Archives of biochemistry and biophysics最新文献

{"title":"New magnetic iron nanoparticle doped with selenium nanoparticles and the mechanisms of their cytoprotective effect on cortical cells under ischemia-like conditions.","authors":"Egor A Turovsky, Egor Y Plotnikov, Alexander V Simakin, Sergey V Gudkov, Elena G Varlamova","doi":"10.1016/j.abb.2024.110241","DOIUrl":"10.1016/j.abb.2024.110241","url":null,"abstract":"<p><p>Ischemic stroke is the cause of high mortality and disability Worldwide. The material costs of stroke treatment and recovery are constantly increasing, making the search for effective and more cost-effective treatment approaches an urgent task for modern biomedicine. In this study, iron nanoparticles doped with selenium nanoparticles, FeNP@SeNPs, which are three-layered structures, were created and characterized using physical methods. Fluorescence microscopy, inhibitor and PCR analyzes were used to determine the signaling pathways involved in the activation of the Ca²⁺ signaling system of cortical astrocytes and the protection of cells from ischemia-like conditions (oxygen-glucose deprivation and reoxygenation). In particular, when using magnetic selenium nanoparticles together with electromagnetic stimulation, an additional pathway for nanoparticle penetration into the cell is activated through the activation of TRPV4 channels and the mechanism of their endocytosis is facilitated. It has been shown that the use of magnetic selenium nanoparticles together with magnetic stimulation represents an advantage over the use of classical selenium nanoparticles, as the effective concentration of nanoparticles can be reduced many times over.</p>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110241"},"PeriodicalIF":3.8,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biochemical and structural insights into pinoresinol hydroxylase from Pseudomonas sp","authors":"Teresa Benedetta Guerriere ,&nbsp;Marco W. Fraaije ,&nbsp;Andrea Mattevi","doi":"10.1016/j.abb.2024.110247","DOIUrl":"10.1016/j.abb.2024.110247","url":null,"abstract":"<div><div>The vanillyl alcohol oxidase/<em>p</em>-cresol methylhydroxylase (VAO/PCMH) flavoprotein family comprises a broad spectrum of enzymes capable of catalyzing the oxidative bioconversions of various substrates. Among them, pinoresinol hydroxylase (PinH) from the 4-alkylphenol oxidizing subgroup initiates the oxidative degradation of (+)-pinoresinol, a lignan important for both lignin structure and plant defense. In this study, we present a detailed biochemical and structural characterization of PinH from <em>Pseudomonas</em> sp., with focus on its substrate specificity and product formation. PinH was expressed in <em>E. coli</em> and purified as FAD-containing, soluble protein. The flavoenzyme catalyzes the hydroxylation of both (+)-pinoresinol and eugenol. Structural analysis reveals its dimeric form, non-covalent flavin binding, and a large active site. AlphaFold models of the PinH-cytochrome complex demonstrate cytochrome's dual role in electron transfer and modulating PinH's conformation. A distinctive feature of PinH is a large cavity that hosts its multi-ring (+)-pinoresinol substrate. The capability of converting bulky lignans is particularly attractive for biotechnological applications aimed at producing high-value compounds from phenolic precursors. These insights expand our knowledge on the structure and mechanism of the VAO/PCMH flavoenzyme family members.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"764 ","pages":"Article 110247"},"PeriodicalIF":3.8,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conservation of mechanism in flavoprotein-catalyzed amine oxidation.","authors":"Paul F Fitzpatrick","doi":"10.1016/j.abb.2024.110242","DOIUrl":"10.1016/j.abb.2024.110242","url":null,"abstract":"<p><p>The goals of this presentation are to summarize the present understanding of the mechanism of amine oxidation by flavoproteins and to examine the possibility that a member of the monoamine oxidase family catalyzes oxidation of a carbon-carbon bond. In the discussion of mechanism, the emphasis is on the protonation state of the amine substrate, since the once-controversial mechanism of oxidation appears to be resolved. The argument will be made that flavoproteins catalyzing amine oxidation preferentially bind the form of the substrate in which the reacting nitrogen is uncharged. The reaction of a member of L-6-hydroxynicotine oxidase, which has been proposed to oxidize a carbon-carbon bond in its substrate during nicotine catabolism, is then discussed. Analysis of the reaction product establishes that the enzyme catalyzes oxidation of a carbon-nitrogen. The effects of site-directed mutagenesis and analysis of the substrate specificity identify the key residues for substrate binding.