Molecular Biology Reports最新文献

{"title":"RXLR effectors of Phytophthora infestans: delivery, host targets and immune suppression.","authors":"Oshin Saini, Anita Arora, Amrinder Kaur, Shubham Saini","doi":"10.1007/s11033-026-12983-5","DOIUrl":"10.1007/s11033-026-12983-5","url":null,"abstract":"<p><p>Phytophthora infestans, the pathogen responsible for the devastating potato disease known as late blight, poses a significant threat to plant health. A major determinant of its pathogenic success is the deployment of cytoplasmic effector proteins, particularly the RXLR class of effectors, which accumulate within the host cells and manipulate plant immune responses. These effectors function as key virulence factors that interfere with multiple layers of plant defense, including pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). Recent studies have revealed that RXLR effectors target diverse host cellular processes such as transcriptional regulation, post-translational modifications, vesicle trafficking, autophagy, chloroplast-mediated immune signalling, and protein stability. By converging on these critical immune hubs, RXLR effectors reprogram host cellular networks to promote pathogen colonization and disease progression. Advances in genomics, structural biology, and host-interactor screening have significantly expanded our understanding of RXLR effector diversity, their molecular mechanisms, and their interactions with host susceptibility factors. In this review, we synthesize current knowledge on the functional roles of RXLR effectors of P. infestans, highlighting their subcellular localization, host targets, and mechanisms of immune suppression. We also discuss emerging concepts in effector biology and their implications for developing durable resistance strategies against late blight disease.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149238879","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":"GSTP1 promoter hypermethylation in prostate cancer detection: current evidence, clinical positioning, and translational gaps.","authors":"Jun-Lynn Joo, Rebecca Shin-Yee Wong, Bey Hing Goh, Nancy Choon-Si Ng","doi":"10.1007/s11033-026-13011-2","DOIUrl":"10.1007/s11033-026-13011-2","url":null,"abstract":"<p><p>GSTP1 promoter hypermethylation is one of the most consistently documented molecular alterations in prostate cancer, with high prevalence in malignant tissue and a well-established relationship with transcriptional silencing. However, despite more than two decades of biological and diagnostic investigation, GSTP1-based testing has not acquired a clearly defined stand-alone role in contemporary prostate cancer detection. This narrative review examines why extensive biological evidence has not translated into routine clinical use and where, if anywhere, GSTP1 testing might provide meaningful value within current diagnostic pathways. Evidence from prostate tissue, urine and circulating cell-free DNA is considered alongside the effects of biospecimen selection, preanalytical handling, CpG target selection, assay design and interpretation thresholds. Tissue demonstrates the most reproducible signal and has achieved partial clinical translation through multiplex testing such as ConfirmMDx, whereas urinary and blood-based approaches remain investigational. Recent urinary findings, including in men with moderately elevated PSA, are promising but remain preliminary and have not established incremental value beyond contemporary risk assessment, biomarkers and multiparametric MRI. The translational priority is therefore not to demonstrate again that GSTP1 detects prostate cancer, but to determine whether a standardised assay provides reproducible, nonredundant and clinically actionable information at a defined decision point. Future development should prioritise clearly specified target populations, analytically validated assay configurations, clinically significant prostate cancer as the relevant endpoint, and prospective evaluation against contemporary diagnostic pathways.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13687363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149238834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HOTAIR in cancer: a context-dependent regulatory platform linking molecular mechanisms, tumor progression, and clinical translation.","authors":"Qingmiao Shi, Chengran Gao, Chen Xue","doi":"10.1007/s11033-026-12973-7","DOIUrl":"10.1007/s11033-026-12973-7","url":null,"abstract":"<p><p>Long non-coding RNA HOX transcript antisense intergenic RNA (HOTAIR) has emerged as a representative cancer-associated lncRNA with diverse regulatory functions in tumor biology. Initially characterized as an epigenetic scaffold that recruits polycomb repressive complex 2 (PRC2) and lysine-specific demethylase 1 (LSD1), HOTAIR is now recognized as a multifunctional regulatory platform involved in chromatin remodeling, RNA-mediated regulation, metabolic adaptation, cellular plasticity, and therapeutic resistance. Increasing evidence indicates that the biological effects of HOTAIR are highly context dependent and are influenced by tumor lineage, molecular partners, RNA modifications, and cellular environments, challenging the concept of HOTAIR as a