Cell Death and Differentiation最新文献

{"title":"hMTR4 promotes p53 protein degradation and tumor growth by accelerating rRNA processing and regulating the RPL5-MDM2 axis","authors":"Chen Xie, Xin-Ling Liang, Bin Chen, Sui Chen, Fang-Xin Xiong, Qi-Cheng Wang, Zhan-Li Chen, Feng-Jun He, Yihang Pan, Shi-Mei Zhuang","doi":"10.1038/s41418-025-01541-4","DOIUrl":"https://doi.org/10.1038/s41418-025-01541-4","url":null,"abstract":"<p>hMTR4 is an RNA helicase and an essential co-factor for the nuclear RNA exosome. Its role in the p53 pathway and cell cycle control remains unknown. Here, gain- and loss-of-function analyses in cell models showed that hMTR4 could not affect p53 mRNA levels, but decreased the levels of p53 protein and its downstream target genes by promoting p53 ubiquitination and degradation, thus accelerating cell cycle progression. These effects of hMTR4 were abrogated by nutlin-3A, an inhibitor of E3 ligase MDM2. Mechanistically, hMTR4 promoted rRNA processing in an RNA helicase-dependent manner, thus increased the amount of mature rRNA to bind ribosomal protein L5 (RPL5), resulted in sequestration of RPL5 in the nucleolus and reduced binding of RPL5 to MDM2 in the nucleoplasm, consequently promoted MDM2-mediated degradation of p53 protein. Silencing RPL5 blocked the effect of hMTR4 knockdown in upregulating p53, while hMTR4 overexpression abrogated the role of RPL5 in stimulating p53 activity. Interestingly, hMTR4 reduced the mRNA levels of p53-target genes via repressing p53 activity rather than promoting their RNA degradation. These findings disclose a novel hMTR4-rRNA-RPL5-MDM2-p53 axis and highlight hMTR4 and rRNA processing as important regulators of the p53 pathway. Further investigations on clinical samples showed that hMTR4 and RPL5 were frequently upregulated in different malignancies, including hepatocellular carcinoma (HCC), and they exhibited a positive correlation. High hMTR4 level was correlated with high recurrence of HCC, among patients with high RPL5 levels and wildtype p53 in tumors. Studies using mouse xenograft models revealed that silencing Skiv2l2 (the homologue of human hMTR4) in mouse hepatoma cells inhibited xenograft development, and tumor growth was suppressed by intratumoral injection of antisense oligonucleotides (ASO) targeting Skiv2l2. These data suggest the significance of hMTR4 overexpression in promoting tumor growth and its potential as a therapeutic target.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"6 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144612800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GLUL mediates FOXO3 O-GlcNAcylation to regulate the osteogenic differentiation of BMSCs and senile osteoporosis","authors":"Lu Zhang, Bao Qi, Yanpeng Li, Xiao Liang, Zifang Zhang, Tao Yang, Shu Jia, Xu Gao, Shang Chen, Guangjun Jiao, Yangyang Li, Hongming Zhou, Yunzhen Chen, Yanming Li, Bin Zhang, Gang Li, Chunyang Meng","doi":"10.1038/s41418-025-01543-2","DOIUrl":"https://doi.org/10.1038/s41418-025-01543-2","url":null,"abstract":"<p>The abnormal osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) is an important cause of senile osteoporosis (SOP). Glutamine synthetase (GLUL) is a key enzyme in glutamine biosynthesis; however, its functional role in SOP remains unclear. Here, we found that GLUL expression was downregulated in the BMSCs of SOP patients. Mice with BMSC-specific <i>Glul</i>-knockout (KO) exhibited dysplasia of the skull and phalanges and osteoporosis due to disordered osteogenic differentiation. Mechanistically, GLUL competitively bound to the Tripartite Motif Containing 25 (TRIM25) SPRY subunit, reduced the ubiquitin-mediated degradation of UDP-N-acetylglucosamine pyrophosphorylase 1 (UAP1) and increased the synthesis of uridine 5-diphosphate N-acetylglucosamine (UDP-GlcNAc), thereby regulating the O-linked β-N-acetylglucosamine modification (O-GlcNAcylation) of serine 296 residues and increasing Forkhead Box O3 (FOXO3) stability to reduce oxidative stress. Moreover, blocking the O-GlcNAcylation of FOXO3 at Ser296 inhibited osteogenic differentiation. Finally, GLUL supplementation specifically in BMSCs slowed bone loss in SOP model mice. Overall, our study suggests that GLUL plays an important role in regulating osteogenic differentiation and bone development, which may have implications for SOP treatment.</p><figure><p>Schematic illustration of the molecular mechanism by which GLUL mediates FOXO3 O-GlcNAcylation to regulate the osteogenic differentiation of BMSCs and senile osteoporosis. The graphical abstract was created by figdraw2.0.