发布求助
文献互助 智能选刊 最新文献

FEBS Letters最新文献

筛选
英文 中文
DNA ligase LigE increases bacterial transformation with damaged extracellular DNA. DNA连接酶LigE增加细菌与受损细胞外DNA的转化。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-10-15 DOI: 10.1002/1873-3468.70483
Jolyn Pan, Avi Singh, Shrawani Weralupe Gamladdalage, Joanna Hicks, Adele Williamson
{"title":"DNA ligase LigE increases bacterial transformation with damaged extracellular DNA.","authors":"Jolyn Pan, Avi Singh, Shrawani Weralupe Gamladdalage, Joanna Hicks, Adele Williamson","doi":"10.1002/1873-3468.70483","DOIUrl":"https://doi.org/10.1002/1873-3468.70483","url":null,"abstract":"<p><p>LigE is a periplasm-targeted ATP-dependent DNA ligase found in many Gram-negative bacteria, including Neisseria gonorrhoeae. Although LigE has been shown to have a role in biofilm formation, many LigE-possessing bacteria are also naturally competent, suggesting a possible role in transformation with extracellular DNA. Here, we demonstrate that LigE participates in competence by increasing transformation with nuclease-damaged extracellular DNA that contains single-stranded or cohesive breaks, and that this activity is dependent on its secretion signal peptide, indicating an extra-cytoplasmic location of activity. We show that increased transformation with this restricted DNA is ATP-dependent; however, the physiological source of ATP in the natural host remains unknown. Our findings highlight a potential role of Ngo-LigE in Neisseria gonorrhoeae competence and horizontal gene transfer.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149192217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Collaborating with AIProSaB-A researcher's perspective on patient advocacy for progeria. 与aiprob - a合作，研究患者倡导早衰症的观点。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-10-13 DOI: 10.1002/1873-3468.70481
Giovanna Lattanzi, Lavinia Arseni
{"title":"Collaborating with AIProSaB-A researcher's perspective on patient advocacy for progeria.","authors":"Giovanna Lattanzi, Lavinia Arseni","doi":"10.1002/1873-3468.70481","DOIUrl":"https://doi.org/10.1002/1873-3468.70481","url":null,"abstract":"<p><p>Progeria is an extremely rare genetic disease in which affected individuals age rapidly due to a specific mutation in the LMNA gene, which results in the production of progerin, an abnormal protein that damages cell nuclei and causes progressive multi-organ disease. AIProSaB is an Italian association founded by Sammy Basso, who was diagnosed with progeria at the age of two, and by his parents. The association supports research, promotes experimental therapies, and provides information for families and clinicians, with a strong emphasis on understanding LMNA/progerin biology and developing targeted treatments and gene-editing approaches. As part of our series on patient advocacy, FEBS Letters interviews Dr. Giovanna Lattanzi, a researcher at the CNR Institute of Molecular Genetics 'Luigi Luca Cavalli-Sforza' in Bologna on the aims, achievements, and activities of AIProSaB.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Interaction and co-phase separation of SARS-CoV-2 nucleocapsid protein and human hnRNPA1 and its implications for viral life cycle SARS-CoV-2核衣壳蛋白与人hnRNPA1的相互作用、共相分离及其对病毒生命周期的影响
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-10-12 Epub Date: 2026-05-28 DOI: 10.1002/1873-3468.70375
Parul Gupta, Risabh Sahu, Iman Nandi, Subba Rao Gangi Setty, Saumitra Das, Mahavir Singh
{"title":"Interaction and co-phase separation of SARS-CoV-2 nucleocapsid protein and human hnRNPA1 and its implications for viral life cycle","authors":"Parul Gupta,&nbsp;Risabh Sahu,&nbsp;Iman Nandi,&nbsp;Subba Rao Gangi Setty,&nbsp;Saumitra Das,&nbsp;Mahavir Singh","doi":"10.1002/1873-3468.70375","DOIUrl":"10.1002/1873-3468.70375","url":null,"abstract":"<p>The nucleocapsid (N) protein of SARS-CoV-2 is central to viral assembly and replication. It binds the viral RNA to form a helical nucleocapsid and enables genome packaging and its release into host cells. Human heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1), one of the most abundant RNA-binding proteins in eukaryotes, regulates key aspects of RNA metabolism, including splicing, transcription, localisation, and transport. Here, we report a direct physical interaction between the SARS-CoV-2 N protein and hnRNPA1, primarily mediated through their intrinsically disordered regions. Furthermore, we found that these proteins co-phase separate <i>in vitro</i> and colocalise within stress granules in cells. <i>In vivo</i> studies reveal that hnRNPA1 suppresses viral replication, suggesting that the N protein–hnRNPA1 interaction plays an important role in modulating the viral life cycle.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 19","pages":"2929-2946"},"PeriodicalIF":3.0,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The dual role of lectins in cancer—immunotherapy tools and therapeutic targets 凝集素在癌症免疫治疗工具和治疗靶点中的双重作用。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-10-12 Epub Date: 2026-07-04 DOI: 10.1002/1873-3468.70406
