Journal of Molecular Cell Biology最新文献

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DNAJC12 downregulation induces neuroblastoma progression via increased histone H4K5 lactylation. DNAJC12下调通过增加组蛋白H4K5乳酸化诱导神经母细胞瘤进展。
IF 5.3 2区 生物学
Journal of Molecular Cell Biology Pub Date : 2024-12-23 DOI: 10.1093/jmcb/mjae056
Yaqi Yang, Jiejun Wen, Susu Lou, Yali Han, Yi Pan, Ying Zhong, Qiao He, Yinfeng Zhang, Xi Mo, Jing Ma, Nan She
{"title":"DNAJC12 downregulation induces neuroblastoma progression via increased histone H4K5 lactylation.","authors":"Yaqi Yang, Jiejun Wen, Susu Lou, Yali Han, Yi Pan, Ying Zhong, Qiao He, Yinfeng Zhang, Xi Mo, Jing Ma, Nan She","doi":"10.1093/jmcb/mjae056","DOIUrl":"https://doi.org/10.1093/jmcb/mjae056","url":null,"abstract":"<p><p>Neuroblastoma (NB) is the most common extracranial solid tumor in children. Despite treatment advances, the survival rates of high-risk NB patients remain low. This highlights the urgent need for a deeper understanding of the molecular mechanisms driving NB progression to support the development of new therapeutic strategies. In this study, we demonstrated that the reduced levels of DNAJC12, a protein involved in metabolic regulation, are associated with poor prognosis in NB patients. Our data indicate that low DNAJC12 expression activates glycolysis in NB cells, leading to increased lactic acid production and histone H4 lysine 5 lactylation (H4K5la). Elevated H4K5la upregulates the transcription of COL1A1, a gene implicated in cell metastasis. Immunohistochemistry staining of NB patient samples confirmed that high H4K5la levels correlate with poor clinical outcomes. Furthermore, we showed that inhibiting glycolysis, reducing H4K5la, or targeting COL1A1 can mitigate the invasive behavior of NB cells. These findings reveal a critical link between metabolic reprogramming and epigenetic modifications in the context of NB progression, suggesting that H4K5la could serve as a novel diagnostic and prognostic marker, and shed light on identifying new therapeutic targets within metabolic pathways for the treatment of this aggressive pediatric cancer.</p>","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inhibition of EphA2 by syndecan-4 in wounded skin regulates clustering of fibroblasts. syndecan-4在损伤皮肤中抑制EphA2可调节成纤维细胞的聚集。
IF 5.3 2区 生物学
Journal of Molecular Cell Biology Pub Date : 2024-12-23 DOI: 10.1093/jmcb/mjae054
Rebecca Brooks, Xianhui Wei, Mang Leng Lei, Francisca Cisterna Cid, James A Roper, Rosalind C Williamson, Mark D Bass
{"title":"Inhibition of EphA2 by syndecan-4 in wounded skin regulates clustering of fibroblasts.","authors":"Rebecca Brooks, Xianhui Wei, Mang Leng Lei, Francisca Cisterna Cid, James A Roper, Rosalind C Williamson, Mark D Bass","doi":"10.1093/jmcb/mjae054","DOIUrl":"https://doi.org/10.1093/jmcb/mjae054","url":null,"abstract":"<p><p>Upon injury, fibroblasts in the surrounding tissue become activated, migrating into the wound in a controlled manner. Once they arrive, they contract the wound and remodel the stroma. While certain cell surface receptors promote fibroblast migration, others cause repulsion between fibroblasts upon contact, seemingly opposing their clustering within the wound bed. Eph receptor-ephrin interactions on colliding cells trigger this repulsion, but how fibroblasts transition to clustering behaviour during healing remains unclear. Syndecan-4 modulates transmembrane receptors involved in wound healing, including receptors for the extracellular matrix and growth factors. As a result, Sdc4-/- mice experience delayed healing due to impaired fibroblast recruitment. In this study, we report that syndecan-4 also regulates fibroblast repulsion during wound healing. We discover that syndecan-4 inhibits the expression and signalling of EphA2 by activating PKCα. Changes in syndecan-4 expression, such as those observed during wound healing, alter fibroblast behaviour from repulsion to adhesion upon cell collision by modulating EphA2 levels. Moreover, we find that EphA2 expression is suppressed in wound bed fibroblasts in a syndecan-4-dependent manner, explaining how fibroblast clustering is achieved during wound healing.</p>","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Serum IL-27 and GDF15 levels in second trimester are associated with adverse pregnancy outcomes. 妊娠中期血清IL-27和GDF15水平与不良妊娠结局相关。
