Molecular Biology Reports最新文献

{"title":"Dexpanthenol reduces IL 6 and VEGF gene expression in a rat model of acetic acid induced ulcerative colitis.","authors":"Mina Shahrooei, Kaveh Rahimi, Masoumeh Ezzati Givi, Annahita Rezaie","doi":"10.1007/s11033-026-11890-z","DOIUrl":"https://doi.org/10.1007/s11033-026-11890-z","url":null,"abstract":"<p><strong>Background: </strong>Ulcerative colitis is a chronic inflammatory bowel disease characterized by inflammation of the colonic mucosa. This study aimed to evaluate the effects of dexpanthenol in an acetic acid-induced model of colitis in rats.</p><p><strong>Methods: </strong>Thirty-two adult male Wistar rats were randomly assigned to four groups: Control (intracolonic saline), dexpanthenol, acetic acid (A.A; 4% acetic acid-induced colitis), and treatment (A.A + dexpanthenol 500). Colitis was induced by intracolonic administration of 4% acetic acid. After 7 days, macroscopic and histopathological evaluations of the colon were performed. The mRNA expression levels of IL-6 and VEGF were assessed using real-time PCR. Stool consistency, colon length, and colon weight-to-length ratio were also measured.</p><p><strong>Results: </strong>Dexpanthenol administration significantly ameliorated acetic acid-induced colitis. The A.A + dexpanthenol group showed partial restoration of colon length, improved stool consistency, and a reduced colon weight-to-length ratio compared with the A.A group. Histopathological analysis demonstrated reduced mucosal damage and decreased inflammatory cell infiltration in dexpanthenol-treated rats. In addition, dexpanthenol significantly decreased IL-6 and VEGF mRNA expression compared with the A.A group (P < 0.0001).</p><p><strong>Conclusion: </strong>Dexpanthenol exerts protective effects against experimental ulcerative colitis in rats by attenuating inflammation, improving tissue integrity, and downregulating IL-6 and VEGF gene expression. These findings suggest its potential as a supportive therapeutic agent in ulcerative colitis.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840202","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 protein prenylation in kidney diseases: Molecular basis and therapeutic implications.","authors":"Rohan Bhadange, Anil Bhanudas Gaikwad","doi":"10.1007/s11033-026-11812-z","DOIUrl":"https://doi.org/10.1007/s11033-026-11812-z","url":null,"abstract":"<p><p>Kidney diseases may lead to a life-threatening condition, with their global prevalence increasing day by day. The progressive nature of kidney diseases is driven by a complex interplay of cellular and molecular events, among which protein prenylation plays a pivotal role. Protein prenylation, a lipid-mediated post-translational modification, is essential for the functional regulation of small guanosine triphosphatase binding proteins, including Ras, Rac, Rab, and Rho, which govern cell signaling, proliferation, and membrane dynamics. Aberrant prenylation disrupts these signaling cascades, contributing to podocyte injury, mitochondrial dysfunction, oxidative stress, and renal fibrosis, among others. This review provides an integrated overview of recent advancements in protein prenylation, the effects of these modifications on renal physiology, emerging insights into how altered prenylation drives kidney disease progression and identifies therapeutic strategies targeting this modification. Moreover, we emphasized the potential pharmacological interventions, including bisphosphonates, statins, and others, providing multitargeted therapeutic benefits in various forms of kidney diseases. This review underscores the translational potential of modulating protein prenylation as a novel therapeutic strategy for the management of kidney diseases and for improving clinical outcomes.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147817656","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":"Research progress on active components from natural medicines inhibiting tumor via epigenetic regulation.","authors":"Xiao Han, Zhongtian Yang, Xiaoman Chen, Caiyan Liu, Guixiang Pan","doi":"10.1007/s11033-026-11882-z","DOIUrl":"https://doi.org/10.1007/s11033-026-11882-z","url":null,"abstract":"<p><p>Tumor is a major disease that seriously threatens human health, and its occurrence and progression involve complex interactions between the genome, epigenome, and environmental factors. Epigenetic modifications-such as DNA methylation, histone modifications, non-coding RNA regulation, and mRNA modifications-play key roles in tumor progression, metastasis, and drug resistance. Natural medicines offer multi-target and holistic regulatory effects, showing unique advantages in cancer therapy. Emerging evidence suggests that natural medicines and its active components can exert anti-tumor activities by modulating epigenetic mechanisms. This review summarizes natural medicines-mediated epigenetic regulation against tumors. It details how natural medicines influences DNA methylation by suppressing DNA methyltransferases (DNMTs) and altering tumor