universally oncogenic factor. In this review, we summarize recent advances in understanding the molecular architecture and regulatory mechanisms of HOTAIR, including its interactions with chromatin-modifying complexes, RNA-binding proteins, and post-transcriptional regulatory networks. We further discuss the involvement of HOTAIR in cancer progression, emphasizing its roles in tumor adaptation, metastasis, epithelial-mesenchymal transition, metabolic regulation, and resistance to anticancer therapies. We also summarize current approaches for HOTAIR detection and discuss their potential clinical relevance and limitations. Although HOTAIR represents a promising candidate for biomarker development and therapeutic intervention, several challenges remain before clinical translation, including tumor heterogeneity, insufficient clinical validation, delivery limitations of HOTAIR-targeting agents, potential off-target effects, and the need for precise patient selection. Future studies integrating molecular profiling, functional characterization, and clinical evaluation will be essential to determine the translational value of HOTAIR-based strategies. A deeper understanding of HOTAIR as a context-dependent regulatory hub may facilitate the development of more precise approaches for cancer diagnosis and therapy.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149238849","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":"Pathogenesis of steroid refractoriness in acute graft versus host disease.","authors":"Mohammed Debes, Syed Muhammad Ali, Mohamed Abouzeid, Mohamad Aljrad, Amr Elyasaky","doi":"10.1007/s11033-026-12935-z","DOIUrl":"10.1007/s11033-026-12935-z","url":null,"abstract":"<p><p>Allogenic stem cell transplant (SCT) is the only curative option for many haematologic disorders. However, graft versus host disease (GVHD) remains a major limitation. Given its inflammatory nature, systemic steroids are the first line therapy. Nevertheless, steroid refractoriness (SR) is encountered in about 50% of cases and this cohort have dismal outcome. Therefore, understanding steroid actions and potential mechanisms driving SR is of paramount importance to design targeted therapies and improve steroid responsiveness. Steroid actions encompass a cascade of events starting from activation of its canonical receptors GR[Formula: see text] then nuclear translocation followed by activation of its response elements (GRE) until its effect at gene transcription level. This cascade includes several steps that are subject to alteration and interruption by a plethora of factors that would potentially induce SR. SR could be congenital or acquired, generalised or tissue specific, complete or just partial. Acquired SR could be related to downregulation of its canonical receptors, impaired nuclear translocation, impaired GRE binding and efficacy, upregulation of its antagonist isoform GR[Formula: see text] as well as potential gene transcription alterations and epigenetic effects. In addition to potential non-T cell related mechanisms. Therefore, SR in aGVHD is likely a multifactorial and multi-level phenomenon related to interruption of steroid actions at one or more levels. Here, we attempted to examine potential mechanisms driving SR in aGVHD. This would lay the foundation to overcome SR and improve outcome.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149238908","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":"Antifibrotic activity of Schistosoma japonicum-derived sja-miR-2a-3p in carbon tetrachloride-induced liver fibrosis.","authors":"Haoran Zhong, Bowen Dong, Danting Li, Danlin Zhu, Ruiting Zhang, Ke Lu, Hao Li, Zhiqiang Fu, Yamei Jin","doi":"10.1007/s11033-026-12969-3","DOIUrl":"10.1007/s11033-026-12969-3","url":null,"abstract":"<p><strong>Background: </strong>Liver fibrosis is a common consequence of chronic liver injury and is driven largely by persistent activation of hepatic stellate cells and excessive extracellular matrix deposition. We previously identified Schistosoma japonicum-derived sja-miR-2a-3p as a parasite-derived microRNA with antifibrotic activity in schistosomiasis-associated liver fibrosis. Whether this cross-species regulatory molecule also modulates fibrogenesis beyond the context of schistosome infection remains unclear.</p><p><strong>Methods and results: </strong>We investigated the effects of sja-miR-2a-3p in a carbon tetrachloride-induced mouse model of liver fibrosis. Mice received systemic administration of sja-miR-2a-3p agomir during CCL₄-induced fibrogenesis, followed by assessment of histological liver injury, fibrosis, inflammation, HSC activation, HSC-associated apoptotic activity, and transcriptomic alterations. sja-miR-2a-3p agomir administration increased sja-miR-2a-3p abundance in serum and liver tissues and markedly attenuated CCL₄-induced hepatic injury and fibrosis, as evidenced by reduced liver weight index, Ishak fibrosis scores, collagen deposition, and hepatic hydroxyproline content. sja-miR-2a-3p treatment also suppressed HSC activation and extracellular matrix production, with decreased expression of α-SMA, Col1α1, Col3α1, and TGF-β. Moreover, enhanced cleaved caspase-3 signals were observed in desmin-positive HSCs, consistent with increased apoptotic activity in activated HSCs. Hepatic expression of the inflammatory mediators TNF-α, IL-1β, and IL-6 was also reduced. Whole-liver transcriptomic analysis further showed treatment-associated downregulation of extracellular matrix-, cytokine-, chemokine-, NF-κB-, IL-17-, and TNF-related pathways.