EMBO Journal最新文献_第9页

The human disease-associated gene ZNFX1 controls inflammation through inhibition of the NLRP3 inflammasome. 人类疾病相关基因 ZNFX1 通过抑制 NLRP3 炎性体控制炎症。

IF 9.4 1区生物学

EMBO Journal Pub Date : 2024-11-01 Epub Date: 2024-09-27 DOI: 10.1038/s44318-024-00236-9

Jing Huang, Yao Wang, Xin Jia, Changfeng Zhao, Meiqi Zhang, Mi Bao, Pan Fu, Cuiqin Cheng, Ruona Shi, Xiaofei Zhang, Jun Cui, Gang Wan, Anlong Xu

{"title":"The human disease-associated gene ZNFX1 controls inflammation through inhibition of the NLRP3 inflammasome.","authors":"Jing Huang, Yao Wang, Xin Jia, Changfeng Zhao, Meiqi Zhang, Mi Bao, Pan Fu, Cuiqin Cheng, Ruona Shi, Xiaofei Zhang, Jun Cui, Gang Wan, Anlong Xu","doi":"10.1038/s44318-024-00236-9","DOIUrl":"10.1038/s44318-024-00236-9","url":null,"abstract":"Inherited deficiency of zinc finger NFX1-type containing 1 (ZNFX1), a dsRNA virus sensor, is associated with severe familial immunodeficiency, multisystem inflammatory disease, increased susceptibility to viruses, and early mortality. However, limited treatments for patients with pathological variants of ZNFX1 exist due to an incomplete understanding of the diseases resulting from ZNFX1 mutations. Here, we demonstrate that ZNFX1 specifically inhibits the activation of the NLR family pyrin domain-containing protein 3 (NLRP3) inflammasome in response to NLRP3 activators both in vitro and in vivo. ZNFX1 retains NLRP3 in the cytoplasm and prevents its accumulation in the TGN38 + /TGN46+ vesicles in the resting state. Upon NLRP3 inflammasome activation, ZNFX1 is cleaved by caspase-1, establishing a feed-forward loop that promotes NLRP3 accumulation in the trans-Golgi network (TGN) and amplifies the activity of the downstream cascade. Expression of wild-type ZNFX1, but not of ZNFX1 with human pathogenic mutations, rescues the impairment of NLRP3 inflammasome inhibition. Our findings reveal a dual role of ZNFX1 in virus sensing and suppression of inflammation, which may become valuable for the development of treatments for ZNFX1 mutation-related diseases.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"5469-5493"},"PeriodicalIF":9.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142331677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Autophagy adaptors mediate Parkin-dependent mitophagy by forming sheet-like liquid condensates. 自噬适配体通过形成片状液体凝聚体来介导依赖于Parkin的有丝分裂。

IF 9.4 1区生物学

EMBO Journal Pub Date : 2024-11-01 Epub Date: 2024-10-17 DOI: 10.1038/s44318-024-00272-5

Zi Yang, Saori R Yoshii, Yuji Sakai, Jing Zhang, Haruka Chino, Roland L Knorr, Noboru Mizushima

{"title":"Autophagy adaptors mediate Parkin-dependent mitophagy by forming sheet-like liquid condensates.","authors":"Zi Yang, Saori R Yoshii, Yuji Sakai, Jing Zhang, Haruka Chino, Roland L Knorr, Noboru Mizushima","doi":"10.1038/s44318-024-00272-5","DOIUrl":"10.1038/s44318-024-00272-5","url":null,"abstract":"During PINK1- and Parkin-mediated mitophagy, autophagy adaptors are recruited to damaged mitochondria to promote their selective degradation. Autophagy adaptors such as optineurin (OPTN) and NDP52 facilitate mitophagy by recruiting the autophagy-initiation machinery, and assisting engulfment of damaged mitochondria through binding to ubiquitinated mitochondrial proteins and autophagosomal ATG8 family proteins. Here, we demonstrate that OPTN and NDP52 form sheet-like phase-separated condensates with liquid-like properties on the surface of ubiquitinated mitochondria. The dynamic and liquid-like nature of OPTN condensates is important for mitophagy activity, because reducing the fluidity of OPTN-ubiquitin condensates suppresses the recruitment of ATG9 vesicles and impairs mitophagy. Based on these results, we propose a dynamic liquid-like, rather than a stoichiometric, model of autophagy adaptors to explain the interactions between autophagic membranes (i.e., ATG9 vesicles and isolation membranes) and mitochondrial membranes during Parkin-mediated mitophagy. This model underscores the importance of liquid-liquid phase separation in facilitating membrane-membrane contacts, likely through the generation of capillary forces.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"5613-5634"},"PeriodicalIF":9.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

