Molecular Biology最新文献

{"title":"Exploration of Role of Lycorine against Endometrial Cancer Based on Network Pharmacology, Molecular Docking, and In Vitro Validation","authors":"K. Meng, J. L. Ma, J. S. Li","doi":"10.1134/s0026893325700712","DOIUrl":"https://doi.org/10.1134/s0026893325700712","url":null,"abstract":"Endometrial cancer (EnCa) poses a serious threat to the reproductive health of women worldwide. Lycorine, a natural plant-extract, exerts tumor-suppressive effects towards several cancers, yet its role and related mechanisms in EnCa are largely unknown. The present study first investigated whether lycorine exerts antitumor activity against EnCa cells and then explored the underlying mechanisms. Lycorine reduced viability and clonogenic growth, curtailed migration and invasion, and induced apoptosis in HEC-1-B cells in a concentration-dependent manner, while sparing human endometrial epithelial cells at lower concentrations. To probe the mechanism, we integrated network pharmacology and molecular docking, identifying 90 overlapping lycorine–endometrial cancer targets enriched in PI3K-AKT, NF-κB, mTOR, and NOD-like receptor pathways and predicting favorable binding to three hub proteins (MAPK1, PI3KCA, and CHUK). Consistent with these predictions, lycorine lowered MAPK1, PI3KCA, and CHUK protein levels and dampened downstream signaling. Notably, silencing PI3KCA largely blunted lycorine-induced growth inhibition, apoptosis, and motility changes, indicating that repression of PI3KCA is a key mediator of its effects. Collectively, these findings suggest that lycorine restrains the malignant behaviors of EnCa cells by suppressing PI3KCA-centered signaling and provide a rationale for further validation across additional models and for evaluating rational combinations.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"60 2","pages":"258-268"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147912184","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":"Inhibition of the m6A Reader IGF2BP2 Impairs Cell Cycle Progression and Glycolysis in Ovarian Cancer","authors":"J. Liang, X. Yang, Kaiyuan Ji, G. Zhu, J. Wang, H. Duan, J. Zhou, Zhiqiang Qin","doi":"10.1134/s0026893325700694","DOIUrl":"https://doi.org/10.1134/s0026893325700694","url":null,"abstract":"N6-methyladenosine (m6A) is the most abundant internal RNA modification in eukaryotic mRNAs and plays a crucial role in regulating mRNA stability, translation, and degradation. Dysregulation of m6A regulators has been increasingly implicated in cancer, yet their cell type–specific roles and therapeutic value in ovarian cancer remain clearly unexplored. We conducted an integrative analysis of single-cell and bulk RNA sequencing datasets from ovarian tumors and matched non-malignant tissues to identify m6A regulators associated with tumor progression. Functional experiments, including gene knockdown, flow cytometry, metabolic assays, and RIP-seq analysis, were performed to evaluate the role of candidate regulators. A small-molecule inhibitor of IGF2BP2 (CWI1-2) was also used to assess therapeutic potential in ovarian cancer cell lines. IGF2BP2 was identified as the most significantly upregulated m6A reader in malignant epithelial cells and was associated with poor patient prognosis. Knockdown of IGF2BP2 impaired cell proliferation, induced cell cycle arrest and apoptosis, and suppressed glycolytic activity. RIP-seq data revealed that IGF2BP2 directly binds transcripts of key oncogenes including CDK4, BCL2L2, and SLC2A1, thereby stabilizing their expression. Pharmacological inhibition of IGF2BP2 recapitulated the effects of genetic silencing, confirming its essential role in sustaining oncogenic programs in ovarian cancer cells. Our findings establish IGF2BP2 as a critical m6A reader that post-transcriptionally regulates gene networks driving proliferation, survival, and metabolic reprogramming in ovarian cancer. Targeting IGF2BP2 may represent a promising therapeutic strategy for m6A-based precision oncology in ovarian cancer.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"60 2","pages":"234-246"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147883818","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":"Effect of Berberine on Osteogenic Differentiation of Human Periodontal Ligament Stem Cells in the Inflammatory Microenvironment through Modulation of FOXO1 Phosphorylation","authors":"J. Wang, M. Qin","doi":"10.1134/s0026893325601764","DOIUrl":"https://doi.org/10.1134/s0026893325601764","url":null,"abstract":"The purpose of this study is to explore the effects of berberine (BBR) on osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) in inflammatory environments and the mechanisms involved. hPDLSCs were isolated from human periodontal membrane tissues and identified via flow cytometry detection by evaluating cell surface markers. hPDLSCs were intervened by using different concentrations of BBR, followed by assessing the cell activity for screening the optimal concentration of BBR for subsequent experiments. hPDLSCs cultured with or without osteogenic induction medium were induced by TNF-α and the optimal concentration of BBR, respectively, and