":"<p>Air pollution remains a major environmental challenge, largely driven by urban dust composed of suspended solid particles of diverse origins and chemical compositions. Particulate matter (PM_2.5) and ultrafine urban dust nanoparticles (NPs), with diameters smaller than 2.5 μm and 100 nm, respectively, pose a particular threat to human health. In this study, we present the first evidence that NPs induce pro-inflammatory activation of human bronchial epithelial cells. Exposure to non-cytotoxic concentrations of NPs led to a significant increase in the mRNA levels of pro-inflammatory markers IL-8, IL-1β, IL-6, and ICAM-1, accompanied by increased secretion of the cytokines IL-8 and IL-6. Heat treatment of NPs, which removed their organic components, completely abolished their ability to stimulate cytokine secretion. NP-induced upregulation of pro-inflammatory gene expression depended on both surface-adsorbed organic compounds and inorganic particle constituents.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 2","pages":"245 - 252"},"PeriodicalIF":2.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147441571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Specific Features of Epithelial-Mesenchymal Transition Induced by Driver Mutations in the PI3K/AKT Signaling Pathway in Breast Epithelial Cells","authors":"Ali Dayoub,&nbsp;Anna O. Zholudeva,&nbsp;Artem I. Fokin,&nbsp;Alla S. Ilnitskaya,&nbsp;Maria E. Lomakina,&nbsp;Alexis M. Gautreau,&nbsp;Antonina Yu. Alexandrova","doi":"10.1134/S0006297925603570","DOIUrl":"10.1134/S0006297925603570","url":null,"abstract":"<p>The PI3K/AKT signaling pathway is one of the most critical intracellular pathways, regulating cell proliferation, survival, and migration. Mutations in PI3K/AKT pathway components are frequently associated with progression and metastasis of malignant tumors. The initial stage of metastasis is epithelial-mesenchymal transition (EMT), during which tumor cells acquire the migratory capacity. The data on the impact of PI3K/AKT driver mutations on tumor cell motility are contradictory. We investigated EMT and changes in the motility of breast epithelial cells carrying four driver mutations commonly identified in malignant tumors and affecting different components of the PI3K/AKT pathway. Analysis of cell motility, expression of EMT markers, and morphology of adherens junctions (AJs) revealed that all these mutations induced partial EMT, as E-cadherin expression was preserved in all studied cell lines and cells maintained AJs. Analysis of EMT types induced by different mutations revealed that the increased cell motility did not correlate with the degree of EMT progression toward the mesenchymal phenotype. The greatest increase in the cell migratory capacity was observed for cells carrying the <i>PIK3CA</i> H1047R mutation, which induced the most pronounced mesenchymal phenotype, as well as for <i>PTEN–/–</i> cells, which retained the most epithelial phenotype. Our analysis showed that mutations indirectly affecting the MAPK/ERK pathway and promoting ERK activation have the greatest impact on EMT and cell motility.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 2","pages":"332 - 344"},"PeriodicalIF":2.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147441573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Postprandial Response of Skeletal Muscle Phosphoproteome in Type 2 Diabetes Is Comparable to That in Healthy Individuals","authors":"Elmira I. Yakupova,&nbsp;Nikita V. Podkuychenko,&nbsp;Igor P. Smirnov,&nbsp;Viktor G. Zgoda,&nbsp;Nikita E. Vavilov,&nbsp;Egor M. Lednev,&nbsp;Tatiana F. Vepkhvadze,&nbsp;Alina O. Tomilova,&nbsp;Marina V. Shestakova,&nbsp;Alexander V. Vorotnikov,&nbsp;Daniil V. Popov","doi":"10.1134/S0006297925603855","DOIUrl":"10.1134/S0006297925603855","url":null,"abstract":"<p>Decreased insulin-mediated glucose uptake by skeletal muscle, which accounts for one-third of total body mass, plays a crucial role in the development of type 2 diabetes (T2D). However, the molecular mechanisms underlying this disorder remain poorly understood. In contrast to previous studies examining changes in phosphorylation of individual sites or global phosphoproteome profile of human skeletal muscle