</p>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110242"},"PeriodicalIF":3.8,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting histidinol-phosphate aminotransferase in Acinetobacter baumannii with salvianolic acid B: A structure-based approach to novel antibacterial strategies","authors":"Anamika Singh,&nbsp;Mansi Tanwar,&nbsp;Tej P. Singh,&nbsp;Sujata Sharma,&nbsp;Pradeep Sharma","doi":"10.1016/j.abb.2024.110233","DOIUrl":"10.1016/j.abb.2024.110233","url":null,"abstract":"<div><div>Undoubtedly, <em>Acinetobacter baumannii</em> is a major ESKAPE pathogen that poses a significant threat to public health, causing severe nosocomial infections with high mortality rates in healthcare settings. Due to the rapid development of antibiotic resistance, only a limited number of antibiotics remain effective against infections caused by multidrug-resistant (MDR) <em>Acinetobacter baumannii</em>. The discovery of new class of antibiotic molecules still lags behind the rate of growing worldwide burden of antimicrobial resistance (AMR). To expedite the discovery of new therapeutic molecules, we have focused on HisC from <em>A. baumannii</em> (<em>Ab</em>HisC), a crucial enzyme involved in the seventh step of histidine biosynthesis. This pathway is absent in humans. We have employed the advanced computational techniques to target this promising drug target. <em>Ab</em>HisC was cloned, overexpressed, and purified. Three distinct sets of libraries containing ∼60,000 natural compounds from ZINC database were screened against <em>Ab</em>HisC using Schrödinger's glide module software. Based on the docking score and glide energy, top 25 hits were further subjected to induced fit (IF) docking. Top four out of the twenty five compounds from IF docking were subjected to 100ns molecular dynamics simulations, and it was observed that salvianolic acid B (SA-B) (a naturally occurring compound) complex with <em>Ab</em>HisC, was found to be extremely stable. The glide energy and docking score of SA-B were −88.59 kcal/mol and −10.4 kcal/mol. SA-B was also found to quench the intrinsic fluorescence of tyrosine indicating its binding to the target. The dissociation constant calculated using Surface Plasmon Resonance was found to be 3.4x10⁻⁹ M. Based on these results we can conclude that SA-B can serve as the potential inhibitor of <em>Ab</em>HisC that can further form the basis of structure based drug design against this deadly pathogen.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"764 ","pages":"Article 110233"},"PeriodicalIF":3.8,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Augmenter of liver regeneration inhibits renal fibrosis during acute kidney injury to chronic kidney disease transition by regulating autophagic flux.","authors":"Chunxia Wang, Xujia Zeng, Pengfei Yang, Gang Wang, Zheng Zhang, Xiaohui Liao","doi":"10.1016/j.abb.2024.110218","DOIUrl":"10.1016/j.abb.2024.110218","url":null,"abstract":"<p><strong>Background: </strong>Augmenter of liver regeneration (ALR) is believed to protect against acute kidney injury (AKI). The objective of this study was to investigate the mechanisms of ALR in the transition from AKI to chronic kidney disease (CKD).</p><p><strong>Methods: </strong>ALR Conditional Knockout (CKO) mice were bilateral renal artery clamped to induce AKI and CKD. Serum creatinine, blood urea nitrogen, and uric acid were measured to reflect renal function. Renal histology was used to assess kidney damage. Transcriptome sequencing and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to identify differentially expressed genes (DEGs) and related pathways. TUNEL assay was conducted to assess apoptosis. Polymerase chain reaction and immunohistology were used to analyze autophagy-related factors and kidney fibrosis. AAV9-mRFP-GFP-LC3 was injected to observe autophagy flux.</p><p><strong>Results: </strong>In the murine models of AKI and CKD, loss of ALR led to markedly reduced renal function and renal tubular pathology injury. Multiple autophagy-related pathways were found to be enriched in up-regulated DEGs in transcriptome sequencing of ALR CKO and control groups with AKI. Renal fibrosis was evident in ALR CKO mice, with marked suppression of Beclin-1, a factor associated with the initiation phase of autophagy, and ATG5, an important factor in the extension phase of autophagosomes. The marked accumulation of LC3 and SQSTM1/P62, which is associated with the formation of autophagosomes, was also observed, suggesting an impairment of autophagic processes. Correspondingly, the AAV9-mRFP-GFP-LC3 results indicated that decreased ALR led to the accumulation of autophagosomes and impaired autophagic lysosome generation.</p><p><strong>Conclusions: </strong>Collectively, these results suggested that ALR deficiency led to apoptosis and enhanced renal fibrosis by impairing autophagic flux, which in turn led to the transition of AKI to CKD.