Journal of Cell Biology最新文献_第2页

Identification of coilin interactors reveals coordinated control of Cajal body number and structure. Coilin相互作用者的鉴定揭示了对Cajal体数量和结构的协调控制。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-02-03 Epub Date: 2024-11-27 DOI: 10.1083/jcb.202305081

Dahyana Arias Escayola, Chuyue Zhang, Emily Nischwitz, Leonard Schärfen, Kerstin Dörner, Korinna Straube, Ulrike Kutay, Falk Butter, Karla M Neugebauer

{"title":"Identification of coilin interactors reveals coordinated control of Cajal body number and structure.","authors":"Dahyana Arias Escayola, Chuyue Zhang, Emily Nischwitz, Leonard Schärfen, Kerstin Dörner, Korinna Straube, Ulrike Kutay, Falk Butter, Karla M Neugebauer","doi":"10.1083/jcb.202305081","DOIUrl":"10.1083/jcb.202305081","url":null,"abstract":"The cell nucleus contains distinct biomolecular condensates that form at specific genetic loci, organize chromosomes in 3D space, and regulate RNA processing. Among these, Cajal bodies (CBs) require key \"scaffolding\" proteins for their assembly, which is not fully understood. Here, we employ proximity biotinylation, mass spectrometry, and functional screening to comprehensively identify and test the functions of CB components. We document 144 protein interactors of coilin, of which 70 were newly detected, and establish 25 players needed for CB assembly and/or maintenance. Surprisingly, the depletion of nine coilin interactors-mostly constituents of the 60S ribosome (RPLs)-increased CB number and caused subdomains defined by coilin and the survival motor neuron protein (SMN) to merge. These phenotypes were traceable to altered nuclear levels of dimethylarginine. Our data implicate RPL24 and other players in the regulation of CBs by modulating posttranslational modifications. Moreover, the prevalence of transcription factors among the identified components highlights roles for gene activity in CB assembly and nuclear positioning.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 2","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11602656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142739767","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

Functional genetics reveals modulators of antimicrotubule drug sensitivity. 功能遗传学揭示抗微管药物敏感性的调节因子

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-02-03 Epub Date: 2024-11-21 DOI: 10.1083/jcb.202403065

Kuan-Chung Su, Elena Radul, Nolan K Maier, Mary-Jane Tsang, Claire Goul, Brittania Moodie, Océane Marescal, Heather R Keys, Iain M Cheeseman

{"title":"Functional genetics reveals modulators of antimicrotubule drug sensitivity.","authors":"Kuan-Chung Su, Elena Radul, Nolan K Maier, Mary-Jane Tsang, Claire Goul, Brittania Moodie, Océane Marescal, Heather R Keys, Iain M Cheeseman","doi":"10.1083/jcb.202403065","DOIUrl":"10.1083/jcb.202403065","url":null,"abstract":"Microtubules play essential roles in diverse cellular processes and are important pharmacological targets for treating human disease. Here, we sought to identify cellular factors that modulate the sensitivity of cells to antimicrotubule drugs. We conducted a genome-wide CRISPR/Cas9-based functional genetics screen in human cells treated with the microtubule-destabilizing drug nocodazole or the microtubule-stabilizing drug paclitaxel. We further conducted a focused secondary screen to test drug sensitivity for ∼1,400 gene targets across two distinct human cell lines and to additionally test sensitivity to the KIF11 inhibitor, STLC. These screens defined gene targets whose loss enhances or suppresses sensitivity to antimicrotubule drugs. In addition to gene targets whose loss sensitized cells to multiple compounds, we observed cases of differential sensitivity to specific compounds and differing requirements between cell lines. Our downstream molecular analysis further revealed additional roles for established microtubule-associated proteins and identified new players in microtubule function.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 2","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11590752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681868","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

Epidermal maintenance of Langerhans cells relies on autophagy-regulated lipid metabolism. 朗格汉斯细胞的表皮维持依赖于自噬调节的脂质代谢。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-02-03 Epub Date: 2024-11-13 DOI: 10.1083/jcb.202403178

Florent Arbogast, Raquel Sal-Carro, Wacym Boufenghour, Quentin Frenger, Delphine Bouis, Louise Filippi De La Palavesa, Jean-Daniel Fauny, Olivier Griso, Hélène Puccio, Rebecca Fima, Thierry Huby, Emmanuel L Gautier, Anne Molitor, Raphaël Carapito, Seiamak Bahram, Nikolaus Romani, Björn E Clausen, Benjamin Voisin, Christopher G Mueller, Frédéric Gros, Vincent Flacher