PCPE-1, a brown adipose tissue-derived cytokine, promotes obesity-induced liver fibrosis. PCPE-1是一种源自棕色脂肪组织的细胞因子，可促进肥胖引起的肝纤维化。

IF 9.4 1区生物学

EMBO Journal Pub Date : 2024-11-01 Epub Date: 2024-08-19 DOI: 10.1038/s44318-024-00196-0

Yung Ting Hsiao, Yohko Yoshida, Shujiro Okuda, Manabu Abe, Seiya Mizuno, Satoru Takahashi, Hironori Nakagami, Ryuichi Morishita, Kenya Kamimura, Shuji Terai, Tin May Aung, Ji Li, Takaaki Furihata, Jing Yuan Tang, Kenneth Walsh, Akihito Ishigami, Tohru Minamino, Ippei Shimizu

{"title":"PCPE-1, a brown adipose tissue-derived cytokine, promotes obesity-induced liver fibrosis.","authors":"Yung Ting Hsiao, Yohko Yoshida, Shujiro Okuda, Manabu Abe, Seiya Mizuno, Satoru Takahashi, Hironori Nakagami, Ryuichi Morishita, Kenya Kamimura, Shuji Terai, Tin May Aung, Ji Li, Takaaki Furihata, Jing Yuan Tang, Kenneth Walsh, Akihito Ishigami, Tohru Minamino, Ippei Shimizu","doi":"10.1038/s44318-024-00196-0","DOIUrl":"10.1038/s44318-024-00196-0","url":null,"abstract":"Metabolic dysfunction-associated steatohepatitis (MASH, previously termed non-alcoholic steatohepatitis (NASH)), is a major complication of obesity that promotes fatty liver disease. MASH is characterized by progressive tissue fibrosis and sterile liver inflammation that can lead to liver cirrhosis, cancer, and death. The molecular mechanisms of fibrosis in MASH and its systemic control remain poorly understood. Here, we identified the secreted-type pro-fibrotic protein, procollagen C-endopeptidase enhancer-1 (PCPE-1), as a brown adipose tissue (BAT)-derived adipokine that promotes liver fibrosis in a murine obesity-induced MASH model. BAT-specific or systemic PCPE-1 depletion in mice ameliorated liver fibrosis, whereas, PCPE-1 gain of function in BAT enhanced hepatic fibrosis. High-calorie diet-induced ER stress increased PCPE-1 production in BAT through the activation of IRE-1/JNK/c-Fos/c-Jun signaling. Circulating PCPE-1 levels are increased in the plasma of MASH patients, suggesting a therapeutic possibility. In sum, our results uncover PCPE-1 as a novel systemic control factor of liver fibrosis.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"4846-4869"},"PeriodicalIF":9.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11535236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142005777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Mouse models to investigate in situ cell fate decisions induced by p53. 研究 p53 诱导的原位细胞命运决定的小鼠模型。

IF 9.4 1区生物学

EMBO Journal Pub Date : 2024-10-01 Epub Date: 2024-08-19 DOI: 10.1038/s44318-024-00189-z