the cells were grouped into control, TNF-α, BBR, and TNF-α + BBR groups. Cell proliferation, ALP activity, and osteogenic differentiation were assessed. The expression of RUNX2, OPN, FOXO1, and phosphorylated p-FOXO1 was also evaluated. Compared with the control group, the TNF-α group exhibited decreased cell activity, reduced ALP activity, impaired osteogenic differentiation, downregulated osteogenic proteins RUNX2 and OPN, and increased expression of p-FOXO1/FOXO1. Relative to the TNF-α group, the TNF-α + BBR group indicated increased cell activity, enhanced ALP activity, improved osteogenic differentiation, upregulated RUNX2 and OPN expression, and decreased p-FOXO1/FOXO1 expression. BBR enhances osteogenic differentiation of hPDLSCs in the inflammatory microenvironment via the inhibition of FOXO1 phosphorylation level.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"59 S1","pages":"S170-S178"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147880343","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":"Naringenin Protects MC3T3-E1 Cells from Dexamethasone-Induced Ferroptosis through NRF2 Signaling Pathway","authors":"Guohui Wan, Tao He, Guming Zou, Xing Long","doi":"10.1134/s0026893325700487","DOIUrl":"https://doi.org/10.1134/s0026893325700487","url":null,"abstract":"Ferroptosis is shown to promote osteoblast death and cause bone fracture in osteoporosis. This study aims to explore the role of naringenin in bone development and the underlying molecular mechanism. After treated with dexamethasone, cell proliferation was significantly inhibited in MC3T3-E1 cells. The levels of Fe2+ and ROS were increased when the level of GSH was decreased. The expression levels of GPX4 and SLC7A11, two markers of ferroptosis, were decreased. However, naringenin reduced the levels of Fe2+ and ROS when increased the expression levels of GPX4, SLC7A11, NRF2, HO-1, and Runx2. Furthermore, the ability of cell growth was restored. Conversely, knockdown of NRF2 counteracted the effects of naringenin. In addition, NRF2 was shown to be associated with TFAM based on the String database and knockdown of TFAM increased the levels of Fe2+ and ROS but decreased the level of GSH. Therefore, naringenin exhibited protective role against dexamethasone-induced ferroptosis in MC3T3-E1 cells by inhibiting NRF2 pathway.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"59 6","pages":"1063-1072"},"PeriodicalIF":0.0,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878825","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 Critical Role of m6A-Related HNRNPA1 in Osteoporosis: Modulating Macrophage Polarization via the Glycolytic Pathway","authors":"Xiaoming Liu, Zhelong Liu, Yang Shi","doi":"10.1134/s002689332570044x","DOIUrl":"https://doi.org/10.1134/s002689332570044x","url":null,"abstract":"Abstract Osteoporosis represents a significant public health challenge. Recent studies suggest that macrophage polarization plays a pivotal role in bone homeostasis, with potential modulation by N6-methyladenosine (m6A) modifications. However, the exact mechanisms through which m6A-related genes regulate macrophage polarization and contribute to osteoporosis remain poorly understood. This study aims to explore the involvement of m6A-related genes in osteoporosis, focusing particularly on their effects on macrophage polarization and glycolytic metabolism. Gene expression data related to osteoporosis were retrieved from the GEO database (GSE56816), and differential expression analysis was conducted using the limma package in R. Functional enrichment analysis was performed with clusterProfiler and Metascape, while Weighted Gene Co-expression Network Analysis (WGCNA) was utilized to identify gene modules associated with osteoporosis. The overlap between m6A-related genes, differentially expressed genes (DEGs), and WGCNA-derived genes was examined using Venn diagrams. The role of HNRNPA1 was further investigated both in vitro and in vivo through various techniques, including qRT-PCR, Western blotting, immunofluorescence staining, and ELISA. Differential expression analysis identified 284 key genes linked to osteoporosis. WGCNA clustered these genes into six modules, revealing distinct correlation patterns (positive, negative, or no significant correlation) with osteoporosis. Overexpression of HNRNPA1 was found to upregulate pro-inflammatory cytokines (CXCL9, CXCL10) and glycolytic genes (GLUT1, PFKFB3). In vivo, HNRNPA1 knockdown significantly improved bone metabolic markers in an osteoporosis model, alongside a reduction in the M1 macrophage marker iNOS, an increase in the M2 macrophage marker CD206, and a decrease in the glycolytic gene GLUT1 expression. These results highlight the critical role of HNRNPA1 in regulating macrophage polarization via the glycolytic pathway in the context of osteoporosis. Targeting HNRNPA1 may provide new therapeutic approaches for enhancing bone health and alleviating osteoporosis.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"59 6","pages":"1019-1034"},"PeriodicalIF":0.0,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1134/S002689332570044X.