Biochemical and biophysical research communications最新文献

{"title":"High-resolution imaging of exosome pulmonary spatial distribution via fluorescent mRNA labeling and fMOST","authors":"Tianhui Chao ,&nbsp;Xiaoyu Fu ,&nbsp;Hongyu Sun ,&nbsp;Xianzhen Yin ,&nbsp;Sha Xu ,&nbsp;Ruifang Gao ,&nbsp;Guodong Chen ,&nbsp;Yang Zhao ,&nbsp;Shilin Zhou ,&nbsp;Xiaoliang Li ,&nbsp;Xiaoxu Hao ,&nbsp;Tingting Li ,&nbsp;Yunpeng Zhao ,&nbsp;Yue Wang","doi":"10.1016/j.bbrc.2026.153334","DOIUrl":"10.1016/j.bbrc.2026.153334","url":null,"abstract":"<div><div>Technical limitations hinder the clinical translation of exosomes for precise visualization of their in vivo pharmacokinetics. Conventional fluorescent labelling methods suffer from low signal-to-noise ratios, which hamper three-dimensional (3D), high-resolution, and quantitative analysis of exosome distribution at the whole-organ scale. To address this challenge, this study established an integrated “fluorescent mRNA labelling-fMOST imaging” technology system. Exosomes were labelled with fluorescent mRNA; in vitro characterization confirmed that the nucleic acid tags were efficiently loaded into exosomes without compromising their structural integrity, while demonstrating significantly superior signal-to-noise ratios and stability over traditional DiO dyes. Using light-sheet microscopy and quantitative analysis, we compared the pulmonary distribution of exosomes across different administration routes. The results indicated that lung accumulation following tail-vein injection was 2.48-fold higher than that of intranasal administration. Furthermore, fluorescence Micro-Optical Sectioning Tomography (fMOST) imaging provided a high-resolution 3D map of exosomes throughout the entire lung. The technology platform established in this study achieves single-exosome spatial resolution of in vivo distribution, offering key methodological tools and data support for evaluating the targeting efficiency of exosomal drugs and optimising delivery strategies, thereby facilitating their clinical translation.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"803 ","pages":"Article 153334"},"PeriodicalIF":2.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146076719","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":"The role of the TLR2 gene in regulating proliferation of rabbit dermal papilla cells","authors":"Yu Zhou ,&nbsp;Bohao Zhao ,&nbsp;Shaoning Sun ,&nbsp;Xiaoman Han ,&nbsp;Yongqi Yu ,&nbsp;Jinbao Li ,&nbsp;Yang Chen ,&nbsp;Xinsheng Wu","doi":"10.1016/j.bbrc.2026.153323","DOIUrl":"10.1016/j.bbrc.2026.153323","url":null,"abstract":"<div><div>Hair follicle (HF) morphogenesis, growth, and regeneration are fundamentally governed by reciprocal interactions between the epidermal and dermal compartments of the skin, with dermal papilla cells (DPCs) serving as a central regulatory element in this process. Here, the functional role of Toll-like receptor 2 (TLR2) in the control of DPC proliferation was investigated. The coding sequence (CDS) of the rabbit <em>TLR2</em> gene was successfully cloned and subjected to preliminary bioinformatics analyses to characterize its predicted structural and functional features. Gain- and loss-of-function experiments demonstrated that modulation of <em>TLR2</em> expression significantly altered the transcription of HF growth- and development-associated genes, including <em>BCL2</em>, <em>CCND1</em>, <em>CTNNB1</em>, <em>FGF2</em>, and <em>TGFβ</em>. Functional assays, including CCK-8 proliferation analysis, EdU incorporation, and immunostaining for proliferating cell nuclear antigen (PCNA), consistently showed that <em>TLR2</em> overexpression markedly enhanced DPC proliferation, whereas <em>TLR2</em> knockdown exerted a pronounced inhibitory effect. These results provide mechanistic insight into the role of TLR2 in regulating DPC proliferation and offer a theoretical basis for further investigations into its contribution to hair follicle biology.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"803 ","pages":"Article 153323"},"PeriodicalIF":2.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146049045","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":"DLST mediates the malignant progression of osteosarcoma cells by regulating the p38 MAPK signaling pathway","authors":"Chong Guo ,&nbsp;Kaiqiong Liao ,&nbsp;Kai Xu ,&nbsp;Jiongfeng Zhang ,&nbsp;Guanglong Chen ,&nbsp;Xiaohui Luo ,&nbsp;Jun Yang ,&nbsp;Zhengzai Dai ,&nbsp;Xiao-Bin Lv ,&nbsp;Feifei Zhang ,&nbsp;Zhiping Zhang","doi":"10.1016/j.bbrc.2026.153341","DOIUrl":"10.1016/j.bbrc.2026.153341","url":null,"abstract":"<div><h3>Background</h3><div>This research investigates the function of dihydrolipoic acid succinyltransferase (DLST) in the initiation and progression of osteosarcoma.