suppressor gene promoter methylation. The modulation of histone modifications through targeting histone deacetylases (HDACs), histone lysine methyltransferases (HKMTs), and histone lysine demethylases (HKDMs) is also discussed. Furthermore, the review covers natural medicines's regulation of non-coding RNAs (e.g., lncRNAs, miRNAs, circRNAs) and their downstream pathways, as well as its role in mRNA modifications, notably N6-methyladenosine (m6A). Overall, this work highlights the epigenetic potential of natural medicines in tumor therapy, enhancing the mechanistic understanding of its anti-tumor effects and supporting natural medicines modernization and precision oncology. However, challenges remain due to natural medicines complexity and tumor epigenetic heterogeneity, calling for deeper investigation and clinical validation.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147817689","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":"Astragalus polysaccharide accelerates wound healing by targeting the miR-92a/FGF2 axis in dermal fibroblasts.","authors":"Zexing Tang, Kang Han, Shisong Sang, Shusen Tan, Haitao Meng, Yan Liang, Donghui Bian","doi":"10.1007/s11033-026-11857-0","DOIUrl":"https://doi.org/10.1007/s11033-026-11857-0","url":null,"abstract":"<p><strong>Objective: </strong>Wound healing requires fibroblast activation, including proliferation, migration, and extracellular matrix (ECM) remodeling. Astragalus polysaccharides (APs), derived from Astragalus membranaceus, have been reported to promote tissue repair, but the underlying mechanisms remain unclear. This study examined whether APs facilitate wound healing through the miR-92a/FGF2 axis.</p><p><strong>Methods: </strong>Human foreskin fibroblasts (HFF-1) were incubated with APs, and proliferation, migration, FGF2, and miR-92a expression were evaluated. Functional assays involved miR-92a overexpression or inhibition. A full-thickness skin defect rat model was utilized to assess wound closure and molecular changes following AP treatment with or without miR-92a agomir.</p><p><strong>Results: </strong>APs enhanced fibroblast proliferation and migration, increased FGF2 expression, and suppressed miR-92a levels. miR-92a directly targeted FGF2, thereby inhibiting fibroblast activity. Overexpression of miR-92a weakened the pro-healing effects of APs, whereas inhibition restored them. In rats, APs accelerated wound closure and elevated FGF2 expression, while miR-92a agomir impaired repair and reduced FGF2 expression.</p><p><strong>Conclusion: </strong>APs promote cutaneous wound repair by modulating the miR-92a/FGF2 axis, with miR-92a acting as a negative regulator. Targeting this pathway may strengthen the therapeutic potential of APs in skin regeneration.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147817703","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":"Epigenetic regulation of hyaluronan degradation and melanogenesis by Kawarayomogin I and II from Artemisia capillaris via miR-486-5p and miR-141-3p.","authors":"Kazal Boron Biswas, Satoshi Nakagawa, Kotaro Sakamoto","doi":"10.1007/s11033-026-11887-8","DOIUrl":"https://doi.org/10.1007/s11033-026-11887-8","url":null,"abstract":"<p><strong>Background: </strong>We previously demonstrated that Artemisia capillaris flower extract (ACFE) suppresses the expression of HYBID (hyaluronan-binding protein involved in hyaluronan depolymerization), a hyaluronan-degrading enzyme, and increases the expression of miR-486-5p, a microRNA that downregulates HYBID. In the same study, we isolated two novel active compounds, Kawarayomogin I and II, and reported that they also suppress HYBID expression. However, it remained unclear whether their inhibitory effects on HYBID were mediated through miR-486-5p. Furthermore, because ACFE has been reported to inhibit melanin production, and miR-141-3p and miR-200a-3p are known to regulate melanogenesis, we investigated whether these compounds modulate melanogenesis-related microRNAs.</p><p><strong>Methods and results: </strong>The expressions levels of miR-486-5p in normal human dermal fibroblasts (NHDF) and miR-141-3p and miR-200a-3p in mouse B16 melanocytes were measured by RT-PCR. Melanin content was quantified by lysing the cells using NaOH followed by taking of absorbance at 420 nm. We confirmed for the first time that Kawarayomogin I and II significantly increased the expression of miR-486-5p in NHDF. Among miR-141-3p and miR-200a-3p, ACFE and Kawarayomogin I and II selectively induced miR-141-3p in B16. These findings identify Kawarayomogin I and II as the principal active components responsible for the melanin-suppressing activity of ACFE for the first time. Although these compounds may influence other microRNAs, our results suggest that they selectively regulate miR-486-5p and miR-141-3p, indicating an epigenetic mechanism underlying their biological effects.</p><p><strong>Conclusions: </strong>Collectively, Kawarayomogin I and II represent promising bioactive molecules that selectively and epigenetically regulate microRNA expression to confer dual functions in hyaluronan protection and melanogenesis suppression.