</p>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110218"},"PeriodicalIF":3.8,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of p53 core tetramer stability mediated by multi-interface interactions: A molecular dynamics study","authors":"Han Zhou ,&nbsp;Shiwei Yan","doi":"10.1016/j.abb.2024.110210","DOIUrl":"10.1016/j.abb.2024.110210","url":null,"abstract":"<div><div>p53 is a tumor suppressor protein for impeding cancer development and maintaining genetic integrity. The formation of the p53 core tetramer is regulated by multiple cooperative interaction interfaces. To investigate the internal mechanisms of tetramer stability, we performed all-atom molecular dynamics simulations. Our findings indicate that the symmetric interface maintains highly conserved interactions, while the dimer–dimer interface displays notable flexibility. Additionally, we identified a novel salt bridge at the dimer–dimer interface that significantly contributes to the interaction energy. Moreover, the affinity of p53 for DNA is more than twice that of protein–protein interactions, driven primarily by five key residues that form multiple hydrogen bonds. Through independent simulations of the two dimeric models, we provide a theoretical explanation for why only the symmetric dimeric structure has been observed experimentally. The study identifies key regions and residues that contribute to stability at the inter-molecular interaction interfaces within the p53 tetramer, and highlight the important roles of each contact surface in the formation and stability of the tetramer.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"763 ","pages":"Article 110210"},"PeriodicalIF":3.8,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computational discovery of novel GPX4 inhibitors from herbal sources as potential ferroptosis inducers in cancer therapy","authors":"Mohammad Mahdi Mokhtari Tabar ,&nbsp;Abdolmajid Ghasemian ,&nbsp;Amin Kouhpayeh ,&nbsp;Esmaeil Behmard","doi":"10.1016/j.abb.2024.110231","DOIUrl":"10.1016/j.abb.2024.110231","url":null,"abstract":"<div><div>Ferroptosis, a cell death regulation process dependent on iron levels, represents a promising therapeutic target in cancer treatment. However, the scarcity of potent ferroptosis inducers hinders advancement in this area. This study addresses this gap by screening the PubChem database for compounds with favorable ADMET properties to identify potential GPX4 inhibitors. A structure-based virtual screening was conducted to compare binding affinities of selected compounds to that of RSL3. The candidates—isochondrodendrine, hinokiflavone, irinotecan, and ginkgetin—were further analyzed through molecular dynamics (MD) simulations to assess their stability within the GPX4-ligand complexes. The computed binding free energies for RSL3, isochondrodendrine, hinokiflavone, irinotecan and ginkgetin were −80.12, −107.31, −132.03, and −137.52 and −91.11 kJ/mol, respectively, indicating their significantly higher inhibitory effects compared to RSL3. These findings highlight the potential for developing novel GPX4 inhibitors to promote ferroptosis, warranting further experimental validation.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"764 ","pages":"Article 110231"},"PeriodicalIF":3.8,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clemastine mitigates sepsis-induced acute kidney injury in rats; the role of α-Klotho/TLR-4/MYD-88/NF-κB/ Caspase-3/ p-P38 MAPK signaling pathways","authors":"Mahmoud Abdelnaser ,&nbsp;Mina Ezzat Attya ,&nbsp;Mahmoud A. El-Rehany ,&nbsp;Moustafa Fathy","doi":"10.1016/j.abb.2024.110229","DOIUrl":"10.1016/j.abb.2024.110229","url":null,"abstract":"<div><div>Sepsis is a fatal condition, with an annual incidence of more than 48 million cases as well as 11 million deaths resulting from it. Moreover, sepsis continues to rank as the fifth most prevalent cause of mortality globally. The objective of this study is to investigate if Clemastine (CLM) pretreatment protects against acute kidney injury (AKI) caused by cecal ligation and puncture (CLP) via modulating Toll-like receptor-4 (TLR-4), Myeloid differentiation primary response 88 (MYD-88), nuclear factor kappa B (<em>NF-κB),</em> Bcl-2-associated X (<em>Bax), B-cell lymphoma-2 (Bcl-2), and caspase-3</em> signaling pathways. CLM markedly attenuated sepsis-caused molecular, biochemical, and histopathological alterations. CLM downregulated the levels of the proinflammatory markers, suppressed the expression of cleaved caspase-3, TLR-4 and MYD-88 as well as inactivating NF-κB p-P65 and p-P38 proteins, inhibited <em>Bax, NF-κB,</em> and <em>caspase-3</em> genes expression, and augmented α-Klotho protein expression as well as <em>Bcl-2</em> gene expression. Finally, CLM pretreatment protected against acute kidney injury by preventing TLR-4/p-P38 pathway-mediated apoptotic cell death in rats.