Frontiers in Molecular Biosciences最新文献

{"title":"Investigating the effects of combined treatment of mesalazine with <i>Lactobacillus casei</i> in the experimental model of ulcerative colitis.","authors":"Shabnam Bahrami, Nahid Babaei, Hadi Esmaeili Gouvarchin Ghaleh, Jaleh Mohajeri Borazjani, Mahdieh Farzanehpour","doi":"10.3389/fmolb.2024.1456053","DOIUrl":"https://doi.org/10.3389/fmolb.2024.1456053","url":null,"abstract":"<p><strong>Introduction: </strong>Ulcerative colitis (UC), a common gastrointestinal disorder in affluent nations, involves chronic intestinal mucosal inflammation. This research investigated the effects of combined probiotic treatment of <i>Lactobacillus casei</i> (L. casei) and mesalazine on disease activity index and inflammatory factors in the UC model.</p><p><strong>Methods: </strong>20 male BALB/c mice were utilized and divided into four groups. To induce UC, all groups received 100 μL of 4% acetic acid (AA) intra-rectally. The first group received phosphate-buffered saline (PBS) (as a control group), the second group was treated with L. casei, the third group was treated with mesalazine and, the fourth group was treated with L. casei and mesalazine. Treatment with L. Casei and mesalazine commenced after the manifestation of symptoms resulting from UC induction. Finally, the mice were euthanized and the disease activity index, myeloperoxidase activity, nitric oxide rate, cytokines level (IL-1β, IL-6, TNF-α) and, gene expression (iNOS, COX-2, and cytokines) were evaluated.</p><p><strong>Results: </strong>The combined treatment of L. casei and mesalazine led to a significant decrease in the levels of NO, MPO and inflammatory cytokines. In addition, the expression of cytokines, iNOS and COX-2 genes decreased in mice treated with the combination.</p><p><strong>Discussion: </strong>This study shows that combined treatment of L. casei and mesalazine improves of experimental UC, which can be attributed to the anti-inflammatory properties of L. casei and mesalazine. In conclusion, this combination therapy can be considered a suitable option for the management of UC.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"11 ","pages":"1456053"},"PeriodicalIF":3.9,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142462124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetically predicted 486 blood metabolites in relation to risk of esophageal cancer: a Mendelian randomization study.","authors":"Caiyan Jia, Dan Yi, Mingze Ma, Qian Xu, Yan Ou, Fanming Kong, Yingjie Jia","doi":"10.3389/fmolb.2024.1391419","DOIUrl":"https://doi.org/10.3389/fmolb.2024.1391419","url":null,"abstract":"<p><strong>Background and objective: </strong>Enhancing therapy choices for varying stages of esophageal cancer and improving patient survival depend on timely and precise diagnosis. Blood metabolites may play a role in either causing or preventing esophageal cancer, but further research is needed to determine whether blood metabolites constitute a genetic risk factor for the disease. In order to tackle these problems, we evaluated the causal association between esophageal cancer and 486 blood metabolites that functioned as genetic proxies using a two-sample Mendelian randomization (MR) study.</p><p><strong>Methods: </strong>We utilized two-sample MR analyses to evaluate the causal links between blood metabolites and esophageal cancer. For the exposure, we used a genome-wide association study (GWAS) of 486 metabolites, and a GWAS study on esophageal cancer from Sakaue et al. was used for preliminary analyses. Causal analyses employed randomized inverse variance weighted (IVW) as the main method, supplemented by MR-Egger and weighted median (WM) analyses. Sensitivity analyses included the MR-Egger intercept test, Cochran Q test, MR-PRESSO, and leave-one-out analysis. Additionally, independent esophageal cancer GWAS data were utilized for replication and meta-analysis. FDR correction was applied to discern features with causal relationships. For conclusive metabolite identification, we conducted Steiger tests, linkage disequilibrium score regression, and colocalization analyses. Moreover, we utilized the program MetaboAnalyst 5.0 to analyze metabolic pathways.</p><p><strong>Results: </strong>This study found an important association between esophageal cancer and three metabolites: 1-linoleoylglycerophosphoethanolamine* [odds ratio (OR) = 3.21, 95% confidence interval (CI): 1.42-7.26, <i>p</i> < 0.01], pyroglutamine* (OR = 1.92, 95% CI: 1.17-3.17, <i>p</i> < 0.01), and laurate (12:0) (OR = 3.06, 95% CI: 1.38-6.78, <i>p</i> < 0.01).</p><p><strong>Conclusion: </strong>This study establishes a causal link between three defined blood metabolites and esophageal cancer, offering fresh insights into its pathogenesis.