{"title":"Epidermal maintenance of Langerhans cells relies on autophagy-regulated lipid metabolism.","authors":"Florent Arbogast, Raquel Sal-Carro, Wacym Boufenghour, Quentin Frenger, Delphine Bouis, Louise Filippi De La Palavesa, Jean-Daniel Fauny, Olivier Griso, Hélène Puccio, Rebecca Fima, Thierry Huby, Emmanuel L Gautier, Anne Molitor, Raphaël Carapito, Seiamak Bahram, Nikolaus Romani, Björn E Clausen, Benjamin Voisin, Christopher G Mueller, Frédéric Gros, Vincent Flacher","doi":"10.1083/jcb.202403178","DOIUrl":"10.1083/jcb.202403178","url":null,"abstract":"Macroautophagy (often-named autophagy), a catabolic process involving autophagy-related (Atg) genes, prevents the accumulation of harmful cytoplasmic components and mobilizes energy reserves in long-lived and self-renewing cells. Autophagy deficiency affects antigen presentation in conventional dendritic cells (DCs) without impacting their survival. However, previous studies did not address epidermal Langerhans cells (LCs). Here, we demonstrate that deletion of either Atg5 or Atg7 in LCs leads to their gradual depletion. ATG5-deficient LCs showed metabolic dysregulation and accumulated neutral lipids. Despite increased mitochondrial respiratory capacity, they were unable to process lipids, eventually leading them to ferroptosis. Finally, metabolically impaired LCs upregulated proinflammatory transcripts and showed decreased expression of neuronal interaction receptors. Altogether, autophagy represents a critical regulator of lipid storage and metabolism in LCs, allowing their maintenance in the epidermis.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 2","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11561468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621231","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

Securin regulates the spatiotemporal dynamics of separase. Securin 可调节分离酶的时空动态。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-02-03 Epub Date: 2024-11-18 DOI: 10.1083/jcb.202312099

Christopher G Sorensen Turpin, Dillon Sloan, Marian LaForest, Lindsey Klebanow, Diana Mitchell, Aaron F Severson, Joshua N Bembenek

{"title":"Securin regulates the spatiotemporal dynamics of separase.","authors":"Christopher G Sorensen Turpin, Dillon Sloan, Marian LaForest, Lindsey Klebanow, Diana Mitchell, Aaron F Severson, Joshua N Bembenek","doi":"10.1083/jcb.202312099","DOIUrl":"10.1083/jcb.202312099","url":null,"abstract":"Separase regulates multiple aspects of the metaphase-to-anaphase transition. Separase cleaves cohesin to allow chromosome segregation and localizes to vesicles to promote exocytosis. The anaphase-promoting complex/cyclosome (APC/C) activates separase by ubiquitinating its inhibitory chaperone, securin, triggering its degradation. How this pathway controls the exocytic function of separase is unknown. During meiosis I, securin is degraded over several minutes, while separase rapidly relocalizes from kinetochore structures at the spindle and cortex to sites of action on chromosomes and vesicles at anaphase onset. The loss of cohesin coincides with the relocalization of separase to the chromosome midbivalent at anaphase onset. APC/C depletion prevents separase relocalization, while securin depletion causes precocious separase relocalization. Expression of non-degradable securin inhibits chromosome segregation, exocytosis, and separase localization to vesicles but not to the anaphase spindle. We conclude that APC/C-mediated securin degradation controls separase localization. This spatiotemporal regulation will impact the effective local concentration of separase for more precise targeting of substrates in anaphase.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 2","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648289","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

Genome-wide conditional degron libraries for functional genomics.

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-02-03 Epub Date: 2024-12-18 DOI: 10.1083/jcb.202409007

Eduardo Gameiro, Karla A Juárez-Núñez, Jia Jun Fung, Susmitha Shankar, Brian Luke, Anton Khmelinskii

{"title":"Genome-wide conditional degron libraries for functional genomics.","authors":"Eduardo Gameiro, Karla A Juárez-Núñez, Jia Jun Fung, Susmitha Shankar, Brian Luke, Anton Khmelinskii","doi":"10.1083/jcb.202409007","DOIUrl":"https://doi.org/10.1083/jcb.202409007","url":null,"abstract":"Functional genomics with libraries of knockout alleles is limited to non-essential genes and convoluted by the potential accumulation of suppressor mutations in knockout backgrounds, which can lead to erroneous functional annotations. To address these limitations, we constructed genome-wide libraries of conditional alleles based on the auxin-inducible degron (AID) system for inducible degradation of AID-tagged proteins in the budding yeast Saccharomyces cerevisiae. First, we determined that N-terminal tagging is at least twice as likely to inadvertently impair protein function across the proteome. We thus constructed two libraries with over 5,600 essential and non-essential proteins fused at the C-terminus with an AID tag and an optional fluorescent protein. Approximately 90% of AID-tagged proteins were degraded in the presence of the auxin analog 5-Ph-IAA, with initial protein abundance and tag accessibility as limiting factors. Genome-wide screens for DNA damage response factors revealed a role for the glucose signaling factor GSF2 in resistance to hydroxyurea, highlighting how the AID libraries extend the yeast genetics toolbox.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 2","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846663","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}

引用次数: 0

The kinetochore protein KNL-1 regulates the actin cytoskeleton to control dendrite branching.