Elizabeth Lieschke, Annabella F Thomas, Andrew Kueh, Georgia K Atkin-Smith, Pedro L Baldoni, John E La Marca, Savannah Young, Allan Shuai Huang, Aisling M Ross, Lauren Whelan, Deeksha Kaloni, Lin Tai, Gordon K Smyth, Marco J Herold, Edwin D Hawkins, Andreas Strasser, Gemma L Kelly

{"title":"Mouse models to investigate in situ cell fate decisions induced by p53.","authors":"Elizabeth Lieschke, Annabella F Thomas, Andrew Kueh, Georgia K Atkin-Smith, Pedro L Baldoni, John E La Marca, Savannah Young, Allan Shuai Huang, Aisling M Ross, Lauren Whelan, Deeksha Kaloni, Lin Tai, Gordon K Smyth, Marco J Herold, Edwin D Hawkins, Andreas Strasser, Gemma L Kelly","doi":"10.1038/s44318-024-00189-z","DOIUrl":"10.1038/s44318-024-00189-z","url":null,"abstract":"Investigating how transcription factors control complex cellular processes requires tools that enable responses to be visualised at the single-cell level and their cell fate to be followed over time. For example, the tumour suppressor p53 (also called TP53 in humans and TRP53 in mice) can initiate diverse cellular responses by transcriptional activation of its target genes: Puma to induce apoptotic cell death and p21 to induce cell cycle arrest/cell senescence. However, it is not known how these processes are regulated and initiated in different cell types. Also, the context-dependent interaction partners and binding loci of p53 remain largely elusive. To be able to examine these questions, we here developed knock-in mice expressing triple-FLAG-tagged p53 to facilitate p53 pull-down and two p53 response reporter mice, knocking tdTomato and GFP into the Puma/Bbc3 and p21 gene loci, respectively. By crossing these reporter mice into a p53-deficient background, we show that the new reporters reliably inform on p53-dependent and p53-independent initiation of both apoptotic or cell cycle arrest/senescence programs, respectively, in vitro and in vivo.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"4406-4436"},"PeriodicalIF":9.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11445477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142005776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Reassessing the unifying hypothesis for hypercontractility caused by myosin mutations in hypertrophic cardiomyopathy. 重新评估肥厚型心肌病肌球蛋白突变导致的过度收缩统一假说。

IF 9.4 1区生物学

EMBO Journal Pub Date : 2024-10-01 Epub Date: 2024-08-27 DOI: 10.1038/s44318-024-00199-x

James A Spudich, Neha Nandwani, Julien Robert-Paganin, Anne Houdusse, Kathleen M Ruppel

引用次数: 0

Author Correction: BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation. 作者更正：含 BCL7A 的 SWI/SNF/BAF 复合物在神经祖细胞分化过程中调节线粒体生物能。

IF 9.4 1区生物学

EMBO Journal Pub Date : 2024-10-01 DOI: 10.1038/s44318-024-00157-7

Lena Wischhof, Hang-Mao Lee, Janine Tutas, Clemens Overkott, Eileen Tedt, Miriam Stork, Michael Peitz, Oliver Brüstle, Thomas Ulas, Kristian Händler, Joachim L Schultze, Dan Ehninger, Pierluigi Nicotera, Paolo Salomoni, Daniele Bano

引用次数: 0

Structure of tetrameric forms of the serotonin-gated 5-HT3_A receptor ion channel. 羟色胺门控 5-HT3A 受体离子通道的四聚体结构。

IF 9.4 1区生物学

EMBO Journal Pub Date : 2024-10-01 Epub Date: 2024-09-04 DOI: 10.1038/s44318-024-00191-5

Bianca Introini, Wenqiang Cui, Xiaofeng Chu, Yingyi Zhang, Ana Catarina Alves, Luise Eckhardt-Strelau, Sabrina Golusik, Menno Tol, Horst Vogel, Shuguang Yuan, Mikhail Kudryashev