</p></figure>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"9 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144610974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The PLEKHA1-TACC2 fusion gene drives tumorigenesis via vascular mimicry formation in esophageal squamous-cell carcinoma.","authors":"Ting Yang, Zhi-Rui Lin, Tian-Liang Xia, Shang-Xin Liu, Bo-Yu Yuan, Yi-Ling Luo, Wen-Ting Du, Chao-Bo Lei, Yong-Zhan Nie, Mu-Sheng Zeng, Qian Zhong","doi":"10.1038/s41418-025-01536-1","DOIUrl":"https://doi.org/10.1038/s41418-025-01536-1","url":null,"abstract":"<p><p>Despite advancements of diagnosis and multimodality therapies in esophageal squamous-cell carcinoma (ESCC), the survival is still unsatisfactory. Therefore, it is urgent to identify novel targets for efficient therapeutic strategies. Herein, we identify a fusion gene between PLEKHA1 and TACC2 generated by chromosomal rearrangement by performing RNA sequencing from ESCC tissues. PLEKHA1-TACC2 transcripts are present in ESCC (66/404, 16.3%) and head and neck squamous cell carcinoma (58/402, 14.4%) tissues, correlated with poor prognosis of patients. Mechanistically, the fusion proteins upregulate the EphA2/AKT/MMP2 signaling pathway and promote vascular mimicry formation by reducing the ubiquitylation of EphA2. Moreover, EphA2 inhibitors dasatinib and ALW II-41-27 remarkably suppress the progression of tumors expressing PLEKHA1-TACC2 in vivo. Functionally, PLEKHA1-TACC2 fusion and Trp53 deletion significantly increases tumor incidence, tumor multiplicity, and mouse mortality in transgenic ESCC mouse model, which could be suppressed by regorafenib, a EphA2 inhibitor approved by FDA in solid tumors. Together, our data indicate that PLEKHA1-TACC2 fusion protein has oncogenic activities and serves as a promising prognosis marker and therapeutic target.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":" ","pages":""},"PeriodicalIF":13.7,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144564623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GSDME-mediated pyroptosis in microglia exacerbates demyelination and neuroinflammation in multiple sclerosis: insights from humans and cuprizone-induced demyelination model mice","authors":"Danjie Wang, Tongtong Zhang, Qi Shao, Xinyi Wu, Xiaoqiang Zhao, Hongyu Zhang, Yumeng Wang, Jingxian Sun, Xuechun Chang, Keying Zhu, Shuai Wu, Li Cao, Wankun Chen, Jun Wang","doi":"10.1038/s41418-025-01537-0","DOIUrl":"https://doi.org/10.1038/s41418-025-01537-0","url":null,"abstract":"<p>Demyelination, a hallmark of multiple sclerosis (MS), disrupts neural conduction due to myelin sheath degradation. Microglia-mediated inflammation plays a pivotal role in this process, with emerging evidence implicating gasdermin E (GSDME) in neuroinflammation and neurodegeneration. However, the specific role of GSDME in MS remains unclear. Here, we investigated the involvement of GSDME in MS using brain tissues from MS patients and cuprizone (CPZ)-induced demyelination model mice. We observed elevated GSDME expression in the central nervous system (CNS) lesions of MS patients, with pronounced GSDME cleavage in microglia at injury sites. Genetic knockout of <i>Gsdme</i> alleviated CPZ-induced motor deficits, demyelination, and neuroinflammation. Furthermore, caspase-3 inhibition significantly suppressed GSDME activation, resulting in reduced demyelination, motor coordination impairment, and neuroinflammation. In an experimental autoimmune encephalomyelitis (EAE) model, caspase-3/GSDME-mediated microglial pyroptosis critically mediated the progression of neuroinflammation and white matter demyelination. Transcriptome sequencing revealed that GSDME regulated the expression of genes related to disease-associated microglia (DAMs) and impaired microglial autophagy, a process critical for myelin debris clearance. <i>Gsdme</i> knockout downregulated the expression of genes associated with DAMs and CPZ-induced microglia-driven demyelination while increasing the expression of remyelination-related genes (<i>Cybb</i> and <i>Cd74</i>). In vitro, GSDME suppression promoted microglial autophagy and myelin debris clearance. Collectively, our findings highlight GSDME-mediated pyroptosis as a key driver of demyelination and neuroinflammation in MS, suggesting novel therapeutic targets for neuroinflammatory disorders.