IF 5.3 2区 生物学
Journal of Molecular Cell Biology Pub Date : 2024-12-23 DOI: 10.1093/jmcb/mjae053
Xue Li, Luping Liu, Li Jiang, Peihong Chen, Hua Jin, Enhao Li, Jiarong Dai, Jufen Yi, Xuemei Yu, Shan Zhang
{"title":"Serum IL-27 and GDF15 levels in second trimester are associated with adverse pregnancy outcomes.","authors":"Xue Li, Luping Liu, Li Jiang, Peihong Chen, Hua Jin, Enhao Li, Jiarong Dai, Jufen Yi, Xuemei Yu, Shan Zhang","doi":"10.1093/jmcb/mjae053","DOIUrl":"https://doi.org/10.1093/jmcb/mjae053","url":null,"abstract":"","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Modeling gastric intestinal metaplasia in 3D organoids using nitrosoguanidine. 利用亚硝基胍在三维有机体中模拟胃肠化生。
IF 5.3 2区 生物学
Journal of Molecular Cell Biology Pub Date : 2024-12-20 DOI: 10.1093/jmcb/mjae030
Yuan Li, Jiena Chen, Tao Li, Jie Lin, Haocheng Zheng, Nadia Johnson, Xuebiao Yao, Xia Ding
{"title":"Modeling gastric intestinal metaplasia in 3D organoids using nitrosoguanidine.","authors":"Yuan Li, Jiena Chen, Tao Li, Jie Lin, Haocheng Zheng, Nadia Johnson, Xuebiao Yao, Xia Ding","doi":"10.1093/jmcb/mjae030","DOIUrl":"10.1093/jmcb/mjae030","url":null,"abstract":"<p><p>Gastric intestinal metaplasia (GIM) represents a precancerous stage characterized by morphological and pathophysiological changes in the gastric mucosa, where gastric epithelial cells transform into a phenotype resembling that of intestinal cells. Previous studies have demonstrated that the intragastric administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) induces both gastric carcinoma and intestinal metaplasia in mice. Here, we show that MNNG induces GIM in three-dimensional (3D) mouse organoids. Our histological analyses reveal that MNNG-induced gastric organoids undergo classical morphological alterations, exhibiting a distinct up-regulation of CDX2 and MUC2, along with a down-regulation of ATP4B and MUC6. Importantly, metaplastic cells observed in MNNG-treated organoids originate from MIST1+ cells, indicating their gastric chief cell lineage. Functional analyses show that activation of the RAS signaling pathway drives MNNG-induced metaplasia in 3D organoids, mirroring the characteristics observed in human GIM. Consequently, modeling intestinal metaplasia using 3D organoids offers valuable insights into the molecular mechanisms and spatiotemporal dynamics of the gastric epithelial lineage during the development of intestinal metaplasia within the gastric mucosa. We conclude that the MNNG-induced metaplasia model utilizing 3D organoids provides a robust platform for developing preventive and therapeutic strategies to mitigate the risk of gastric cancer before precancerous lesions occur.</p>","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11744189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141995874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
ZW10: an emerging orchestrator of organelle dynamics during the cell division cycle. ZW10:细胞分裂周期中细胞器动力学的新兴协调者
IF 5.3 2区 生物学
Journal of Molecular Cell Biology Pub Date : 2024-12-20 DOI: 10.1093/jmcb/mjae026
Sm Faysal Bellah, Fengrui Yang, Fangyuan Xiong, Zhen Dou, Xuebiao Yao, Xing Liu
{"title":"ZW10: an emerging orchestrator of organelle dynamics during the cell division cycle.","authors":"Sm Faysal Bellah, Fengrui Yang, Fangyuan Xiong, Zhen Dou, Xuebiao Yao, Xing Liu","doi":"10.1093/jmcb/mjae026","DOIUrl":"10.1093/jmcb/mjae026","url":null,"abstract":"<p><p>Zeste white 10 (ZW10) was first identified as a centromere/kinetochore protein encoded by the ZW10 gene in Drosophila. ZW10 guides the spindle assembly checkpoint signaling during mitotic chromosome segregation in metazoans. Recent studies have shown that ZW10 is also involved in membrane-bound organelle interactions during interphase and plays a vital role in membrane transport between the endoplasmic reticulum and Golgi apparatus. Despite these findings, the precise molecular mechanisms by which ZW10 regulates interactions between membrane-bound organelles in interphase and the assembly of membraneless organelle kinetochore in mitosis remain elusive. Here, we highlight how ZW10 forms context-dependent protein complexes during the cell cycle. These complexes are essential for mediating membrane trafficking in interphase and ensuring the accurate segregation of chromosomes in mitosis.