</div></div><div><h3>Methods</h3><div>Cellular functions were assessed using CCK-8, colony formation, scratch assays, transwell assays, and flow cytometry. The expression of relevant genes at both mRNA and protein levels was detected using quantitative real-time PCR (qRT-PCR) and Western blotting techniques. The regulatory mechanism of DLST was analyzed through RNA-sequencing. Finally, tumor growth in vivo was evaluated using established animal models.</div></div><div><h3>Results</h3><div>DLST was highly expressed in osteosarcoma. Knockdown of DLST limited the proliferative, migratory, invasive, and anti-apoptotic abilities of osteosarcoma cells. RNA-seq was employed to analyze its mechanism, which showed that DLST can influence the p38 MAPK signaling pathway. Functional validation further showed that the p38 MAPK signaling pathway inhibitor was able to reverse the malignant functional changes in osteosarcoma cells that had been caused by DLST knockdown. Finally, in in vivo experiments, knocking down the DLST gene in the osteosarcoma animal model slowed down tumor growth.</div></div><div><h3>Conclusion</h3><div>In this study, we found that DLST promotes the proliferation, migration, invasion, anti-apoptosis of osteosarcoma cells, as well as tumor growth, regulated through the p38 MAPK signaling pathway. These results could offer novel and valuable perspectives for the clinical management of osteosarcoma.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"803 ","pages":"Article 153341"},"PeriodicalIF":2.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146076709","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":"Neuropeptide INS-14 modulates apoptotic cell clearance in Caenorhabditis elegans","authors":"Yunmin Xie ,&nbsp;Lu Chen ,&nbsp;Fuqiao Liu,&nbsp;Qian Zheng,&nbsp;Lei Yuan,&nbsp;Hui Xiao,&nbsp;Hui Wang","doi":"10.1016/j.bbrc.2026.153337","DOIUrl":"10.1016/j.bbrc.2026.153337","url":null,"abstract":"<div><div>Apoptosis, a principal form of programmed cell death, is integral to animal development. Neuropeptides, which are crucial signaling molecules in the nervous system, play roles in various physiological and behavioral processes. Until now, there has been no evidence of neuropeptides being involved in the clearance of apoptotic cells. Consequently, utilizing <em>Caenorhabditis elegans</em>—an exemplary model organism for investigating apoptosis and its regulatory mechanisms—we performed a comprehensive functional screening of neuropeptide genes via RNA interference (RNAi) technology to identify pivotal neuropeptide genes involved in apoptosis and apoptotic cell clearance. <em>C. elegans</em> possesses 113 neuropeptide genes. Our screening identified 9 neuropeptide genes as preliminary regulators of apoptosis, with 2 neuropeptide genes specifically involved in apoptotic cell clearance. Among these, the neuropeptide gene <em>ins-14</em> exhibited the most significant regulatory phenotype. Further mechanistic investigations revealed that, during the late stage of apoptotic cell clearance, disruptions in <em>ins-14</em> function markedly affect the recruitment efficiency of the key protein LAAT-1 to phagosomes and disrupt the normal acidification process within phagosomes. Moreover, we found that <em>ins-14</em> modulated <em>laat-1</em> expression at the transcriptional level. This study is the first to elucidate the regulatory role of neuropeptides in apoptotic cell clearance in <em>C. elegans</em>, offering novel experimental evidence for a more profound understanding of neuropeptide-mediated apoptotic regulatory networks.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"803 ","pages":"Article 153337"},"PeriodicalIF":2.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146049046","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":"Role of WNK4 and FKBP5 in asthma: Insights from bioinformatics analysis, machine learning, and preliminary validation","authors":"Meng Liu,&nbsp;Yue Li,&nbsp;Tianci Jiang,&nbsp;Lingling Dai,&nbsp;Zhe Cheng","doi":"10.1016/j.bbrc.2026.153351","DOIUrl":"10.1016/j.bbrc.2026.153351","url":null,"abstract":"<div><h3>Background</h3><div>The complex and heterogeneous molecular mechanisms of asthma are currently unclear, and treatment outcomes are dismal in some patients. This study aimed to identify biomarkers with diagnostic and therapeutic potential.</div></div><div><h3>Methods</h3><div>Gene Expression Omnibus was used to obtain asthma-related gene expression data for identifying differentially expressed genes. They were subjected to functional and pathway enrichment analyses using the Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Disease Ontology. Gene Set Enrichment Analysis and Gene Set Variation Analysis were used to explore potential asthma-related mechanisms. Candidate biomarkers were identified using two machine learning algorithms and evaluated via ROC curve analysis. Immune cell fractions were assessed using CIBERSORT, and biomarker expression was validated in external database, in vivo, and in vitro studies.