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-02-03 Epub Date: 2024-12-03 DOI: 10.1083/jcb.202311147

Henrique Alves Domingos, Mattie Green, Vasileios R Ouzounidis, Cameron Finlayson, Bram Prevo, Dhanya K Cheerambathur

{"title":"The kinetochore protein KNL-1 regulates the actin cytoskeleton to control dendrite branching.","authors":"Henrique Alves Domingos, Mattie Green, Vasileios R Ouzounidis, Cameron Finlayson, Bram Prevo, Dhanya K Cheerambathur","doi":"10.1083/jcb.202311147","DOIUrl":"10.1083/jcb.202311147","url":null,"abstract":"The function of the nervous system is intimately tied to its complex and highly interconnected architecture. Precise control of dendritic branching in individual neurons is central to building the complex structure of the nervous system. Here, we show that the kinetochore protein KNL-1 and its associated KMN (Knl1/Mis12/Ndc80 complex) network partners, typically known for their role in chromosome-microtubule coupling during mitosis, control dendrite branching in the Caenorhabditis elegans mechanosensory PVD neuron. KNL-1 restrains excess dendritic branching and promotes contact-dependent repulsion events, ensuring robust sensory behavior and preventing premature neurodegeneration. Unexpectedly, KNL-1 loss resulted in significant alterations of the actin cytoskeleton alongside changes in microtubule dynamics within dendrites. We show that KNL-1 modulates F-actin dynamics to generate proper dendrite architecture and that its N-terminus can initiate F-actin assembly. These findings reveal that the postmitotic neuronal KMN network acts to shape the developing nervous system by regulating the actin cytoskeleton and provide new insight into the mechanisms controlling dendrite architecture.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 2","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11613958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769302","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 function of TPL/TBL1-type corepressors is to nucleate the assembly of the preinitiation complex.

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-02-03 Epub Date: 2024-12-09 DOI: 10.1083/jcb.202404103

Alexander R Leydon, Benjamin Downing, Janet Solano Sanchez, Raphael Loll-Krippleber, Nathan M Belliveau, Ricard A Rodriguez-Mias, Andrew J Bauer, Isabella J Watson, Lena Bae, Judit Villén, Grant W Brown, Jennifer L Nemhauser

{"title":"A function of TPL/TBL1-type corepressors is to nucleate the assembly of the preinitiation complex.","authors":"Alexander R Leydon, Benjamin Downing, Janet Solano Sanchez, Raphael Loll-Krippleber, Nathan M Belliveau, Ricard A Rodriguez-Mias, Andrew J Bauer, Isabella J Watson, Lena Bae, Judit Villén, Grant W Brown, Jennifer L Nemhauser","doi":"10.1083/jcb.202404103","DOIUrl":"10.1083/jcb.202404103","url":null,"abstract":"The plant corepressor TPL is recruited to diverse chromatin contexts, yet its mechanism of repression remains unclear. Previously, we leveraged the fact that TPL retains its function in a synthetic transcriptional circuit in the yeast model Saccharomyces cerevisiae to localize repressive function to two distinct domains. Here, we employed two unbiased whole-genome approaches to map the physical and genetic interactions of TPL at a repressed locus. We identified SPT4, SPT5, and SPT6 as necessary for repression with SPT4 acting as a bridge connecting TPL to SPT5 and SPT6. We discovered the association of multiple additional constituents of the transcriptional preinitiation complex at TPL-repressed promoters, specifically those involved early in transcription initiation. These findings were validated in yeast and plants, including a novel method to analyze the conditional loss of function of essential genes in plants. Our findings support a model where TPL nucleates preassembly of the transcription activation machinery to facilitate the rapid onset of transcription once repression is relieved.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 2","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11627113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800933","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

One step 4× and 12× 3D-ExM enables robust super-resolution microscopy of nanoscale cellular structures.