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147914738","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":"Protective Effects of Luteolin in an In Vitro Model of Ethanol-Induced Gastric Epithelial Injury: Insights into ROS Modulation and Inflammatory Response","authors":"Xiong Zhu, Yun Shao, J. P. Wang","doi":"10.1134/s0026893325700426","DOIUrl":"https://doi.org/10.1134/s0026893325700426","url":null,"abstract":"Ethanol-induced gastric injury is a prevalent clinical issue characterized by oxidative stress, inflammation, and apoptosis in gastric epithelial cells. Luteolin, a naturally occurring flavonoid with potent antioxidant and anti-inflammatory properties, has shown promise as a therapeutic agent for managing such damage. This study explores the protective effects of luteolin on ethanol-induced injury in gastric epithelial cells (GES-1) and investigates the underlying mechanisms, with a focus on the Keap1/Nrf2 signaling pathway. Our findings demonstrate that luteolin significantly enhances cell viability, reduces lactate dehydrogenase (LDH) release, and helps maintain mitochondrial membrane potential (MMP) in ethanol-treated cells. Luteolin also mitigates oxidative stress by increasing the activity of antioxidant enzyme activities (CAT, SOD) and glutathione (GSH) levels and decreasing malondialdehyde (MDA) levels. Additionally, it suppresses inflammation by reducing the expression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and inhibits apoptosis by modulating the expression of Bax, caspase-3, and Bcl-2. Mechanistically, luteolin activates the Keap1/Nrf2 signaling pathway, which restores redox balance and reduces inflammation, highlighting its central role in luteolin’s protective effects. These results provide valuable insights into the therapeutic potential of luteolin in addressing alcohol-related gastric injuries and oxidative stress-driven disorders, offering a mechanistic basis for its application in clinical settings.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"59 6","pages":"993-1003"},"PeriodicalIF":0.0,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147919241","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":"USP43 Promotes Colorectal Cancer Progression by Enhancing Wnt/β-catenin Signaling Pathway","authors":"D. Li, Fanghao Yang, Dalong Ma, Wei Li, Hui Zhang, Ruilong Sheng","doi":"10.1134/s0026893325700396","DOIUrl":"https://doi.org/10.1134/s0026893325700396","url":null,"abstract":"Wnt/β-catenin signaling is a cellular signaling pathway that plays a crucial role in various biological processes, including embryonic development, cell differentiation, and tissue homeostasis. And, its imbalance is closely linked to tumorigenesis. Here, we report USP43, a deubiquitinase, as a positive regulator of Wnt/β-catenin signaling. Our study revealed that USP43 directly binds to β-catenin and stabilizes β-catenin through K48-linked deubiquitination, leading to the hyperactivation of downstream Wnt signaling. Functionally, USP43 promotes the migration and growth of colorectal cancer (CRC)and contributes to the survival of murine CRC organoids. These findings provide comprehensive understanding of USP43's impact on the Wnt/β-catenin pathway, offering further insights into colonic epithelial-related diseases.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"59 6","pages":"951-963"},"PeriodicalIF":0.0,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147887731","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":"GSDME-Driven Regulation of Pyroptosis and PD1/PD-L1 Inhibitor Sensitivity in Cervical Cancer","authors":"Hui Wang, Pan Liu, Dilidaer Sidike, Lun Suo, H. Niyazi","doi":"10.1134/s0026893325700475","DOIUrl":"https://doi.org/10.1134/s0026893325700475","url":null,"abstract":"To investigate the role of Gasdermin E (GSDME) and its interaction with the PD1/PD-L1 pathway in the progression of cervical cancer, focusing on apoptosis, migration, and invasion of cancer cells. Primary and metastatic cervical cancer tissues were collected, and histological changes were observed using HE staining. Immunohistochemistry was performed to detect the expression of GSDME. The expression levels of GSDME and Caspase-3 were assessed by RT-qPCR and Western blot. GSDME was knocked down in HeLa cells, and PD1/PD-L1 inhibitors were administered. Caspase-3 expression, cell apoptosis, migration, and invasion abilities were evaluated. Subsequently, HeLa cells were co-cultured with CD8+ T cells, and the effects of GSDME knockdown combined with PD1/PD-L1 inhibitor treatment on Caspase-3 expression and related cellular behaviors were further assessed. Compared to primary cervical cancer tissues, the expression of GSDME and Caspase-3 was significantly lower in metastatic cervical cancer tissues. GSDME knockdown significantly inhibited the expression of Caspase-3 in HeLa cells, reduced cell apoptosis, and enhanced cell migration and invasion abilities. PD1/PD-L1 inhibitor treatment significantly upregulated the expression of GSDME and Caspase-3, promoted cell apoptosis, and inhibited cell migration and invasion, reversing the inhibition of apoptosis caused by GSDME knockdown. After co-culturing with CD8+ T cells and PD1/PD-L1 inhibitor treatment, GSDME expression and cell apoptosis significantly increased, while migration and invasion significantly decreased. Levels of perforin, granzyme B, and IFN-γ were significantly elevated. GSDME knockdown weakened the therapeutic effects of CD8+ T cells and PD1/PD-L1 inhibitors. GSDME plays a pivotal role in regulating apoptosis, migration, and invasion in cervical cancer, particularly in the context of the PD1/PD-L1 pathway. Targeting GSDME and PD1/PD-L1 interactions may offer a novel therapeutic strategy for metastatic cervical cancer.