</div></div><div><h3>Results</h3><div>The 168 differentially expressed genes (96 upregulated and 72 downregulated) were enriched for xenobiotic stimuli, glutathione transferase activity, negative regulation of proteolysis, and endopeptidase inhibitor activity; the pathways for glutathione metabolism, xenobiotic metabolism via cytochrome P450, and chemical carcinogenesis involving DNA adducts; and for periodontitis and asthma. WNK4 and FKBP5 were identified as critical genes and were validated using ROC assays. Correlations were found between WNK4 and M2-macrophages, and between FKBP5 expression and mast cells, resting NK cells, and T cells. Our findings demonstrated increased FKBP5 expression and decreased WNK4 expression in the asthmatic cohort, aligning with the results from dataset analyses. This concordance reinforces the reliability and validity of the bioinformatics assessments.</div></div><div><h3>Conclusions</h3><div>This study identified WNK4 and FKBP5 as candidate biomarkers of asthma warranting further clinical validation, thus contributing to a deeper understanding of asthma pathogenesis and offering a theoretical basis for future treatment strategies.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"803 ","pages":"Article 153351"},"PeriodicalIF":2.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146076710","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":"Localization of Asgard archaeal ESCRT proteins to eukaryotic cellular structures","authors":"Kishore Babu Naripogu ,&nbsp;Yee Han Tee ,&nbsp;Yosuke Senju ,&nbsp;Alexander Bershadsky ,&nbsp;Robert C. Robinson","doi":"10.1016/j.bbrc.2026.153301","DOIUrl":"10.1016/j.bbrc.2026.153301","url":null,"abstract":"<div><div>The emergence of internal membrane systems was a defining step in eukaryogenesis, but how pre-eukaryotic proteins were adapted to these novel compartments and structures remains unclear. Asgard archaea, the closest known prokaryotic relatives of eukaryotes, encode homologs of ESCRT (Endosomal Sorting Complex Required for Transport) proteins, which mediate membrane remodeling in eukaryotic cells, processes ranging from endosomal sorting to cytokinetic abscission. Here, we show that ESCRT-II and ESCRT-III homologs, VSP4 and ubiquitin from the Asgard achaeon <em>Promethearchaeum syntrophicum</em> (MK-D1) are recruited to discrete structures when expressed in human cells. These archaeal proteins localize to canonical eukaryotic ESCRT recruitment sites, midbodies and centrosomes, structures which are absent from MK-D1. This localization reflects conserved molecular interactions that predate the emergence of eukaryotic internal membranes and other eukaryotic cellular structures. These findings support a model in which protein machines were repurposed to support cellular complexity during eukaryogenesis, allowing the integration of ancestral ESCRT molecular functions and networks in to novel cellular architectures.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153301"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146025591","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":"Opposing effects of Gα12 and Gα13 loss on myotube size regulation via mTORC1 signaling","authors":"Mai Kubota ,&nbsp;Shuhei Fujita ,&nbsp;Ryohei Kamata ,&nbsp;Kazuma Tamura ,&nbsp;Keiichiro Sugimoto ,&nbsp;Tomoya Kitakaze ,&nbsp;Naoki Harada ,&nbsp;Ryoichi Yamaji","doi":"10.1016/j.bbrc.2026.153326","DOIUrl":"10.1016/j.bbrc.2026.153326","url":null,"abstract":"<div><div>To reduce the risk of diseases caused by a reduction in skeletal muscle mass and quality, it is important to understand the molecular mechanisms underlying the maintenance and improvement of skeletal muscle mass and quality. Gα12 and/or Gα13 have been implicated in the regulation of myotube size through the mechanistic target of rapamycin complex 1 (mTORC1) signaling; however, their specific and potentially distinct molecular mechanisms remain unknown. Knockdown and rescue experiments revealed that the loss of Gα12 decreased myotube size, whereas the loss of Gα13 increased it. Gα12 knockdown reduced the phosphorylation levels of mTORC1 signaling components (Akt, mTOR, and p70S6K) and the levels of puromycin-labeled proteins, whereas Gα13 knockdown increased these levels. Loss of Gα12 or Gα13 suppressed SRF-RE-dependent transcriptional activity. While expression of a constitutively active form of RhoA (RhoA-CA) activated SRF-RE activity, notably, RhoA-CA expression did not affect myotube size, nor did it alter myotube atrophy induced by Gα12 knockdown or hypertrophy induced by Gα13 knockdown. Depletion of Gα12 increased the mRNA expression of oxidative myosin heavy chain (MyHC) isoforms <em>Myh7</em> and <em>Myh2</em> and decreased the mRNA expression of <em>Myh1</em> and <em>Myh4</em>, whereas depletion of Gα13 increased the mRNA expression of <em>Myh7</em>, <em>Myh2</em>, <em>Myh1</em>, and <em>Myh4</em>. These results indicate that loss of Gα12 induces myotube atrophy by suppressing mTORC1 signaling and protein synthesis, whereas loss of Gα13 induces myotube hypertrophy by enhancing these processes, likely independent of SRF-RE-mediated transcription. Notably, Gα12 and Gα13 oppositely regulated the mRNA expression of MyHC isoforms, particularly <em>Myh1</em> and <em>Myh4</em>.