</p><p><strong>Conclusions: </strong>sja-miR-2a-3p attenuates CCL₄-induced liver fibrosis in mice, accompanied by reduced HSC activation and extracellular matrix accumulation, enhanced HSC-associated apoptotic activity, and attenuation of inflammatory signaling. These findings extend the biological activity of sja-miR-2a-3p from schistosomiasis-associated fibrosis to a chemically induced fibrosis model and support further investigation of helminth-derived regulatory miRNAs as modulators of host fibrotic responses.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149238905","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":"Lactobacillus brevis cell-free supernatant attenuates inflammation-associated gene expression and differentially modulates host defense-associated genes in DSS-stimulated HT-29 cells.","authors":"Alireza Moghanlou, Shima Rasouli, Sheyda Asadi Lanjavani, Sarvenaz Falsafi, Ava Behrouzi","doi":"10.1007/s11033-026-12890-9","DOIUrl":"10.1007/s11033-026-12890-9","url":null,"abstract":"<p><strong>Background: </strong>Dysregulated Toll-like receptor (TLR) signaling in intestinal epithelial cells contributes to persistent mucosal inflammation in inflammatory bowel disease (IBD). Although Lactobacillus brevis has demonstrated anti-inflammatory potential, the transcriptional effects of its secreted metabolites on inflammatory and host defense-associated components of epithelial innate immune signaling remain insufficiently characterized. This study investigated the effects of L. brevis cell-free supernatant (CFS) on TLR-associated gene expression in DSS-stimulated HT-29 cells.</p><p><strong>Methods: </strong>1% DSS stimulated HT-29 human intestinal epithelial cells (inflammatory epithelial model) were treated with 50% L. brevis CFS (48 h) following viability assessment using MTT assay. Transcriptional profiling of 84 key genes involved in the TLR signaling pathway was performed using the RT² Profiler™ PCR Array. Differential gene expression was analyzed using the ΔΔCt method, followed by pathway-level mapping of the MyD88- and TRIF-dependent branches. Raw p-values were adjusted for multiple comparisons using the Benjamini-Hochberg FDR procedure.</p><p><strong>Results: </strong>Treatment with L. brevis CFS was associated with significant downregulation of multiple inflammation-associated genes, including TLR2, TLR4, MYD88, TIRAP, IRAK1, IRAK4, MAP3K7, NFKB1, IL1A, IL1B, IL6, IL12A, CCL2, and PTGS2. Host defense-associated genes exhibited a non-uniform transcriptional response. Components of the TRIF-dependent antiviral axis, including TLR3, TICAM1, TBK1, IRF3, and CXCL10, were downregulated, whereas TLR1, TLR10, TICAM2, and BTK were upregulated, and several other immune-response genes showed no significant change. These findings indicate differential modulation of TLR-associated transcription rather than uniform suppression of all examined immune-related genes.</p><p><strong>Conclusions: </strong>L. brevis CFS attenuated the expression of multiple inflammation-associated genes and differentially modulated host defense-associated genes in DSS-stimulated HT-29 cells. This non-uniform transcriptional pattern indicates selective modulation of the TLR-associated gene network rather than indiscriminate suppression of all examined immune-related genes.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228337","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":"Reply to 'Correspondence to AdipoRon promotes angiogenesis in B-cell leukemia by modulating pro-angiogenic factors through AdipoR1'.","authors":"Marta Mallardo, Rosita Russo, Aurora Daniele, Angela Chambery, Ersilia Nigro","doi":"10.1007/s11033-026-12866-9","DOIUrl":"https://doi.org/10.1007/s11033-026-12866-9","url":null,"abstract":"","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228266","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":"PRKAR2A/RIIα as a candidate spatial cAMP-PKA signal router in triple-negative breast cancer metastasis: evidence boundaries, competing models and decisive experiments.","authors":"Tanzeel Muzaffar, Biswajit Saha","doi":"10.1007/s11033-026-12975-5","DOIUrl":"10.1007/s11033-026-12975-5","url":null,"abstract":"<p><p>Metastatic relapse remains the principal lethal event in triple-negative breast cancer (TNBC), yet the contribution of PRKAR2A, which encodes the type IIα regulatory subunit (RIIα) of protein kinase A (PKA), remains unresolved. RIIα creates a mechanistic duality: it restrains catalytic PKA within the holoenzyme while recruiting type II PKA to A-kinase anchoring protein (AKAP) microdomains. A targeted critical narrative search identified no eligible published study in the searched sources that causally linked PRKAR2A to a TNBC metastasis endpoint. Direct evidence is limited to four association or detection contexts: PRKAR2A mRNA differed at the adjusted-significance boundary between pathological complete response and residual disease but was not retained