The EMBO Journal最新文献_第3页

miRNA-mediated gene silencing in Drosophila larval development involves GW182-dependent and independent mechanisms. 果蝇幼虫发育过程中 miRNA 介导的基因沉默涉及 GW182 依赖性和独立机制。

The EMBO Journal Pub Date : 2024-09-25 DOI: 10.1038/s44318-024-00249-4

Eriko Matsuura-Suzuki,Kaori Kiyokawa,Shintaro Iwasaki,Yukihide Tomari

{"title":"miRNA-mediated gene silencing in Drosophila larval development involves GW182-dependent and independent mechanisms.","authors":"Eriko Matsuura-Suzuki,Kaori Kiyokawa,Shintaro Iwasaki,Yukihide Tomari","doi":"10.1038/s44318-024-00249-4","DOIUrl":"https://doi.org/10.1038/s44318-024-00249-4","url":null,"abstract":"MicroRNAs (miRNAs) regulate a wide variety of biological processes by silencing their target genes. Argonaute (AGO) proteins load miRNAs to form an RNA-induced silencing complex (RISC), which mediates translational repression and/or mRNA decay of the targets. A scaffold protein called GW182 directly binds AGO and the CCR4-NOT deadenylase complex, initiating the mRNA decay reaction. Although previous studies have demonstrated the critical role of GW182 in cultured cells as well as in cell-free systems, its biological significance in living organisms remains poorly explored, especially in Drosophila melanogaster. Here, we generated gw182-null flies using the CRISPR/Cas9 system and found that, unexpectedly, they can survive until an early second-instar larval stage. Moreover, in vivo miRNA reporters can be effectively repressed in gw182-null first-instar larvae. Nevertheless, gw182-null flies have defects in the expression of chitin-related genes and the formation of the larval trachea system, preventing them from completing larval development. Our results highlight the importance of both GW182-dependent and -independent silencing mechanisms in vivo.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142325123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TBK1-Zyxin signaling controls tumor-associated macrophage recruitment to mitigate antitumor immunity. TBK1-Zyxin信号控制肿瘤相关巨噬细胞的招募，从而减轻抗肿瘤免疫。

The EMBO Journal Pub Date : 2024-09-20 DOI: 10.1038/s44318-024-00244-9

Ruyuan Zhou,Mengqiu Wang,Xiao Li,Yutong Liu,Yihan Yao,Ailian Wang,Chen Chen,Qian Zhang,Qirou Wu,Qi Zhang,Dante Neculai,Bing Xia,Jian-Zhong Shao,Xin-Hua Feng,Tingbo Liang,Jian Zou,Xiaojian Wang,Pinglong Xu

{"title":"TBK1-Zyxin signaling controls tumor-associated macrophage recruitment to mitigate antitumor immunity.","authors":"Ruyuan Zhou,Mengqiu Wang,Xiao Li,Yutong Liu,Yihan Yao,Ailian Wang,Chen Chen,Qian Zhang,Qirou Wu,Qi Zhang,Dante Neculai,Bing Xia,Jian-Zhong Shao,Xin-Hua Feng,Tingbo Liang,Jian Zou,Xiaojian Wang,Pinglong Xu","doi":"10.1038/s44318-024-00244-9","DOIUrl":"https://doi.org/10.1038/s44318-024-00244-9","url":null,"abstract":"Mechanical control is fundamental for cellular localization within a tissue, including for tumor-associated macrophages (TAMs). While the innate immune sensing pathways cGAS-STING and RLR-MAVS impact the pathogenesis and therapeutics of malignant diseases, their effects on cell residency and motility remain incompletely understood. Here, we uncovered that TBK1 kinase, activated by cGAS-STING or RLR-MAVS signaling in macrophages, directly phosphorylates and mobilizes Zyxin, a key regulator of actin dynamics. Under pathological conditions and in STING or MAVS signalosomes, TBK1-mediated Zyxin phosphorylation at S143 facilitates rapid recruitment of phospho-Zyxin to focal adhesions, leading to subsequent F-actin reorganization and reduced macrophage migration. Intratumoral STING-TBK1-Zyxin signaling was evident in TAMs and critical in antitumor immunity. Furthermore, myeloid-specific or global disruption of this signaling decreased the population of CD11b+ F4/80+ TAMs and promoted PD-1-mediated antitumor immunotherapy. Thus, our findings identify a new biological function of innate immune sensing pathways by regulating macrophage tissue localization, thus providing insights into context-dependent mitigation of antitumor immunity.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142275152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A shorter splicing isoform antagonizes ZBP1 to modulate cell death and inflammatory responses. 一种较短的剪接异构体可拮抗 ZBP1，从而调节细胞死亡和炎症反应。