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153326"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146025602","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":"Structural characterization of a glucose-activated β-glucosidase from Bacillus thermoamylovorans","authors":"Wendi Yang ,&nbsp;Panpan Dong ,&nbsp;Guosi Li ,&nbsp;Hanyu Wu ,&nbsp;Lanlan Li ,&nbsp;Min Gao ,&nbsp;Lin Li ,&nbsp;Yunkun Wu","doi":"10.1016/j.bbrc.2026.153261","DOIUrl":"10.1016/j.bbrc.2026.153261","url":null,"abstract":"<div><div>β-glucosidases play crucial roles in lignocellulosic biomass conversion, but their applications were limited by thermostability and glucose sensitivity. In this study, the high-resolution crystal structure of a thermostable glucose-activated β-glucosidase Bgl52 from <em>Bacillus thermoamylovorans</em> was determined at 2.00 Å. Bgl52 belongs to the GH1 family, and exhibited a canonical (β/α)₈ TIM barrel architecture typical to GH1 enzymes. Comparison analysis and site-directed mutagenesis revealed that its catalytic sites were Glu166 and Glu353 and its gatekeeper residues were Trp169 and Leu173, which involved in the glucose tolerance. Features contributing to its thermostability were also explored, including the composition of amino acids, number of mobile loops, total area of major hydrophobic clusters and number of salt bridges. Our study shed light on the molecular basis for glucose tolerance and thermostability of GH1 β-glucosidases and provide possibility of improving the characteristics for potential industrial applications by structure-guided engineering.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153261"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146006638","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":"Clinical advances in CD47-SIRPα axis-targeted cancer immunotherapy: Mechanisms, strategies, challenges, and future perspectives","authors":"Yuanyuan Li ,&nbsp;Xiaomei He ,&nbsp;Hongli Zhou,&nbsp;Yu Tian,&nbsp;Qingqing Zhang,&nbsp;Yiguo Zhou,&nbsp;Jianyun Zhou","doi":"10.1016/j.bbrc.2026.153330","DOIUrl":"10.1016/j.bbrc.2026.153330","url":null,"abstract":"<div><div>The CD47-SIRPα signaling axis has emerged as a promising target in cancer immunotherapy by disrupting the “don't eat me” signal, thereby promoting macrophage-mediated phagocytosis. However, its clinical translation confronts a significant challenge due to the “on-target off-tumor” effect, primarily leading to hematological toxicity, notably anemia. This challenge was underscored by a pivotal setback in the field: the Phase III trial of Magrolimab, the first anti-CD47 therapy to reach this stage, which failed to meet its primary endpoint and ultimately led to the discontinuation of its development program. This comprehensive review systematically traces the evolution of therapeutic strategies targeting the CD47-SIRPα axis, from first-generation monoclonal antibodies to advanced fusion proteins, bispecific antibodies, and cutting-edge approaches such as oncolytic viruses and CAR-macrophages. It also provides a detailed summary of the clinical trial landscape, analyzing the differential efficacy observed between hematological malignancies and solid tumors. Furthermore, we summarize the major clinical challenges, including safety concerns, resistance mechanisms, and diagnostic complexities. By synthesizing these key findings, this review provides valuable insights for optimizing future drug design, refining combination regimens, and guiding patient selection strategies, thereby offering a crucial reference for overcoming current limitations and fully realizing the therapeutic potential of this promising axis.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153330"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146026172","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":"Corrigendum to “Plasmodium falciparum Raf kinase inhibitor is a lipid binding protein that interacts with and regulates the activity of PfCDPK1, an essential plant-like kinase required for red blood cell invasion” [Biochem. Biophys. Res. Commun. 749 (2025) 151350]","authors":"Manish Sharma ,&nbsp;Deepak Krishnan ,&nbsp;Ayushi Singh ,&nbsp;Pooja Negi ,&nbsp;Komal Rani ,&nbsp;Amjesh Revikumar ,&nbsp;Manoj Munde ,&nbsp;Abhisheka Bansal","doi":"10.1016/j.bbrc.2026.153375","DOIUrl":"10.1016/j.bbrc.2026.153375","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153375"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112171","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}