Milena Dziewicka, Agnieszka Graczyk-Jarzynka
{"title":"The dual role of lectins in cancer—immunotherapy tools and therapeutic targets","authors":"Milena Dziewicka,&nbsp;Agnieszka Graczyk-Jarzynka","doi":"10.1002/1873-3468.70406","DOIUrl":"10.1002/1873-3468.70406","url":null,"abstract":"<p>Altered glycosylation is a hallmark of cancer that shapes immune recognition within the tumor microenvironment. Lectins—glycan-binding proteins—play a dual role in this process: they interpret tumor-associated glycan patterns and can also be exploited as therapeutic tools. In this review, we discuss emerging strategies that harness lectins in cancer immunotherapy. Engineered lectin-based constructs, including antibody–lectin chimeras, lectin–drug conjugates, and glycan-targeting CAR-T cells, enable recognition of tumor-specific glycosylation signatures. At the same time, endogenous lectin pathways such as the galectin-polyLacNAc and sialic acid-Siglec axes function as glyco-immune checkpoints that suppress anti-tumor responses and represent promising therapeutic targets. Understanding how lectins regulate tumor–immune interactions may guide the development of next-generation immunotherapies integrating antigen recognition with glycan sensing.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 19","pages":"2817-2832"},"PeriodicalIF":3.0,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70406","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148381827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Epigenetic reprogramming of lineage switching in cancer 癌症谱系转换的表观遗传重编程。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-10-12 Epub Date: 2026-08-15 DOI: 10.1002/1873-3468.70433
Ezgi Boyvatlı, Burcu Akman, Ezgi Bağırsakçı, Nese Atabey, Serap Erkek-Ozhan
{"title":"Epigenetic reprogramming of lineage switching in cancer","authors":"Ezgi Boyvatlı,&nbsp;Burcu Akman,&nbsp;Ezgi Bağırsakçı,&nbsp;Nese Atabey,&nbsp;Serap Erkek-Ozhan","doi":"10.1002/1873-3468.70433","DOIUrl":"10.1002/1873-3468.70433","url":null,"abstract":"<p>Lineage plasticity develops as tumor cells overcome terminal differentiation barriers, adapt to environmental stressors, and acquire metastatic, therapy-resistant phenotypes. These phenotypic transitions are driven by nonmutational epigenetic mechanisms, including dynamic shifts in chromatin accessibility, histone modifications, DNA methylation, and noncoding RNA activity beyond genetic alterations. While epithelial–mesenchymal plasticity (EMP) remains a foundational model, cancer-cell plasticity extends into a broader pan-plasticity spectrum encompassing dedifferentiation, transdifferentiation into neuroendocrine or squamous lineages, and stem cell–like reprogramming. In this review, we evaluate how the antagonistic interplay between Polycomb and Trithorax complexes, chromatin modifier activity, and enhancer reprogramming affects lineage identity and enables multi-lineage plasticity in cancer. We further discuss extrinsic mechanisms reinforced by the tumor microenvironment, particularly hypoxia, chronic inflammation, and metabolic stress, that rewire the epigenetic landscape to stabilize plastic states. Collectively, these data underscore epigenetic deregulation as a primary driver of lineage plasticity and intratumoral heterogeneity, while revealing therapeutic vulnerabilities and the potential to reverse plasticity and overcome therapy resistance by targeting the epigenome.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 19","pages":"2850-2873"},"PeriodicalIF":3.0,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70433","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148759223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Decoding the dynamic extracellular matrix in cancer—3D models and bioscaffolds rewire the rules of tumor progression 解码癌症三维模型和生物支架中的动态细胞外基质，重新连接肿瘤进展的规则。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-10-12 Epub Date: 2026-07-03 DOI: 10.1002/1873-3468.70402