The EMBO Journal Pub Date : 2024-09-19 DOI: 10.1038/s44318-024-00238-7

Masahiro Nagata,Yasmin Carvalho Schäfer,Laurens Wachsmuth,Manolis Pasparakis

{"title":"A shorter splicing isoform antagonizes ZBP1 to modulate cell death and inflammatory responses.","authors":"Masahiro Nagata,Yasmin Carvalho Schäfer,Laurens Wachsmuth,Manolis Pasparakis","doi":"10.1038/s44318-024-00238-7","DOIUrl":"https://doi.org/10.1038/s44318-024-00238-7","url":null,"abstract":"Z-DNA-binding protein 1 (ZBP1) is an interferon-inducible sensor of Z-DNA and Z-RNA, which has emerged as a critical regulator of cell death and inflammation. ZBP1 binds Z-DNA and Z-RNA via its Zα domains, and signals by engaging RIPK3 and RIPK1 via its RIP homotypic interaction motifs (RHIMs). Here, we show that mice express an alternatively-spliced shorter ZBP1 isoform (ZBP1-S), which harbours the Zα domains but lacks the RHIMs, and acts as an endogenous inhibitor of the full-length protein (ZBP1-L). Mice and cells expressing only ZBP1-S are resistant to ZBP1-mediated cell death and inflammation. In contrast, cells lacking ZBP1-S show increased ZBP1-L-induced death compared to cells expressing both isoforms. Moreover, loss of the short isoform accelerates and exacerbates skin inflammation induced by ZBP1-mediated necroptosis of RIPK1-deficient keratinocytes, revealing an important physiological role of ZBP1-S. Mechanistically, ZBP1-S suppresses ZBP1-L-mediated cell death by binding to Z-nucleic acids via its Zα domains. Therefore, ZBP1-S acts as an endogenous inhibitor that competes with full-length ZBP1-L for binding Z-nucleic acid ligands to fine-tune ZBP1-mediated cell death and inflammation.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142273518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Astrocyte allocation during brain development is controlled by Tcf4-mediated fate restriction. 大脑发育过程中星形胶质细胞的分配受 Tcf4 介导的命运限制控制。

The EMBO Journal Pub Date : 2024-09-19 DOI: 10.1038/s44318-024-00218-x

Yandong Zhang,Dan Li,Yuqun Cai,Rui Zou,Yilan Zhang,Xin Deng,Yafei Wang,Tianxiang Tang,Yuanyuan Ma,Feizhen Wu,Yunli Xie

{"title":"Astrocyte allocation during brain development is controlled by Tcf4-mediated fate restriction.","authors":"Yandong Zhang,Dan Li,Yuqun Cai,Rui Zou,Yilan Zhang,Xin Deng,Yafei Wang,Tianxiang Tang,Yuanyuan Ma,Feizhen Wu,Yunli Xie","doi":"10.1038/s44318-024-00218-x","DOIUrl":"https://doi.org/10.1038/s44318-024-00218-x","url":null,"abstract":"Astrocytes in the brain exhibit regional heterogeneity contributing to regional circuits involved in higher-order brain functions, yet the mechanisms controlling their distribution remain unclear. Here, we show that the precise allocation of astrocytes to specific brain regions during development is achieved through transcription factor 4 (Tcf4)-mediated fate restriction based on their embryonic origin. Loss of Tcf4 in ventral telencephalic neural progenitor cells alters the fate of oligodendrocyte precursor cells to transient intermediate astrocyte precursor cells, resulting in mislocalized astrocytes in the dorsal neocortex. These ectopic astrocytes engage with neocortical neurons and acquire features reminiscent of dorsal neocortical astrocytes. Furthermore, Tcf4 functions as a suppressor of astrocyte fate during the differentiation of oligodendrocyte precursor cells derived from the ventral telencephalon, thereby restricting the fate to the oligodendrocyte lineage in the dorsal neocortex. Together, our findings highlight a previously unappreciated role for Tcf4 in regulating astrocyte allocation, offering additional insights into the mechanisms underlying neurodevelopmental disorders linked to Tcf4 mutations.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142273453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Acetylation of TIR domains in the TLR4-Mal-MyD88 complex regulates immune responses in sepsis. TLR4-Mal-MyD88复合物中TIR结构域的乙酰化调节败血症中的免疫反应。