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"11 ","pages":"1391419"},"PeriodicalIF":3.9,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11479936/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142462122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The evolving hematopoietic niche during development.","authors":"Raúl Sánchez-Lanzas, Amanda Jiménez-Pompa, Miguel Ganuza","doi":"10.3389/fmolb.2024.1488199","DOIUrl":"https://doi.org/10.3389/fmolb.2024.1488199","url":null,"abstract":"<p><p>Mammalian hematopoietic stem cells (HSCs) emerge from the hemogenic endothelium in the major embryonic arteries. HSCs undergo a complex journey first migrating to the fetal liver (FL) and from there to the fetal bone marrow (FBM), where they mostly remain during adult life. In this process, a pool of adult HSCs is produced, which sustains lifelong hematopoiesis. Multiple cellular components support HSC maturation and expansion and modulate their response to environmental and developmental cues. While the adult HSC niche has been extensively studied over the last two decades, the niches present in the major embryonic arteries, FL, FBM and perinatal bone marrow (BM) are poorly described. Recent investigations highlight important differences among FL, FBM and adult BM niches and emphasize the important role that inflammation, microbiota and hormonal factors play regulating HSCs and their niches. We provide a review on our current understanding of these important cellular microenvironments across ontogeny. We mainly focused on mice, as the most widely used research model, and, when possible, include relevant insights from other vertebrates including birds, zebrafish, and human. Developing a comprehensive picture on these processes is critical to understand the earliest origins of childhood leukemia and to achieve multiple goals in regenerative medicine, such as mimicking HSC development <i>in vitro</i> to produce HSCs for broad transplantation purposes in leukemia, following chemotherapy, bone marrow failure, and in HSC-based gene therapy.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"11 ","pages":"1488199"},"PeriodicalIF":3.9,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11480086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142462031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Branched oncolytic peptides target HSPGs, inhibit metastasis, and trigger the release of molecular determinants of immunogenic cell death in pancreatic cancer.","authors":"Alessandro Rencinai, Eva Tollapi, Giulia Marianantoni, Jlenia Brunetti, Tania Henriquez, Alessandro Pini, Luisa Bracci, Chiara Falciani","doi":"10.3389/fmolb.2024.1429163","DOIUrl":"https://doi.org/10.3389/fmolb.2024.1429163","url":null,"abstract":"<p><p>Immunogenic cell death (ICD) can be exploited to treat non-immunoreactive tumors that do not respond to current standard and innovative therapies. Not all chemotherapeutics trigger ICD, among those that do exert this effect, there are anthracyclines, irinotecan, some platinum derivatives and oncolytic peptides. We studied two new branched oncolytic peptides, BOP7 and BOP9 that proved to elicit the release of damage-associated molecular patterns DAMPS, mediators of ICD, in pancreatic cancer cells. The two BOPs selectively bound and killed tumor cells, particularly PANC-1 and Mia PaCa-2, but not cells of non-tumor origin such as RAW 264.7, CHO-K1 and pgsA-745. The cancer selectivity of the two BOPs may be attributed to their repeated cationic sequences, which enable multivalent binding to heparan sulfate glycosaminoglycans (HSPGs), bearing multiple anionic sulfation patterns on cancer cells. This interaction of BOPs with HSPGs not only fosters an anti-metastatic effect <i>in vitro</i>, as demonstrated by reduced adhesion and migration of PANC-1 cancer cells, but also shows promising tumor-specific cytotoxicity and low hemolytic activity. Remarkably, the cytotoxicity induced by BOPs triggers the release of DAMPs, particularly HMGB1, IFN-β and ATP, by dying cells, persisting longer than the cytotoxicity of conventional chemotherapeutic agents such as irinotecan and daunorubicin. An <i>in vivo</i> assay in nude mice showed an encouraging 20% inhibition of tumor grafting and growth in a pancreatic cancer model by BOP9.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"11 ","pages":"1429163"},"PeriodicalIF":3.9,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11479992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142462117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endoplasmic reticulum stress alters myelin associated protein expression and extracellular vesicle composition in human oligodendrocytes.","authors":"Ethan D Evalt, Saranraj Govindaraj, Madison T Jones, Nesve Ozsoy, Han Chen, Ashley E Russell","doi":"10.3389/fmolb.2024.1432945","DOIUrl":"https://doi.org/10.3389/fmolb.2024.1432945","url":null,"abstract":"<p><p>Myelination of the central nervous system is mediated by specialized glial cells called oligodendrocytes (OLs). Multiple sclerosis (MS) is characterized by loss of myelination and subsequent clinical symptoms that can severely impact the quality of life and mobility of those affected by the disease. The major protein components of myelin sheaths are synthesized in the endoplasmic reticulum (ER), and ER stress has been observed in patients with MS. Extracellular vesicles (EVs) have been shown to carry bioactive cargo and have the potential to be utilized as noninvasive biomarkers for various diseases. In the current study, we sought to determine how ER stress in OLs affected the production of key myelination proteins and EV release and composition. To achieve this, tunicamycin was used to induce ER stress in a human oligodendroglioma cell line and changes in myelination protein expression and markers of autophagy were assessed. EVs were also separated from the conditioned cell culture media through size exclusion chromatography and characterized. Significant reductions in the expression of myelination proteins and alterations to autophagosome formation were observed in cells undergoing ER stress. EVs released from these cells were slightly smaller relative to controls, and had strong expression of LC3B. We also observed significant upregulation of miR-29a-3p in ER stress EVs when compared to controls. Taken together, these data suggest that ER stress negatively impacts production of key myelination proteins and induces cells to release EVs that may function to preemptively activate autophagic pathways in neighboring cells.