Sylvia Mangani, Konstantinos Spanopoulos, Zoi Piperigkou, Nikos K. Karamanos
{"title":"Decoding the dynamic extracellular matrix in cancer—3D models and bioscaffolds rewire the rules of tumor progression","authors":"Sylvia Mangani,&nbsp;Konstantinos Spanopoulos,&nbsp;Zoi Piperigkou,&nbsp;Nikos K. Karamanos","doi":"10.1002/1873-3468.70402","DOIUrl":"10.1002/1873-3468.70402","url":null,"abstract":"<p>Cancer progression is regulated by the dynamic matrix code of the tumor microenvironment, which influences cellular behavior and disease development. Importantly, matrix remodeling in three-dimensional cancer models more accurately reflects <i>in vivo</i> conditions compared to conventional two-dimensional systems. Matrix engineering through bioscaffolds supports physiologically relevant tumor modeling, while matrix-based platforms offer valuable tools for preclinical research and therapeutic development.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 19","pages":"2874-2875"},"PeriodicalIF":3.0,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70402","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148381849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Proteasomes in extracellular vesicles—Emerging roles in cancer progression and intercellular communication 细胞外囊泡中的蛋白酶体-在癌症进展和细胞间通讯中的新作用。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-10-12 Epub Date: 2026-07-21 DOI: 10.1002/1873-3468.70416
Irina Viktorovna Kondakova, Natalia Valerievna Yunusova, Evgenia Alexandrovna Sidenko, Alexey Anatolievich Belogurov, Vadim L'vovich Karpov, Alexey Vladimirovich Morozov
{"title":"Proteasomes in extracellular vesicles—Emerging roles in cancer progression and intercellular communication","authors":"Irina Viktorovna Kondakova,&nbsp;Natalia Valerievna Yunusova,&nbsp;Evgenia Alexandrovna Sidenko,&nbsp;Alexey Anatolievich Belogurov,&nbsp;Vadim L'vovich Karpov,&nbsp;Alexey Vladimirovich Morozov","doi":"10.1002/1873-3468.70416","DOIUrl":"10.1002/1873-3468.70416","url":null,"abstract":"<p>Intercellular communication via extracellular vesicles (EVs) is a means by which cells exchange various molecules, including proteins, protein complexes, lipids, nucleic acids, and others. This communication is essential for cellular adaptation to stress, the formation of specialized niches, and the maintenance of homeostasis in organs and tissues. Recent studies have shown that proteasomes, which are multi-subunit cellular proteases, play an emerging role in these processes. The transfer of proteasomes from one cell to another affects the profile of peptides presented on cell membranes, prevents the accumulation of potentially toxic protein aggregates, and modulates various cellular signaling pathways. This review summarizes the current understanding of the significance and mechanisms of proteasome transfer between cells via EVs, with a focus on cancer.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 19","pages":"2833-2849"},"PeriodicalIF":3.0,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70416","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
KSRP-dependent immunogenic cell death induced by pyridazinone derivative IMB5036 drives antitumor immunity in neuroblastoma 吡嗪酮衍生物IMB5036诱导的ksrp依赖性免疫原性细胞死亡驱动神经母细胞瘤的抗肿瘤免疫。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-10-12 Epub Date: 2026-05-26 DOI: 10.1002/1873-3468.70364
Yanqun Dong, Yanfeng Xu, Junyi Zhang, Hanyu Hong, Lingli Gao, Hanrui Wei, Yijia Zheng, Xing Lv, Yan-Bo Zheng, Jigang Yang, Jian-Hua Gong
{"title":"KSRP-dependent immunogenic cell death induced by pyridazinone derivative IMB5036 drives antitumor immunity in neuroblastoma","authors":"Yanqun Dong,&nbsp;Yanfeng Xu,&nbsp;Junyi Zhang,&nbsp;Hanyu Hong,&nbsp;Lingli Gao,&nbsp;Hanrui Wei,&nbsp;Yijia Zheng,&nbsp;Xing Lv,&nbsp;Yan-Bo Zheng,&nbsp;Jigang Yang,&nbsp;Jian-Hua Gong","doi":"10.1002/1873-3468.70364","DOIUrl":"10.1002/1873-3468.70364","url":null,"abstract":"<p>The small-molecule pyridazinone derivative IMB5036 (IMB) exhibits significant cytotoxicity against multiple cancer cell lines, and KH-type splicing regulatory protein (KSRP) is confirmed as its direct binding partner. However, KSRP's functional role in neuroblastoma (NB) and the mechanism mediating IMB's antitumor effects remain unclear. This study analyzed public tumor databases and found KSRP expression negatively correlates with NB patients' median survival. Experiments showed IMB induces NB cell pyroptosis, immunogenic cell death (ICD, with calreticulin exposure), and cGAS-STING activation (to boost antitumor immunity), while CRISPR-Cas9-mediated KSRP knockout notably attenuates these effects. Transcriptome sequencing further confirmed KSRP mediates IMB's regulation of HSPA6/RSAD2. This study clarifies KSRP-dependent ICD drives NB antitumor immunity, providing a basis for KSRP-targeted NB immunotherapies.