The EMBO Journal Pub Date : 2024-09-18 DOI: 10.1038/s44318-024-00237-8

Xue Li,Xiangrong Li,Pengpeng Huang,Facai Zhang,Juanjuan K Du,Ying Kong,Ziqiang Shao,Xinxing Wu,Weijiao Fan,Houquan Tao,Chuanzan Zhou,Yan Shao,Yanling Jin,Meihua Ye,Yan Chen,Jong Deng,Jimin Shao,Jicheng Yue,Xiaju Cheng,Y Eugene Chinn

{"title":"Acetylation of TIR domains in the TLR4-Mal-MyD88 complex regulates immune responses in sepsis.","authors":"Xue Li,Xiangrong Li,Pengpeng Huang,Facai Zhang,Juanjuan K Du,Ying Kong,Ziqiang Shao,Xinxing Wu,Weijiao Fan,Houquan Tao,Chuanzan Zhou,Yan Shao,Yanling Jin,Meihua Ye,Yan Chen,Jong Deng,Jimin Shao,Jicheng Yue,Xiaju Cheng,Y Eugene Chinn","doi":"10.1038/s44318-024-00237-8","DOIUrl":"https://doi.org/10.1038/s44318-024-00237-8","url":null,"abstract":"Activation of the Toll-like receptor 4 (TLR4) by bacterial endotoxins in macrophages plays a crucial role in the pathogenesis of sepsis. However, the mechanism underlying TLR4 activation in macrophages is still not fully understood. Here, we reveal that upon lipopolysaccharide (LPS) stimulation, lysine acetyltransferase CBP is recruited to the TLR4 signalosome complex leading to increased acetylation of the TIR domains of the TLR4 signalosome. Acetylation of the TLR4 signalosome TIR domains significantly enhances signaling activation via NF-κB rather than IRF3 pathways. Induction of NF-κB signaling is responsible for gene expression changes leading to M1 macrophage polarization. In sepsis patients, significantly elevated TLR4-TIR acetylation is observed in CD16+ monocytes combined with elevated expression of M1 macrophage markers. Pharmacological inhibition of HDAC1, which deacetylates the TIR domains, or CBP play opposite roles in sepsis. Our findings highlight the important role of TLR4-TIR domain acetylation in the regulation of the immune responses in sepsis, and we propose this reversible acetylation of TLR4 signalosomes as a potential therapeutic target for M1 macrophages during the progression of sepsis.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142246978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Acidity suppresses CD8 + T-cell function by perturbing IL-2, mTORC1, and c-Myc signaling. 酸性物质通过扰乱 IL-2、mTORC1 和 c-Myc 信号转导抑制 CD8 + T 细胞功能。

The EMBO Journal Pub Date : 2024-09-16 DOI: 10.1038/s44318-024-00235-w

Romain Vuillefroy de Silly,Laetitia Pericou,Bili Seijo,Isaac Crespo,Melita Irving