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"763 ","pages":"Article 110229"},"PeriodicalIF":3.8,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142745523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling the structural and functional perspectives of a bifunctional α-l-arabinofuranosidase/endo-β-1,4-xylanase (BoGH43_35) from Bacteroides ovatus","authors":"Madhulika Shrivastava,&nbsp;Arun Goyal","doi":"10.1016/j.abb.2024.110232","DOIUrl":"10.1016/j.abb.2024.110232","url":null,"abstract":"<div><div>Arabinoxylan, a complex hemicellulose, can be degraded to its constituent sugars by concerted action of hemicellulases like α-<span>l</span>-arabinofuranosidase, endo-β-1,4-xylanase and xylosidase. In this study, a novel bifunctional α-<span>l</span>-arabinofuranosidase/endo-β-1,4-xylanase (<em>Bo</em>GH43_35) of glycoside hydrolase family 43 subfamily 35 from <em>Bacteroides ovatus</em> was characterized by computational and experimental approaches. Sequence analysis identified Asp34 and Glu251 as the conserved catalytic residues. Structure analysis of <em>Bo</em>GH43_35 disclosed 5-bladed β-propeller fold adopted by the N-terminal GH43 catalytic module followed by two independently folded carbohydrate-binding modules family 6 (CBM6A and CBM6B), displaying jellyroll type β-sandwich fold. Molecular Dynamics simulation of <em>Bo</em>GH43_35 for 200 ns showed RMSD 0.35 nm, confirming structural stability and compactness of modeled structure. Molecular docking of <em>Bo</em>GH43_35 with arabino-xylooligosaccharides and xylooligosaccharides by using AutoDock 4.2.7 demonstrated most favourable binding with arabinose (−5.01 kcal/mol) followed by arabinoxylobiose (−4.35 kcal/mol), xylotriose (−4.65 kcal/mol), xylotetraose (−4.18 kcal/mol) and xylobiose (−3.66 kcal/mol) showing affinity with both types of oligosaccharides. RMSD value of <em>Bo</em>GH43_35-arabinose complex decreased to 0.28 nm upon MD simulation from 0.35 nm for only <em>Bo</em>GH43_35, indicating stability of enzyme-substrate complex throughout the trajectory. The binding analysis of <em>Bo</em>GH43_35 with wheat arabinoxylan by fluorescence spectroscopy gave <em>K</em>_<em>a</em>, 3.1 × 10² M⁻¹, ΔG -14.2 kJ mole⁻¹ and number of binding sites 2.2. Dynamic light scattering of <em>Bo</em>GH43_35 showed hydrodynamic radius (<em>R</em>_<em>h</em>) of 4.0 nm, slightly higher than the radius of gyration (2.69 nm) from MD simulation. Additionally, zeta potential measurements (−9.3 mV at 0.5 mg/mL and −9.4 mV at 1.0 mg/mL) denoted its fair resistance towards aggregation in aqueous solution.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"764 ","pages":"Article 110232"},"PeriodicalIF":3.8,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myrtenol promotes skin flap survival by inhibiting apoptosis and promoting autophagy via the MEK/ERK pathway","authors":"Jialong Yang ,&nbsp;Shenchuyue Ni ,&nbsp;An Wang ,&nbsp;Kaitao Wang ,&nbsp;Jiapeng Deng ,&nbsp;Zijie Li ,&nbsp;Yizhen Cai ,&nbsp;Yiqi Chen ,&nbsp;Guodong Chen ,&nbsp;Dingsheng Lin","doi":"10.1016/j.abb.2024.110230","DOIUrl":"10.1016/j.abb.2024.110230","url":null,"abstract":"<div><div>Skin flaps are often used for repair and reconstruction, including oral cavity and palate. However, postoperative flap necrosis limited applications. Myrtenol, a plant-derived bicyclic monoterpene, has pharmacological effects including inhibiting apoptosis and promoting autophagy. But any impact on skin flaps survival remains unclear. Thus, we established modified McFarlane flaps on 24 Sprague-Dawley rats and applied myrtenol. They were randomly divided into low-dose myrtenol (L-Myr), high-dose myrtenol (H-Myr), inhibitor and control groups. On postoperative day 7, flap survival rate was increased and Laser Doppler images showed blood circulation improvement under myrtenol treatment. Hematoxylin and eosin staining (H&amp;E) results indicated that it increased micro vessel density (MVD) and decreased neutrophil numbers. Besides, kits detection showed that it improved anti-oxidant stress factors activities and reduced pro-oxidant stress factors contents. Moreover, immunofluorescence and Western blot results demonstrated that it upregulated the expression of pro-angiogenic factors, anti-apoptotic proteins, pro-autophagic proteins, mitogen-activated protein kinase 1/2 (MEK1/2) and extracellular signal-regulated kinases 1/2 (ERK1/2) and downregulated the expression of pro-inflammatory cytokines, pro-apoptotic proteins and anti-autophagic proteins. The specific inhibitor U0126 of MEK/ERK pathway partially reversed these effects. Overall, Myrtenol promoted angiogenesis, reduced oxidative stress, ameliorated inflammation, inhibited apoptosis and upregulated autophagy via MEK/ERK pathway to promote flap survival.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"763 ","pages":"Article 110230"},"PeriodicalIF":3.8,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142723765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}