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147817621","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":"Miniaturization of CRISPRa plasmids for efficient delivery into renal epithelial cells and Pkd1 transactivation.","authors":"Anubhav Chakraborty, Alan S L Yu","doi":"10.1007/s11033-026-11872-1","DOIUrl":"https://doi.org/10.1007/s11033-026-11872-1","url":null,"abstract":"<p><strong>Background: </strong>Autosomal Dominant Polycystic Kidney Disease is caused by loss-of-function mutations in PKD1 or PKD2 genes, leading to reduced polycystin protein levels. Increasing PKD1 expression via CRISPR activation (CRISPRa) represents a promising therapeutic strategy; however, delivery of large CRISPRa plasmids into renal epithelial cells, and particularly primary cells, remains inefficient due to size-related barriers. We aimed to enable Pkd1 transactivation by miniaturizing CRISPRa plasmids into ~ 6 kb vectors using a one-pot method to enhance cellular uptake in mouse kidney epithelial cells.</p><p><strong>Methods and results: </strong>Using type IIS restriction enzymes, we excised the mammalian expression cassette from full-length large 9-11 kB plasmids. The excised cassette was engineered to have complimentary overhangs. Thermocycling with T4 DNA ligase promoted circularization of the excised cassette (forming ~ 6kB mini-CRISPRa vectors), and T5 exonuclease digestion removed residual backbone fragments. These mini vectors substantially enhanced nucleofection efficiency from 16.10% ± 0.53 to 54.17% ± 2.10 in Pkd1^RC/- cells, and from 10.14% ± 1.40 to 31.27% ± 0.12 in primary Pkd1^RC/Cond; Pkhd1^Cre+ cells. Functionally, the mini-CRISPRa plasmid (mdCas9-VPR) with Pkd1-targeting sgRNAs induced robust endogenous Pkd1 upregulation compared with non-targeting controls: a 4.1-fold increase in Pkd1^RC/- cells (p < 0.001) and a 2.9-fold increase in primary cells (p < 0.001). Full-length plasmids produced no significant activation in either cell type.</p><p><strong>Conclusions: </strong>Miniaturization of CRISPRa vectors with this one-pot approach overcomes delivery limitations in hard-to-transfect renal epithelial cells and enables efficient, functional Pkd1 activation, in vitro.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147816681","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":"Emerging roles for SNRPB2 in governing the cell cycle and steering tumor immune modulation in breast cancer.","authors":"Jiazhennan Zhang, Hu Wang, Yizhen Jia, Adalaiti Yasheng, Xiaoye Ai, Xiuli Wang","doi":"10.1007/s11033-026-11874-z","DOIUrl":"10.1007/s11033-026-11874-z","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer is a common malignant tumor with limited treatment options and poor prognosis. SNRPB2, a core spliceosomal component involved in pre-mRNA splicing, is dysregulated in multiple cancers, but its role in breast cancer remains incompletely understood.</p><p><strong>Methods and results: </strong>We analyzed SNRPB2 expression in breast cancer using TCGA, CPTAC, and HPA databases, and assessed its prognostic value via Kaplan-Meier plotter. The biological function of SNRPB2 was evaluated through in vitro cell line assay, and the underlying molecular mechanisms were determined via RNA-seq, RT-qPCR, and additional GEO datasets. Our findings demonstrated that SNRPB2 was significantly overexpressed in breast cancer tissues and correlated with malignant progression and poor prognosis. Knockdown of SNRPB2 induced G2/M cell cycle arrest in cancer cells, decreased expression of numerous genes related to cell cycle and immune modulation, and triggered alterations in multiple alternative splicing events. Mechanistically, SNRPB2 knockdown might promote cancer cell cycle arrest by regulating HMGA2 splicing and expression, while simultaneously suppressing the expression of immune-related genes such as CSF1, CSF1R, IL6, and CX3CL1. Immune infiltration analysis revealed that SNRPB2 expression correlated with increased infiltration of activated inflammatory cells and myeloid-derived suppressor cells.</p><p><strong>Conclusions: </strong>SNRPB2 potentially plays a dual role in promoting breast cancer progression and shaping the immunosuppressive microenvironment, partly through HMGA2 splicing modulation and immune-regulatory gene suppression. These findings suggest that SNRPB2 may represent a promising therapeutic target for breast cancer.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147817667","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":"SPP1 integrates trophoblast-endothelial crosstalk via the αVβ3-PI3K/Akt-MMP-9 axis to govern vascular remodeling in preeclampsia.","authors":"Xuyuan Ma, Hongfang Kong, Fang Wang, Yuan Su, Yaqing Chang, Hong Xin","doi":"10.1007/s11033-026-11867-y","DOIUrl":"10.1007/s11033-026-11867-y","url":null,"abstract":"<p><strong>Background: </strong>Preeclampsia (PE) is a major hypertensive disorder of pregnancy rooted in defective placental vascular remodeling. Osteopontin (SPP1) is implicated in placental development, but its role in orchestrating the critical paracrine dialogue between trophoblasts and endothelial cells remains undefined.