{"title":"Structure of tetrameric forms of the serotonin-gated 5-HT3A receptor ion channel.","authors":"Bianca Introini, Wenqiang Cui, Xiaofeng Chu, Yingyi Zhang, Ana Catarina Alves, Luise Eckhardt-Strelau, Sabrina Golusik, Menno Tol, Horst Vogel, Shuguang Yuan, Mikhail Kudryashev","doi":"10.1038/s44318-024-00191-5","DOIUrl":"10.1038/s44318-024-00191-5","url":null,"abstract":"Multimeric membrane proteins are produced in the endoplasmic reticulum and transported to their target membranes which, for ion channels, is typically the plasma membrane. Despite the availability of many fully assembled channel structures, our understanding of assembly intermediates, multimer assembly mechanisms, and potential functions of non-standard assemblies is limited. We demonstrate that the pentameric ligand-gated serotonin 5-HT3A receptor (5-HT3AR) can assemble to tetrameric forms and report the structures of the tetramers in plasma membranes of cell-derived microvesicles and in membrane memetics using cryo-electron microscopy and tomography. The tetrameric structures have near-symmetric transmembrane domains, and asymmetric extracellular domains, and can bind serotonin molecules. Computer simulations, based on our cryo-EM structures, were used to decipher the assembly pathway of pentameric 5-HT3R and suggest a potential functional role for the tetrameric receptors.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"4451-4471"},"PeriodicalIF":9.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11480441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142134356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

The fitness cost of spurious phosphorylation. 虚假磷酸化的健康代价

IF 9.4 1区生物学

EMBO Journal Pub Date : 2024-10-01 Epub Date: 2024-09-10 DOI: 10.1038/s44318-024-00200-7

David Bradley, Alexander Hogrebe, Rohan Dandage, Alexandre K Dubé, Mario Leutert, Ugo Dionne, Alexis Chang, Judit Villén, Christian R Landry

{"title":"The fitness cost of spurious phosphorylation.","authors":"David Bradley, Alexander Hogrebe, Rohan Dandage, Alexandre K Dubé, Mario Leutert, Ugo Dionne, Alexis Chang, Judit Villén, Christian R Landry","doi":"10.1038/s44318-024-00200-7","DOIUrl":"10.1038/s44318-024-00200-7","url":null,"abstract":"The fidelity of signal transduction requires the binding of regulatory molecules to their cognate targets. However, the crowded cell interior risks off-target interactions between proteins that are functionally unrelated. How such off-target interactions impact fitness is not generally known. Here, we use Saccharomyces cerevisiae to inducibly express tyrosine kinases. Because yeast lacks bona fide tyrosine kinases, the resulting tyrosine phosphorylation is biologically spurious. We engineered 44 yeast strains each expressing a tyrosine kinase, and quantitatively analysed their phosphoproteomes. This analysis resulted in ~30,000 phosphosites mapping to ~3500 proteins. The number of spurious pY sites generated correlates strongly with decreased growth, and we predict over 1000 pY events to be deleterious. However, we also find that many of the spurious pY sites have a negligible effect on fitness, possibly because of their low stoichiometry. This result is consistent with our evolutionary analyses demonstrating a lack of phosphotyrosine counter-selection in species with tyrosine kinases. Our results suggest that, alongside the risk for toxicity, the cell can tolerate a large degree of non-functional crosstalk as interaction networks evolve.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"4720-4751"},"PeriodicalIF":9.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11480408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142300040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

The unfolded protein response regulates ER exit sites via SNRPB-dependent RNA splicing and contributes to bone development. 未折叠蛋白反应通过 SNRPB 依赖性 RNA 剪接调节 ER 出口位点，并促进骨骼发育。

IF 9.4 1区生物学

EMBO Journal Pub Date : 2024-10-01 Epub Date: 2024-08-19 DOI: 10.1038/s44318-024-00208-z

Muhammad Zahoor, Yanchen Dong, Marco Preussner, Veronika Reiterer, Sabrina Shameen Alam, Margot Haun, Utku Horzum, Yannick Frey, Renata Hajdu, Stephan Geley, Valerie Cormier-Daire, Florian Heyd, Loydie A Jerome-Majewska, Hesso Farhan