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"11 ","pages":"1432945"},"PeriodicalIF":3.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11473301/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142462121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Profiling genetic variants in cardiovascular disease genes among a Heterogeneous cohort of Mendelian conditions patients and electronic health records.","authors":"Nadia Akawi, Ghadeera Al Mansoori, Anwar Al Zaabi, Andrea Badics, Noura Al Dhaheri, Aisha Al Shamsi, Amal Al Tenaiji, Bashar Alzohily, Fatmah S A Almesmari, Hamad Al Hammadi, Nahid Al Dhahouri, Manal Irshaid, Praseetha Kizhakkedath, Fatema Al Shibli, Mohammed Tabouni, Mushal Allam, Ibrahim Baydoun, Hiba Alblooshi, Bassam R Ali, Roger S Foo, Fatma Al Jasmi","doi":"10.3389/fmolb.2024.1451457","DOIUrl":"https://doi.org/10.3389/fmolb.2024.1451457","url":null,"abstract":"<p><strong>Introduction: </strong>This study addresses the rising cardiovascular disease (CVD) rates in the United Arab Emirates (UAE) by investigating the occurrence and impact of genetic variants in CVD-related genes.</p><p><strong>Methods: </strong>We collected all genes linked to heritable CVD from public and diagnostic databases and mapped them to their corresponding biological processes and molecular pathways. We then evaluated the types and burden of genetic variants within these genes in 343 individuals from the Emirati Mendelian Study Cohort and 3,007 national electronic health records.</p><p><strong>Results: </strong>We identified a total of 735 genes associated with heritable CVD, covering a range of cardiovascular conditions. Enrichment analysis revealed key biological processes and pathways, including Apelin, FoxO, and Ras signaling, that are implicated across all forms of heritable CVD. Analysis of a UAE cohort of 3,350 individuals showed a predominance of rare and unique CVD variants specific to the population. The study found a significant burden of pathogenic variants in families with CVD within the Emirati Mendelian cohort and re-assessed the pathogenicity of 693 variants from national health records, leading to the discovery of new CVD-causing variants.</p><p><strong>Discussion: </strong>This study underscores the importance of continuously updating our understanding of genes and pathways related to CVD. It also highlights the significant underrepresentation of the UAE population in public databases and clinical literature on CVD genetics, offering valuable insights that can inform future research and intervention strategies.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"11 ","pages":"1451457"},"PeriodicalIF":3.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11473968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142462027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Semantic segmentation-based detection algorithm for challenging cryo-electron microscopy RNP samples.","authors":"J Vargas, A Modrego, H Canabal, J Martin-Benito","doi":"10.3389/fmolb.2024.1473609","DOIUrl":"https://doi.org/10.3389/fmolb.2024.1473609","url":null,"abstract":"<p><p>In this study, we present a novel and robust methodology for the automatic detection of influenza A virus ribonucleoproteins (RNPs) in single-particle cryo-electron microscopy (cryo-EM) images. Utilizing a U-net architecture-a type of convolutional neural network renowned for its efficiency in biomedical image segmentation-our approach is based on a pretraining phase with a dataset annotated through visual inspection. This dataset facilitates the precise identification of filamentous RNPs, including the localization of the filaments and their terminal coordinates. A key feature of our method is the application of semantic segmentation techniques, enabling the automated categorization of micrograph pixels into distinct classifications of particle and background. This deep learning strategy allows to robustly detect these intricate particles, a crucial step in achieving high-resolution reconstructions in cryo-EM studies. To encourage collaborative advancements in the field, we have made our routines, the pretrained U-net model, and the training dataset publicly accessible. The reproducibility and accessibility of these resources aim to facilitate further research and validation in the realm of cryo-EM image analysis.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"11 ","pages":"1473609"},"PeriodicalIF":3.