</p><p><strong>Methods: </strong>Placental SPP1 expression and microvessel density (MVD) were analyzed in PE and control pregnancies. An in vitro hypoxia-reoxygenation (H/R) model with SPP1 manipulation in HTR-8/SVneo trophoblasts was used to assess cell functions. Trophoblast-endothelial communication was evaluated via a Transwell co-culture system with HUVECs. Key signaling (integrin αVβ3-PI3K/Akt/FAK) and the MMP-9/TIMP-1 balance were examined. Serum SPP1, sFlt-1, and PlGF were measured. In vivo, we established an N-nitro-L-arginine methyl ester (L-NAME)-induced PE rat model, and evaluated the therapeutic effect of recombinant SPP1 supplementation on PE-like phenotypes, placental vascular remodeling and the underlying signaling changes.</p><p><strong>Results: </strong>SPP1 was downregulated in PE placentas and positively correlated with MVD. H/R reduced SPP1 secretion, impairing trophoblast invasion/proliferation and suppressing endothelial tube formation via paracrine signaling. Mechanistically, trophoblast-derived SPP1 promoted angiogenesis by activating endothelial integrin αVβ3-PI3K/Akt/FAK signaling and restoring the MMP-9/TIMP-1 balance. Downregulated SPP1 disrupts EVT-endothelial paracrine signaling required for spiral artery‑like remodeling. In vivo, SPP1 supplementation ameliorated PE phenotypes, restored placental vascular density, and reversed signaling defects in a rat model. Clinically, serum SPP1 levels were reduced in PE and inversely correlated with the sFlt-1/PlGF ratio and disease severity, highlighting its predictive value.</p><p><strong>Conclusion: </strong>SPP1 is a central paracrine mediator of trophoblast-endothelial crosstalk, and its hypoxia-induced reduced expression drives vascular dysfunction in PE via the integrin αVβ3-PI3K/Akt-MMP-9/TIMP-1 axis. Our findings nominate SPP1 as both a promising biomarker and a potential therapeutic target for PE.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13132967/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776265","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":"Recent advances in miRNAs mediated agronomical advantageous traits improvement in rice.","authors":"Tilak Chandra, Saurabh Gangola, Sarika Jaiswal, Mir Asif Iquebal","doi":"10.1007/s11033-026-11884-x","DOIUrl":"https://doi.org/10.1007/s11033-026-11884-x","url":null,"abstract":"<p><p>A central enigma in crop improvement lies in introducing beneficial traits without fitness trade-offs. Rice, the cornerstone of global food security, demands multifaceted genetic innovation to sustain yield, quality, and resilience in the face of mounting climatic constraints. With the global population projected to surpass ten billion, functional master regulators such as miRNAs stand out as transformative molecular tools, capable of orchestrating complex trait networks and offering a tangible path toward the next green revolution. These are robust fine-tuners that orchestrate a myriad of functional processes and provide a value addition in emerging technologies such as assisted breeding, genome editing, and genomic selection to make rice production feasible. Herein, we have provided a comprehensive synthesis and updates on functional miRNA-mediated agronomically advantageous trait improvement exclusively for rice. It represents the latest functional understanding of miRNAs and their involvement as signatures of domestication and divergence processes, in support of the previously established notion and recent updates on emerging miRNA-assisted resources and technologies, such as their application as artificial solutions for improving genotypes, coding, and dietary potentialities for environmental safeguards and innovative biotherapeutics. Recent updates signify their robust cross-kingdom communicators' potential for multifaceted non-host dialoguing, and their integrative action relies on the coordination with other non-coding regulatory elements for various downstream trait regulation. Moreover, specific highlights refer to the application of miRNAs for rice agronomical trait improvements, broadly classified into three functional domains, viz., biotic and abiotic stresses and yield and quality traits. Such updated functional aspects of different miRNA modules would strengthen rice improvement by facilitating a foundation and future roadmap for miRNA-mediated trait discovery and improvement.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776238","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 m6A modification in spermatogenic dysfunction.","authors":"Jiale Wang, Xiaobao Zhang, Pingping Tang, Xiaohan Tang, Wenyu Cao, Yang Xu, Suyun Li","doi":"10.1007/s11033-026-11784-0","DOIUrl":"https://doi.org/10.1007/s11033-026-11784-0","url":null,"abstract":"","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776426","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}