</p>","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11757092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141236270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Sterile activation of RNA-sensing pathways in autoimmunity. 无菌激活自身免疫中的 RNA 传感途径
IF 5.3 2区 生物学
Journal of Molecular Cell Biology Pub Date : 2024-12-20 DOI: 10.1093/jmcb/mjae029
Jiaxin Li, Junyan Zhu, Hui Yang, Fajian Hou
{"title":"Sterile activation of RNA-sensing pathways in autoimmunity.","authors":"Jiaxin Li, Junyan Zhu, Hui Yang, Fajian Hou","doi":"10.1093/jmcb/mjae029","DOIUrl":"10.1093/jmcb/mjae029","url":null,"abstract":"<p><p>RNA-sensing pathways play a pivotal role in host defense against pathogenic infections to maintain cellular homeostasis. However, in the absence of infection, certain endogenous RNAs can serve as the activators of RNA-sensing pathways as well. The inappropriate activation of RNA-sensing pathways by self-ligands leads to systemic inflammation and autoimmune diseases. In this review, we summarize current findings on the sterile activation of RNA sensors, as well as its implications in autoimmunity, inflammatory diseases, and therapeutics.</p>","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11659683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141982557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
PHLDA2 is critical for p53-mediated ferroptosis and tumor suppression. PHLDA2 对 p53 介导的铁变态反应和肿瘤抑制至关重要。
IF 5.3 2区 生物学
Journal of Molecular Cell Biology Pub Date : 2024-12-20 DOI: 10.1093/jmcb/mjae033
Xin Yang, Wei Gu
{"title":"PHLDA2 is critical for p53-mediated ferroptosis and tumor suppression.","authors":"Xin Yang, Wei Gu","doi":"10.1093/jmcb/mjae033","DOIUrl":"10.1093/jmcb/mjae033","url":null,"abstract":"","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11713609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Single-cell landscape of alternative polyadenylation in human lymphoid hematopoiesis. 人类淋巴造血过程中替代多腺苷酸化的单细胞图谱。
IF 5.3 2区 生物学
Journal of Molecular Cell Biology Pub Date : 2024-12-20 DOI: 10.1093/jmcb/mjae027
Jiaqi Qiang, Shan Yu, Jun Li, Yu Rong, Xiaoshuang Wang, Yong Zhu, Fang Wang
{"title":"Single-cell landscape of alternative polyadenylation in human lymphoid hematopoiesis.","authors":"Jiaqi Qiang, Shan Yu, Jun Li, Yu Rong, Xiaoshuang Wang, Yong Zhu, Fang Wang","doi":"10.1093/jmcb/mjae027","DOIUrl":"10.1093/jmcb/mjae027","url":null,"abstract":"<p><p>Alternative polyadenylation (APA) is an essential post-transcriptional process that produces mature mRNA isoforms by regulating the usage of polyadenylation sites (PASs). APA is involved in lymphocyte activation; however, its role throughout the entire differentiation trajectory remains elusive. Here, we analyzed single-cell 3'-end transcriptome data from healthy subjects to construct a dynamic-APA landscape from hematopoietic stem and progenitor cells (HSPCs) to terminally differentiated lymphocytes. This analysis covered 19973 cells of 12 clusters from five lineages (B cells, CD4+ T cells, CD8+ T cells, natural killer cells, and plasmacytoid dendritic cells). A total of 2364 genes exhibited differential 3'-untranslated region (3'UTR) PAS usage, and 3021 genes displayed differential intronic cleavage during lymphoid differentiation. We observed a global trend of 3'UTR shortening during lymphoid differentiation. Nevertheless, specific events of both 3'UTR shortening and lengthening were also identified within each cluster. The APA patterns delineated three differentiation stages: HSPCs, precursor cells, and mature cells. Moreover, we demonstrated that the conversion of naïve T cells to memory T cells was accompanied by dynamic APA in transcription factor-encoding genes (TCF7 and NFATC2IP), immune function-related genes (BCL2, CD5, CD28, GOLT1B, and TMEM59), and protein ubiquitination-related genes (UBE2G1, YPEL5, and SUMO3). These findings expand our understanding of the underlying molecular mechanisms of APA and facilitate studies on the regulatory role of APA in lymphoid hematopoiesis.</p>","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141563561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Prospects for PARG inhibitors in cancer therapy. PARG 抑制剂在癌症治疗中的应用前景。