in response to insulin (euglycemic-hyperinsulinemic clamp test), the present study is the first to investigate changes in skeletal muscle signaling in response to a mixed meal normalized to body mass (a model of physiological postprandial response). Using mass spectrometry-based phosphoproteomics, postprandial changes across 4205 phosphorylation sites in 1208 proteins/protein groups were analyzed in healthy individuals (<i>n</i> = 8) and patients with obesity and T2D (<i>n</i> = 8) and key kinases associated with these changes were identified. Food intake altered phosphorylation levels of 70 sites in healthy individuals and 36 sites in patients. However, postprandial phosphorylation of canonical insulin cascade proteins was comparable between the groups, which might be attributed to significantly elevated postprandial blood insulin levels in the patients caused by a reduced insulin-dependent glucose uptake by tissues and a greater food intake compared to healthy individuals. Only healthy individuals exhibited changes in postprandial phosphorylation levels of several proteins regulating the translocation and/or exposure of GLUT4-containing vesicles (SRBS1, CIP4/2, ABI1, SVIL, CPZIP, PLEC, and COBL), suggesting that impaired insulin-dependent glucose uptake in skeletal muscle in patients with obesity and T2D is primarily due to impaired regulation of GLUT4-containing vesicles trafficking.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 2","pages":"345 - 357"},"PeriodicalIF":2.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147441641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biochemical Rationale for the Development of a Rapid Spectrophotometric Assay for Diagnosis of Mineral Homeostasis Disorders in Patients with Cardiovascular Disease","authors":"Daria K. Shishkova,&nbsp;Anastasia I. Lazebnaya,&nbsp;Egor A. Kondratiev,&nbsp;Alexey A. Isametov,&nbsp;Victoria E. Markova,&nbsp;Leo A. Bogdanov,&nbsp;Arina E. Tyurina,&nbsp;Vera G. Matveeva,&nbsp;Anton G. Kutikhin","doi":"10.1134/S000629792560351X","DOIUrl":"10.1134/S000629792560351X","url":null,"abstract":"<p>Patients with coronary and cerebral atherosclerosis are characterized by increased levels of total serum calcium, ionized calcium, and phosphate, against a background of reduced levels of total serum protein and albumin. Here we aimed to develop a rapid diagnostic assay for mineral homeostasis disorders, based on assessing capacity of the acidic plasma proteins to bind excess calcium and phosphate ions. Plasma from bony fish, amphibians, reptiles, birds, mice, and patients with myocardial infarction was incubated with excess concentrations of calcium and phosphate at 37°C for varying time periods. The following assay readouts were defined: (i) plasma optical density after supersaturation with calcium and phosphate ions, reflecting excessive formation of calciprotein particles (CPPs); and (ii) CPP concentration in plasma. CPPs were formed in all vertebrates. The most pronounced plasma calcification propensity was observed in the human and mouse plasma, suggesting an evolutionary significance of CPP formation as a mechanism for clearance of excess circulating calcium and phosphate ions in mammals. Among the 11 protocols of supersaturation with calcium and phosphate ions, stable increase in plasma optical density at 620 nm wavelength (normalized OD₆₂₀, a measure of plasma calcification propensity) was achieved by adding solutions of CaCl₂ (+2 mmol/L, +50 µL), Na₂HPO₄∙12H₂O (+2 mmol/L, +50 µL), and NaCl (+15.4 mmol/L, +20 µL) to plasma (80 µL). Increase in the normalized OD₆₂₀ was consistently detected within 10 min from the reaction onset during incubation in a microplate shaker (37°C), with mild-to-moderate variability across the parallel or sequential measurements and between the different operators. These results support relevance of validating the developed diagnostic assay for assessing mineral homeostasis disorders in the expanded cohorts of patients with myocardial infarction and ischemic stroke.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 2","pages":"309 - 331"},"PeriodicalIF":2.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147441569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}