in the final consensus predictor; its transcript was induced in a lipid-adapted TNBC heterospheroid state without gene-specific perturbation; RIIα was detected in mitochondria-endoplasmic-reticulum contact fractions whose local PKA activity controlled calcium transfer and apoptosis without isolating RIIα; and PRKAR2A entered a multigene prognostic signature without independent or cell-resolved validation. AKAP2 depletion altered focal-adhesion signalling, invasion, primary-tumour growth and lung signal, but neither the operative PKA regulatory subunit nor a burden-independent metastatic effect was established. These boundaries support four competing interpretations: PRKAR2A may be a driver, compensatory brake, localisation determinant or passenger state marker. Decisive tests require inducible depletion, near-endogenous domain-resolved rescue, compartment-targeted PKA reporters, endogenous complex mapping and stage-resolved metastasis assays. Until then, RIIα is best treated as a candidate spatial signal router rather than a validated biomarker or therapeutic target.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228201","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":"The role of the mitochondrial phosphate carrier in modulating mitochondrial homeostasis and enhancing radiosensitivity in tumor cells.","authors":"Lichen Shen, Xinyu Liu, Yijun Lu, Kaiwei Wang, Hongcang Gu, Shuanghu Yuan, Junchao Qian","doi":"10.1007/s11033-026-12779-7","DOIUrl":"10.1007/s11033-026-12779-7","url":null,"abstract":"<p><strong>Background: </strong>The mitochondrial phosphate carrier (PiC) is a key protein in maintaining mitochondrial homeostasis, and its dysfunction is closely associated with cell fate determination. Recent studies suggest that PiC may regulate mitochondrial permeability transition pore (MPTP) opening. However, its precise role during radiotherapy and the mechanisms by which it regulates cell death remain elusive.</p><p><strong>Methods and results: </strong>Focusing on the clinical challenge of radioresistance in glioma, this study reveals for the first time that radiation specifically suppresses PiC expression, thereby inducing mitochondrial energy metabolism failure, collapse of membrane potential, dysregulation of mtDNA replication, and significantly promoting sustained MPTP opening. Further mechanistic investigations demonstrated that this cascade of mitochondrial damage activates the mitochondrial apoptotic pathway involving Bax/Bcl-2, cytochrome c, and caspase-3, ultimately driving apoptosis in glioma cells. Consistently, concordant alterations in apoptotic markers were observed in murine tumor models, further validating these findings in vivo.</p><p><strong>Conclusions: </strong>This study identifies PiC as a critical regulator of the radiotherapy response in glioma, demonstrating for the first time that radiation-induced PiC suppression drives apoptosis via mitochondrial dysfunction and MPTP opening. Targeting the PiC-MPTP axis represents a novel potential strategy for overcoming radioresistance and enhancing radiosensitivity in glioma.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228197","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":"Therapeutic potential of varenicline in neuropsychiatric disorders: insights into its molecular mechanisms.","authors":"Abdolkarim Talebi Taheri, Michael Aschner, Fatemeh Rahmati-Dehkordi, Omid Reza Tamtaji","doi":"10.1007/s11033-026-12921-5","DOIUrl":"10.1007/s11033-026-12921-5","url":null,"abstract":"<p><p>Neuropsychiatric disorders pose significant health challenges. Current drug therapies are often inadequate, highlighting the urgent need for new and effective treatments. The α4β2 nicotinic receptor has been implicated in the pathophysiology of various neuropsychiatric disorders. In this context, varenicline, its selective agonist, has garnered increasing attention for its potential therapeutic effects across a range of neuropsychiatric conditions. Emerging preclinical evidence suggests that varenicline may exert neuroprotective effects through modulation of pathways that include synaptic plasticity and synaptic proteins, neuroinflammation, microglial activation, apoptosis, and autophagy. However, direct target engagement for many of these pathways has not yet been established. In this review, we provide a comprehensive review of the cellular and molecular mechanisms by which varenicline might be expected to exert therapeutic effects in a range of neuropsychiatric disorders. Most previous reviews of varenicline have concentrated on its use as a smoking cessation aid or on its potential to treat individual diseases. The current review takes a different approach, focusing at the molecular level on the various pathways that are affected in different diseases, and discussing within each section the evidence that currently exists in relation to each of these in studies conducted in rodent models and in clinical trials. The review seeks to provide insight into the potential benefits and drawbacks of using a single compound to treat a variety of disorders, and to highlight areas for future research.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228204","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}