IF 5.3 2区 生物学
Journal of Molecular Cell Biology Pub Date : 2024-12-12 DOI: 10.1093/jmcb/mjae050
Yangchan Hu, Yuxin Meng, Zirui Zhuang, Yuancong Li, Junjun Nan, Ning Xu, Zu Ye, Ji Jing
{"title":"Prospects for PARG inhibitors in cancer therapy.","authors":"Yangchan Hu, Yuxin Meng, Zirui Zhuang, Yuancong Li, Junjun Nan, Ning Xu, Zu Ye, Ji Jing","doi":"10.1093/jmcb/mjae050","DOIUrl":"https://doi.org/10.1093/jmcb/mjae050","url":null,"abstract":"<p><p>Poly(ADP-ribose) glycosylhydrolase (PARG) is an enzyme involved in hydrolyzing the ribose-ribose bonds present in poly(ADP-ribose) (PAR), which are primarily found in the nucleus. Along with poly(ADP-ribose) polymerase (PARP), PARG regulates the level of PAR in cells, playing a crucial role in DNA maintenance and repair processes. Recent studies have revealed elevated levels of PARG in various cancers, such as breast, liver, prostate, and esophageal cancers, indicating a link to unfavorable cancer outcomes. PARG is a significant molecular target for treating PAR-related cancers. This review provides a comprehensive overview of the physiological role of PARG and the development of its inhibitors, highlighting its potential as an innovative target for cancer treatment.</p>","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Blockade of TNF-α/TNFR2 signalling suppresses colorectal cancer and enhances the efficacy of anti-PD1 immunotherapy by decreasing CCR8+T regulatory cells. 阻断TNF-α/TNFR2信号抑制结直肠癌癌症,并通过减少CCR8+T调节细胞来增强抗PD1免疫疗法的疗效。
IF 5.3 2区 生物学
Journal of Molecular Cell Biology Pub Date : 2024-11-25 DOI: 10.1093/jmcb/mjad067
Yixian Guo, Feng Xie, Xu Liu, Shouyu Ke, Jieqiong Chen, Yi Zhao, Ning Li, Zeyu Wang, Gang Yi, Yanying Shen, Dan Li, Chunchao Zhu, Zizhen Zhang, Gang Zhao, Hong Lu, Bin Li, Wenyi Zhao
{"title":"Blockade of TNF-α/TNFR2 signalling suppresses colorectal cancer and enhances the efficacy of anti-PD1 immunotherapy by decreasing CCR8+T regulatory cells.","authors":"Yixian Guo, Feng Xie, Xu Liu, Shouyu Ke, Jieqiong Chen, Yi Zhao, Ning Li, Zeyu Wang, Gang Yi, Yanying Shen, Dan Li, Chunchao Zhu, Zizhen Zhang, Gang Zhao, Hong Lu, Bin Li, Wenyi Zhao","doi":"10.1093/jmcb/mjad067","DOIUrl":"10.1093/jmcb/mjad067","url":null,"abstract":"<p><p>The enrichment of regulatory T cells (Tregs) in the tumour microenvironment (TME) has been recognized as one of the major factors in the initiation and development of resistance to immune checkpoint inhibitors. C-C motif chemokine receptor 8 (CCR8), a marker of activated suppressive Tregs, has a significant impact on the functions of Tregs in the TME. However, the regulatory mechanism of CCR8 in Tregs remains unclear. Here, we revealed that a high level of TNF-α in the colorectal cancer (CRC) microenvironment upregulated CCR8 expression in Tregs via the TNFR2/NF-κB signalling pathway and the FOXP3 transcription factor. Furthermore, in both anti-programmed cell death protein 1 (anti-PD1)-responsive and anti-PD1-unresponsive tumour models, PD1 blockade induced CCR8+ Treg infiltration. In both models, Tnfr2 depletion or TNFR2 blockade suppressed tumour progression by reducing CCR8+ Treg infiltration and thus augmented the efficacy of anti-PD1 therapy. Finally, we identified that TNFR2+CCR8+ Tregs but not total Tregs were positively correlated with adverse prognosis in patients with CRC and gastric cancer. Our work reveals the regulatory mechanisms of CCR8 in Tregs and identifies TNFR2 as a promising target for immunotherapy.</p>","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11587560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71482559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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