</p><figure></figure>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"36 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144479013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"p53 prophylactic therapy for cancer prevention","authors":"Christian Krueger, Kanaga Sabapathy","doi":"10.1038/s41418-025-01538-z","DOIUrl":"https://doi.org/10.1038/s41418-025-01538-z","url":null,"abstract":"<p>Germline mutations in the tumor suppressor <i>TP53</i> lead to cancer predisposition, as seen in Li-Fraumeni syndrome (LFS). Currently, no strategies exist to delay or prevent cancer development in this population. Our work is based on the hypothesis that modulating wild-type p53 levels could serve as a prophylactic approach to mitigate cancer risk. By introducing a third copy of <i>Trp53</i>, either constitutively or in an inducible manner in adulthood, we demonstrate that tumor development is delayed, and mice live longer without observable side effects in both the <i>Eu-myc</i> lymphoma and LFS models. Mechanistically, <i>Trp53</i> loss of heterozygosity is reduced in the LFS model, accompanied by an enhanced p53 transcriptional response. Our findings therefore provide genetic evidence supporting this approach, which could be leveraged to identify compounds that modulate p53 levels and benefit LFS carriers and other cancer-prone populations with reduced p53 activity.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"35 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144488898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cullin-associated and neddylation-dissociated protein 1 (CAND1) promotes cardiomyocyte proliferation and heart regeneration by enhancing the ubiquitinated degradation of Mps one binder kinase activator 1b (Mob1b)","authors":"Xingda Li, Lingmin Zhang, Tao Tian, Yao Pei, Kaile Wang, Shuang Wang, Xuan Ning, Pinhan Zhao, Yueying Qu, Haiyu Gao, Chenhong Li, Xuening Liu, Jiming Yang, Yingzi Zhang, Hongbin Gao, Lina Xuan, Yang Zhang, Yanjie Lu, Benzhi Cai, Baofeng Yang, Zhenwei Pan","doi":"10.1038/s41418-025-01540-5","DOIUrl":"https://doi.org/10.1038/s41418-025-01540-5","url":null,"abstract":"<p>Activation of the intrinsic regenerative potential of adult mammalian hearts by promoting cardiomyocyte proliferation holds great potential in heart repair. CAND1 (Cullin-associated and neddylation-dissociated protein 1) functions as a critical regulator of cellular protein homeostasis by fine-tuning the ubiquitinated degradation of specific abnormally expressed protein substrates. Here, we identified that cardiac-specific transgenic overexpression of CAND1 reduced the infarct size, restored cardiac function, and promoted cardiomyocyte proliferation after myocardial infarction in juvenile (7-day-old) and adult (8-week-old) mice. Conversely, CAND1 deficiency blunted the regenerative capacity of neonatal hearts after apex resection. MS and functional verification demonstrated that CAND1 enhanced the assembly of Cullin1, FBXW11(F-box/WD repeat-containing protein 11), and Mob1b (Mps one binder kinase activator 1b) complexes, and thus promotes the degradation of Mob1b. The ubiquitination of Mob1b occurred at K108 and was linked by K48 of ubiquitin. Mob1b deletion partially rescued the loss of regenerative capacity in neonatal hearts induced by CAND1 deficiency and improved cardiac function in adult mice post-MI. Moreover, CAND1 promoted the proliferation of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). Our data demonstrate that CAND1 promotes cardiomyocyte proliferation via FBXW11-mediated K48-linked ubiquitination degradation of Mob1b, and improves heart regeneration after cardiac injury. The findings provide a novel strategy to promote cardiac regeneration and repair.</p><figure><p>Schematic diagram of the role of CAND1 in regulating ubiquitination and degradation of Mob1b and cardiomyocyte proliferation and heart regeneration. Under CAND1-High condition, CAND1 promotes the incorporation of Cullin1, FBXW11, and Mob1b complexes, and accelerates SCF^FBXW11-mediated K48-linked ubiquitination of Mob1b at the K108 site, which leads to the degradation of Mob1b and thus suppresses the Hippo signaling pathway and facilitates cardiomyocyte proliferation and heart regeneration post-MI.</p></figure>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"45 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144371137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic targeting of cancer cells through simultaneous inhibition of key metabolic enzymes","authors":"Jan Dreute, Julia Stengel, Jonas Becher, David van den Borre, Maximilian Pfisterer, Marek Bartkuhn, Vanessa M. Beutgen, Benardina Ndreshkjana, Ulrich Gärtner, Johannes Graumann, Michael Huck, Stephan Klatt, Chloe Leff, Henner F. Farin, Andrea Nist, Roland Schmitz, Thorsten Stiewe, Julia Teply-Szymanski, Jochen Wilhelm, Alfredo Cabrera-Orefice, M. Lienhard Schmitz","doi":"10.1038/s41418-025-01532-5","DOIUrl":"https://doi.org/10.1038/s41418-025-01532-5","url":null,"abstract":"<p>As cancer cell specific rewiring of metabolic networks creates potential therapeutic opportunities, we conducted a synthetic lethal screen utilizing inhibitors of metabolic pathways. Simultaneous administration of (R)-GNE-140 and BMS-986205 (Linrodostat) preferentially halted proliferation of ovarian cancer cells, but not of their non-oncogenically transformed progenitor cells. While (R)-GNE-140 inhibits lactate dehydrogenase (LDH)A/B and thus effective glycolysis, BMS-986205, in addition to its known inhibitory activity on Indoleamine 2,3-dioxygenase (IDO1), also restricts oxidative phosphorylation (OXPHOS), as revealed here. BMS-986205, which is being tested in multiple Phase III clinical trials, inhibits the ubiquinone reduction site of respiratory complex I and thus compromises mitochondrial ATP production. The energetic catastrophe caused by simultaneous interference with glycolysis and OXPHOS resulted in either cell death or the induction of senescence in tumor cells, with the latter being eliminated by senolytics. The frequent synergy observed with combined inhibitor treatment was comprehensively confirmed through testing on tumor cell lines from the DepMap panel and on human colorectal cancer organoids. These experiments revealed highly synergistic activity of the compounds in a third of the tested tumor cell lines, correlating with alterations in genes with known roles in metabolic regulation and demonstrating the therapeutic potential of metabolic intervention.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"26 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144341112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanisms of immune cell death in immunosenescence","authors":"Joost Verduijn, Kelly Coutant, Mitchell E. Fane, Lorenzo Galluzzi","doi":"10.1038/s41418-025-01535-2","DOIUrl":"https://doi.org/10.1038/s41418-025-01535-2","url":null,"abstract":"<p>Along with organismal aging, multiple compartments of the immune system undergo a progressive functional degeneration that may contribute to – or at least allow for – disease, a scenario that is commonly known as “immunosenescence”. While not all immune cell populations suffer from organismal aging through similar mechanisms, immunosenescence appears to involve numerical alterations in specific immune cell types that – at least in some settings – result from the unscheduled activation of regulated cell death (RCD), often along with unbalanced hematopoietic output downstream of thymic involution and bone marrow defects. Here, we critically discuss core RCD mechanisms including apoptosis, necroptosis, ferroptosis, pyroptosis and NETosis as key regulators of global immune homeostasis in the context of immunosenescence.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"12 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144341027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial cells-derived SEMA3G suppresses glioblastoma stem cells by inducing c-Myc degradation","authors":"Peng-Xiang Min, Li-Li Feng, Yi-Xuan Zhang, Chen-Chen Jiang, Hong-Zhen Zhang, Yan Chen, Kohji Fukunaga, Fang Liu, Yu-Jie Zhang, Takuya Sasaki, Xu Qian, Katsuhisa Horimoto, Jian-Dong Jiang, Ying-Mei Lu, Feng Han","doi":"10.1038/s41418-025-01534-3","DOIUrl":"https://doi.org/10.1038/s41418-025-01534-3","url":null,"abstract":"<p>The poor prognosis of glioblastoma (GBM) patients is attributed mainly to abundant neovascularization and presence of glioblastoma stem cells (GSCs). GSCs are preferentially localized to the perivascular niche to maintain stemness. However, the effect of abnormal communication between endothelial cells (ECs) and GSCs on GBM progression remains unknown. Here, we reveal that ECs-derived SEMA3G, which is aberrantly expressed in GBM patients, impairs GSCs by inducing c-Myc degradation. SEMA3G activates NRP2/PLXNA1 in a paracrine manner, subsequently inducing the inactivation of Cdc42 and dissociation of Cdc42 and WWP2 in GSCs. Once released, WWP2 interacts with c-Myc and mediates c-Myc degradation via ubiquitination. Genetic deletion of <i>Sema3G</i> in ECs accelerates GBM growth, whereas <i>SEMA3G</i> overexpression or recombinant SEMA3G protein prolongs the survival of GBM bearing mice. These findings illustrate that ECs play an intrinsic inhibitory role in GSCs stemness via the SMEA3G-c-Myc distal regulation paradigm. Targeting SEMA3G signaling may have promising therapeutic benefits for GBM patients.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"45 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144311686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Daniel Aberdam, the legacy of a mentor.","authors":"Huiqing Zhou, Bernard Attali, Neil Lagali, Ruby Shalom-Feuerstein","doi":"10.1038/s41418-025-01520-9","DOIUrl":"https://doi.org/10.1038/s41418-025-01520-9","url":null,"abstract":"","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":" ","pages":""},"PeriodicalIF":13.7,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}