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 19","pages":"2899-2916"},"PeriodicalIF":3.0,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148014135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Rab14 regulates the transport of human papillomavirus to the trans-Golgi network for infectious cell entry Rab14调节人乳头瘤病毒的运输到反式高尔基网络的感染性细胞进入。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-10-12 Epub Date: 2026-05-26 DOI: 10.1002/1873-3468.70365
Yoshiyuki Ishii, Iwao Kukimoto
{"title":"Rab14 regulates the transport of human papillomavirus to the trans-Golgi network for infectious cell entry","authors":"Yoshiyuki Ishii,&nbsp;Iwao Kukimoto","doi":"10.1002/1873-3468.70365","DOIUrl":"10.1002/1873-3468.70365","url":null,"abstract":"<p>Human papillomavirus (HPV) utilizes multiple host proteins to infect epithelial cells. Here we identified Rab14, a small GTPase belonging to the Rab family, as a critical host factor in HPV infection. Rab14 knockout (KO) cells exhibited resistance to HPV pseudovirion (PsV) infection. Confocal microscopy revealed that PsV transport to the <i>trans</i>-Golgi network (TGN) was significantly reduced in Rab14 KO cells. Reintroduction of wild-type Rab14 restored infection levels, but neither GDP-bound (S25N) nor GTP-bound (Q70L) mutants did. S25N preferentially localized to the TGN, while Q70L exhibited similar localization in the early endosome and the TGN. PsV showed reduced colocalization with S25N, whereas the opposite was observed for Q70L. These results indicate that Rab14 GTPase cycling controls HPV transport to the TGN.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 19","pages":"2917-2928"},"PeriodicalIF":3.0,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70365","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148014133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Structural insights and therapeutic targets in Acinetobacter baumannii capsule biosynthesis 鲍曼不动杆菌胶囊生物合成的结构见解和治疗靶点。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-10-12 Epub Date: 2026-06-17 DOI: 10.1002/1873-3468.70390
Woo Cheol Lee, Junho Jeong, Chae Yeong Lee, Hyunjoon Cho, Man Hwan Oh, Je Chul Lee, Jee-Young Lee, Yangmee Kim
{"title":"Structural insights and therapeutic targets in Acinetobacter baumannii capsule biosynthesis","authors":"Woo Cheol Lee,&nbsp;Junho Jeong,&nbsp;Chae Yeong Lee,&nbsp;Hyunjoon Cho,&nbsp;Man Hwan Oh,&nbsp;Je Chul Lee,&nbsp;Jee-Young Lee,&nbsp;Yangmee Kim","doi":"10.1002/1873-3468.70390","DOIUrl":"10.1002/1873-3468.70390","url":null,"abstract":"<p>Gram-negative bacteria produce nonulosonic acids, a family of nine-carbon sugars that mimic host sialic acids and may contribute to bacterial virulence. The nonulosonic acid C8-epimeric 5,7-di-<i>N</i>-acetyllegionaminic acid (8-epi-Leg5,7Ac2) is a component of the K-locus 49 (KL49) capsule of hypervirulent <i>Acinetobacter baumannii</i>, and its epimerization is proposed to be mediated by ElaA, ElaB, and ElaC. We identified a KL49 strain that induces lethal sepsis in mice and found deletion of <i>elaA</i>, <i>elaB</i>, or <i>elaC</i> abolished lethality and markedly reduced capsule production. Crystal structures of ElaB, ElaA, and ElaC revealed conserved <i>N</i>-acetyl recognition underlying CMP-Leg5,7Ac2 synthesis and regioselective C8 epimerization. Together, these genetic, structural, and <i>in vivo</i> findings identify ElaABC as potential antivirulence targets in emerging hypervirulent KL49 <i>A. baumannii</i> strains.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 19","pages":"2947-2960"},"PeriodicalIF":3.0,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70390","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
下一页 尾页
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整，为了账户安全，请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们：info@booksci.cn Book学术提供免费学术资源搜索服务，方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号：604180095
Book学术官方微信
小红书