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-02-03 Epub Date: 2024-12-03 DOI: 10.1083/jcb.202407116

Roshan X Norman, Yu-Chia Chen, Emma E Recchia, Jonathan Loi, Quincy Rosemarie, Sydney L Lesko, Smit Patel, Nathan Sherer, Motoki Takaku, Mark E Burkard, Aussie Suzuki

{"title":"One step 4× and 12× 3D-ExM enables robust super-resolution microscopy of nanoscale cellular structures.","authors":"Roshan X Norman, Yu-Chia Chen, Emma E Recchia, Jonathan Loi, Quincy Rosemarie, Sydney L Lesko, Smit Patel, Nathan Sherer, Motoki Takaku, Mark E Burkard, Aussie Suzuki","doi":"10.1083/jcb.202407116","DOIUrl":"10.1083/jcb.202407116","url":null,"abstract":"Super-resolution microscopy has become an indispensable tool across diverse research fields, offering unprecedented insights into biological architectures with nanometer scale resolution. Compared with traditional nanometer-scale imaging methods such as electron microscopy, super-resolution microscopy offers several advantages, including the simultaneous labeling of multiple target biomolecules with high specificity and simpler sample preparation, making it accessible to most researchers. In this study, we introduce two optimized methods of super-resolution imaging: 4-fold and 12-fold 3D-isotropic and preserved Expansion Microscopy (4× and 12× 3D-ExM). 3D-ExM is a straightforward expansion microscopy technique featuring a single-step process, providing robust and reproducible 3D isotropic expansion for both 2D and 3D cell culture models. With standard confocal microscopy, 12× 3D-ExM achieves a lateral resolution of <30 nm, enabling the visualization of nanoscale structures, including chromosomes, kinetochores, nuclear pore complexes, and Epstein-Barr virus particles. These results demonstrate that 3D-ExM provides cost-effective and user-friendly super-resolution microscopy, making it highly suitable for a wide range of cell biology research, including studies on cellular and chromatin architectures.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 2","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11613959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769247","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

Real-time imaging reveals a role for macrophage protrusive motility in melanoma invasion. 实时成像揭示了巨噬细胞在黑色素瘤侵袭中的突出运动作用。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-02-03 Epub Date: 2024-11-21 DOI: 10.1083/jcb.202403096

Gayathri Ramakrishnan, Veronika Miskolci, Miranda Hunter, Morgan A Giese, Daniela Münch, Yiran Hou, Kevin W Eliceiri, Michael R Lasarev, Richard M White, Anna Huttenlocher

引用次数: 0

Neuronal constitutive endolysosomal perforations enable α-synuclein aggregation by internalized PFFs.

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-02-03 Epub Date: 2024-12-23 DOI: 10.1083/jcb.202401136

Anwesha Sanyal, Gustavo Scanavachi, Elliott Somerville, Anand Saminathan, Athul Nair, Ricardo F Bango Da Cunha Correia, Beren Aylan, Ewa Sitarska, Athanasios Oikonomou, Nikos S Hatzakis, Tom Kirchhausen

{"title":"Neuronal constitutive endolysosomal perforations enable α-synuclein aggregation by internalized PFFs.","authors":"Anwesha Sanyal, Gustavo Scanavachi, Elliott Somerville, Anand Saminathan, Athul Nair, Ricardo F Bango Da Cunha Correia, Beren Aylan, Ewa Sitarska, Athanasios Oikonomou, Nikos S Hatzakis, Tom Kirchhausen","doi":"10.1083/jcb.202401136","DOIUrl":"https://doi.org/10.1083/jcb.202401136","url":null,"abstract":"Endocytosis, required for the uptake of receptors and their ligands, can also introduce pathological aggregates such as α-synuclein (α-syn) in Parkinson's Disease. We show here the unexpected presence of intrinsically perforated endolysosomes in neurons, suggesting involvement in the genesis of toxic α-syn aggregates induced by internalized preformed fibrils (PFFs). Aggregation of endogenous α-syn in late endosomes and lysosomes of human iPSC-derived neurons (iNs), seeded by internalized α-syn PFFs, caused the death of the iNs but not of the parental iPSCs and non-neuronal cells. Live-cell imaging of iNs showed constitutive perforations in ∼5% of their endolysosomes. These perforations, identified by 3D electron microscopy in iNs and CA1 pyramidal neurons and absent in non-neuronal cells, may facilitate cytosolic access of endogenous α-syn to PFFs in the lumen of endolysosomes, triggering aggregation. Inhibiting the PIKfyve phosphoinositol kinase reduced α-syn aggregation and associated iN death, even with ongoing PFF endolysosomal entry, suggesting that maintaining endolysosomal integrity might afford a therapeutic strategy to counteract synucleinopathies.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 2","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142877267","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}

引用次数: 0