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11473350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142462028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Revisiting the challenges and opportunities in cancer drug resistance.","authors":"Tikam Chand Dakal, Narendra Kumar Sharma, Amit Sharma","doi":"10.3389/fmolb.2024.1497754","DOIUrl":"https://doi.org/10.3389/fmolb.2024.1497754","url":null,"abstract":"","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"11 ","pages":"1497754"},"PeriodicalIF":3.9,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11471640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142462120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lapatinib-induced enhancement of mitochondrial respiration in HER2-positive SK-BR-3 cells: mechanism revealed by analysis of proteomic but not transcriptomic data.","authors":"Dmitry Kamashev, Nina Shaban, Galina Zakharova, Alexander Modestov, Мargarita Kamynina, Sergey Baranov, Anton Buzdin","doi":"10.3389/fmolb.2024.1470496","DOIUrl":"https://doi.org/10.3389/fmolb.2024.1470496","url":null,"abstract":"<p><p>Dual inhibitors of HER2 and EGFR, such as lapatinib, have shown significant efficacy for the therapy of HER2-positive breast cancer. Previous experiments showed that in cell cultures, the efficacy of lapatinib was significantly reduced by exposure to human serum and human epidermal growth factor (EGF). At the proteomic and transcriptomic levels, we examined the changes in the HER2-positive breast cancer cell line SK-BR-3 profiles upon treatment with lapatinib, either alone or in combination with human serum or EGF. Proteomic profiling revealed 350 differentially expressed proteins (DEPs) in response to lapatinib treatment at concentrations that induced cell growth arrest. Addition of human serum or EGF in combination with lapatinib prevented cell growth inhibition, and this combination treatment returned the expression of ∼93% of DEPs to drug-free levels for both human serum and EGF. Gene ontology enrichment and OncoboxPD pathway activation level analysis showed that lapatinib addition influenced mostly common functional processes revealed in RNA- and protein-based assays. However, a specific feature was observed at the proteome level: addition of lapatinib increased the expression of proteins associated with mitochondrial function and cellular respiration. This feature was not observed when using RNA sequencing data for the same experiments. However, it is consistent with the results of the resazurin test, which showed a 1.8-fold increase in SK-BR-3 cellular respiration upon exposure to lapatinib. Thus, we conclude that enhanced cellular respiration is a novel additional mechanism of action of lapatinib on HER2-positive cancer cells.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"11 ","pages":"1470496"},"PeriodicalIF":3.9,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11472020/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142462025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Visualizing multimerization of plasticity-related gene 5 at the plasma membrane using FLIM-FRET.","authors":"Franziska Köper, Danara Vonk, Malte W Dirksen, Isabel Gross, Axel Heep, Torsten Plösch, Mark S Hipp, Anja U Bräuer","doi":"10.3389/fmolb.2024.1478291","DOIUrl":"https://doi.org/10.3389/fmolb.2024.1478291","url":null,"abstract":"<p><p>Plasticity-related gene (PRG) 5 is a vertebrate specific membrane protein, that belongs to the family of lipid-phosphate phosphatases (LPPs). It is prominently expressed in neurons and is involved in cellular processes such as growth-cone guidance and spine formation. At a functional level, PRG5 induces filopodia in non-neuronal cell lines, as well as the formation of plasma membrane protrusions in primary cortical and hippocampal neurons. Overexpression of PRG5 in immature neurons leads to the induction of spine-like structures, and regulates spine density and morphology in mature neurons. Understanding spine formation is pivotal, as spine abnormalities are associated with numerous neurological disorders. Although the importance of PRG5 in neuronal function is evident, the precise mechanisms as to how exactly it induces membrane protrusions and orchestrates cellular processes remain unresolved. Here we used <i>in vitro</i> biochemical assays to demonstrate that in HEK293T cells a large fraction of PRG5 can be found in homo dimers and lager multimers. By using Fluorescence Lifetime Imaging (FLIM) to quantify Förster Resonance Energy Transfer (FRET), we were able to visualize and quantify the specific localization of PRG5 multimers in living HEK293T cells and in fixed immature primary hippocampal neurons. Here, we provide the first evidence that PRG5 multimers are specifically localized in non-neuronal filopodia, as well as in neuronal spine-like structures. Our findings indicate a potential functional role for PRG5 multimerization, which might be required for interaction with extracellular matrix molecules or for maintaining the stability of membrane protrusions.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"11 ","pages":"1478291"},"PeriodicalIF":3.9,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11471602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142462032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}