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"59 6","pages":"1043-1054"},"PeriodicalIF":0.0,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147906300","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":"Chrysin Boosts the Cell Death and Anticancer Actions of Doxorubicin by Stimulating the TRPM2 Channel in Glioblastoma Cells","authors":"Yener Yazğan, Kenan Yıldızhan","doi":"10.1134/s0026893325600710","DOIUrl":"https://doi.org/10.1134/s0026893325600710","url":null,"abstract":"The prognosis for glioblastoma multiforme (GBM), the adult brain and spinal cord tumour with the poorest prognosis, has not improved enough with current therapies. Investigating potential molecular routes of tumour growth and metastasis and novel therapeutic methods are, therefore, obviously necessary. Although some natural substances have been shown to increase intracellular Ca2+ concentration and ROS generation by activating TRPM2 channel and potentiate the anticancer effects of doxorubicin (DOX), and chrysin (CHR) has been shown to enhance the anticancer effect of DOX, its anticancer effect through TRPM2-mediated Ca2+ homeostasis and ROS generation in glioblastoma tumour cells (DBTRG) has not been investigated. This work aimed to clarify the molecular processes behind the synergistic chemotherapeutic action of DOX and CHR in DBTRG cells. For this purpose, we investigated the stimulatory role of CHR on DOX-induced cell death via TRPM2 channel activation in DBTRG cells. DOX treatment caused cell cytotoxicity, increased apoptosis (caspase 3 and 9), ROS, lipid peroxidation levels, and decreased cell viability and antioxidant levels. The combination of CHR and DOX made the treatment even more effective. The effects in cells were reduced with treatments with 2APB, a TRPM2 antagonist. In conclusion, the increase in ROS and cell death levels mediated by TRPM2 activation in DOX-induced DBTRG cells was further enhanced by CHR treatment. The combination of CHR and DOX can be used as a successful agent in the treatment of glioblastoma tumours.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"59 5","pages":"784-794"},"PeriodicalIF":0.0,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147330647","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":"OLR1 Knockdown Mitigates Traumatic-Hemorrhagic Shock-Induced Liver Injury by Inhibiting the TLR4/MYD88 Pathway and NLRP3 Inflammasome Activation","authors":"Hongwei Yao, Ningchao Wang, Z. Huan, Ji‐Hye Han, Mei Zhao, X. Ge","doi":"10.1134/s0026893325600539","DOIUrl":"https://doi.org/10.1134/s0026893325600539","url":null,"abstract":"Traumatic-hemorrhagic shock (T/HS) is a critical condition characterized by massive hemorrhage, hypovolemia, tissue hypoxia, and the progression to multi-organ dysfunction syndrome (MODS). To investigate the role of oxidized low-density lipoprotein receptor 1 (OLR1) in T/HS-induced liver injury, male Sprague-Dawley (SD) rats were utilized to establish a resuscitation after hemorrhagic shock (HS/R) model through controlled bloodletting and mean arterial pressure (MAP) monitoring. Immunohistochemical (IHC) staining revealed a significant upregulation of hepatic OLR1 expression following HS/R. Interfering with OLR1 significantly improved coagulation parameters, as evidenced by shortened thrombin time (TT), prothrombin time (PT), and activated partial thromboplastin time (APTT), along with reduced plasma thrombin-antithrombin (TAT) complex levels. Hematoxylin-eosin (HE) staining revealed extensive hepatocellular necrosis following HS/R, which was significantly alleviated by OLR1 knockdown. Biochemical analysis demonstrated reduced serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and pro-inflammatory cytokines (IL-1β and IL-18), highlighting the protective effect of OLR1 inhibition on liver function. Mechanistic studies revealed that OLR1 mediated HS/R-induced liver injury through the activation of the toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88) pathway and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediated pyroptosis, both of which were suppressed by OLR1 knockdown. These findings were corroborated in vitro using BRL-3A cells. In conclusion, OLR1 mediated HS/R-induced liver injury by regulating the TLR4/MyD88/NF-κB pathway and pyroptosis. Targeting OLR1 could offer a potential therapeutic strategy to mitigate liver damage, correct coagulation abnormalities, and improve outcomes in T/HS.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"59 5","pages":"772-783"},"PeriodicalIF":0.0,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147898873","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}