{"title":"The unfolded protein response regulates ER exit sites via SNRPB-dependent RNA splicing and contributes to bone development.","authors":"Muhammad Zahoor, Yanchen Dong, Marco Preussner, Veronika Reiterer, Sabrina Shameen Alam, Margot Haun, Utku Horzum, Yannick Frey, Renata Hajdu, Stephan Geley, Valerie Cormier-Daire, Florian Heyd, Loydie A Jerome-Majewska, Hesso Farhan","doi":"10.1038/s44318-024-00208-z","DOIUrl":"10.1038/s44318-024-00208-z","url":null,"abstract":"Splicing and endoplasmic reticulum (ER)-proteostasis are two key processes that ultimately regulate the functional proteins that are produced by a cell. However, the extent to which these processes interact remains poorly understood. Here, we identify SNRPB and other components of the Sm-ring, as targets of the unfolded protein response and novel regulators of export from the ER. Mechanistically, The Sm-ring regulates the splicing of components of the ER export machinery, including Sec16A, a component of ER exit sites. Loss of function of SNRPB is causally linked to cerebro-costo-mandibular syndrome (CCMS), a genetic disease characterized by bone defects. We show that heterozygous deletion of SNRPB in mice resulted in bone defects reminiscent of CCMS and that knockdown of SNRPB delays the trafficking of type-I collagen. Silencing SNRPB inhibited osteogenesis in vitro, which could be rescued by overexpression of Sec16A. This rescue indicates that the role of SNRPB in osteogenesis is linked to its effects on ER-export. Finally, we show that SNRPB is a target for the unfolded protein response, which supports a mechanistic link between the spliceosome and ER-proteostasis. Our work highlights components of the Sm-ring as a novel node in the proteostasis network, shedding light on CCMS pathophysiology.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"4228-4247"},"PeriodicalIF":9.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11445528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142005778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

A non-canonical repressor function of JUN restrains YAP activity and liver cancer growth. JUN的非典型抑制功能可抑制YAP的活性和肝癌的生长。

IF 9.4 1区生物学

EMBO Journal Pub Date : 2024-10-01 Epub Date: 2024-08-29 DOI: 10.1038/s44318-024-00188-0

Yuliya Kurlishchuk, Anita Cindric Vranesic, Marco Jessen, Alexandra Kipping, Christin Ritter, KyungMok Kim, Paul Cramer, Björn von Eyss

{"title":"A non-canonical repressor function of JUN restrains YAP activity and liver cancer growth.","authors":"Yuliya Kurlishchuk, Anita Cindric Vranesic, Marco Jessen, Alexandra Kipping, Christin Ritter, KyungMok Kim, Paul Cramer, Björn von Eyss","doi":"10.1038/s44318-024-00188-0","DOIUrl":"10.1038/s44318-024-00188-0","url":null,"abstract":"Yes-associated protein (YAP) and its homolog, transcriptional coactivator with PDZ-binding motif (TAZ), are the main transcriptional downstream effectors of the Hippo pathway. Decreased Hippo pathway activity leads to nuclear translocation of YAP/TAZ where they interact with TEAD transcription factors to induce target gene expression. Unrestrained YAP/TAZ activity can lead to excessive growth and tumor formation in a short time, underscoring the evolutionary need for tight control of these two transcriptional coactivators. Here, we report that the AP-1 component JUN acts as specific repressor of YAP/TAZ at joint target sites to decrease YAP/TAZ activity. This function of JUN is independent of its heterodimeric AP-1 partner FOS and the canonical AP-1 function. Since expression of JUN is itself induced by YAP/TAZ, our work identifies a JUN-dependent negative feedback loop that buffers YAP/TAZ activity at joint genomic sites. This negative feedback loop gets disrupted in liver cancer to unlock the full oncogenic potential of YAP/TAZ. Our results thus demonstrate an additional layer of control for the interplay of YAP/TAZ and AP-1.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"4578-4603"},"PeriodicalIF":9.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11480203/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142114395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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