{"title":"Acidity suppresses CD8 + T-cell function by perturbing IL-2, mTORC1, and c-Myc signaling.","authors":"Romain Vuillefroy de Silly,Laetitia Pericou,Bili Seijo,Isaac Crespo,Melita Irving","doi":"10.1038/s44318-024-00235-w","DOIUrl":"https://doi.org/10.1038/s44318-024-00235-w","url":null,"abstract":"CD8 + T cells have critical roles in tumor control, but a range of factors in their microenvironment such as low pH can suppress their function. Here, we demonstrate that acidity restricts T-cell expansion mainly through impairing IL-2 responsiveness, lowers cytokine secretion upon re-activation, and reduces the cytolytic capacity of CD8 + T cells expressing low-affinity TCR. We further find decreased mTORC1 signaling activity and c-Myc levels at low pH. Mechanistically, nuclear/cytoplasmic acidification is linked to mTORC1 suppression in a Rheb-, Akt/TSC2/PRAS40-, GATOR1- and Lkb1/AMPK-independent manner, while c-Myc levels drop due to both decreased transcription and higher levels of proteasome-mediated degradation. In addition, lower intracellular levels of glutamine, glutamate, and aspartate, as well as elevated proline levels are observed with no apparent impact on mTORC1 signaling or c-Myc levels. Overall, we suggest that, due to the broad impact of acidity on CD8 + T cells, multiple interventions will be required to restore T-cell function unless intracellular pH is effectively controlled.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142245242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ER-phagy restrains inflammatory responses through its receptor UBAC2. ER-phagy 通过其受体 UBAC2 抑制炎症反应。

The EMBO Journal Pub Date : 2024-09-16 DOI: 10.1038/s44318-024-00232-z

Xing He,Haowei He,Zitong Hou,Zheyu Wang,Qinglin Shi,Tao Zhou,Yaoxing Wu,Yunfei Qin,Jun Wang,Zhe Cai,Jun Cui,Shouheng Jin

{"title":"ER-phagy restrains inflammatory responses through its receptor UBAC2.","authors":"Xing He,Haowei He,Zitong Hou,Zheyu Wang,Qinglin Shi,Tao Zhou,Yaoxing Wu,Yunfei Qin,Jun Wang,Zhe Cai,Jun Cui,Shouheng Jin","doi":"10.1038/s44318-024-00232-z","DOIUrl":"https://doi.org/10.1038/s44318-024-00232-z","url":null,"abstract":"ER-phagy, a selective form of autophagic degradation of endoplasmic reticulum (ER) fragments, plays an essential role in governing ER homeostasis. Dysregulation of ER-phagy is associated with the unfolded protein response (UPR), which is a major clue for evoking inflammatory diseases. However, the molecular mechanism underpinning the connection between ER-phagy and disease remains poorly defined. Here, we identified ubiquitin-associated domain-containing protein 2 (UBAC2) as a receptor for ER-phagy, while at the same time being a negative regulator of inflammatory responses. UBAC2 harbors a canonical LC3-interacting region (LIR) in its cytoplasmic domain, which binds to autophagosomal GABARAP. Upon ER-stress or autophagy activation, microtubule affinity-regulating kinase 2 (MARK2) phosphorylates UBAC2 at serine (S) 223, promoting its dimerization. Dimerized UBAC2 interacts more strongly with GABARAP, thus facilitating selective degradation of the ER. Moreover, by affecting ER-phagy, UBAC2 restrains inflammatory responses and acute ulcerative colitis (UC) in mice. Our findings indicate that ER-phagy directed by a MARK2-UBAC2 axis may provide targets for the treatment of inflammatory disease.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142245239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Non-autophagic Golgi-LC3 lipidation facilitates TFE3 stress response against Golgi dysfunction. 非自噬高尔基-LC3 脂化促进了 TFE3 对高尔基功能障碍的应激反应。

The EMBO Journal Pub Date : 2024-09-16 DOI: 10.1038/s44318-024-00233-y

Jaemin Kang,Cathena Meiling Li,Namhoon Kim,Jongyeon Baek,Yong-Keun Jung

{"title":"Non-autophagic Golgi-LC3 lipidation facilitates TFE3 stress response against Golgi dysfunction.","authors":"Jaemin Kang,Cathena Meiling Li,Namhoon Kim,Jongyeon Baek,Yong-Keun Jung","doi":"10.1038/s44318-024-00233-y","DOIUrl":"https://doi.org/10.1038/s44318-024-00233-y","url":null,"abstract":"Lipidated ATG8/LC3 proteins are recruited to single membrane compartments as well as autophagosomes, supporting their functions. Although recent studies have shown that Golgi-LC3 lipidation follows Golgi damage, its molecular mechanism and function under Golgi stress remain unknown. Here, by combining DLK1 overexpression as a new strategy for induction of Golgi-specific LC3 lipidation, and the application of Golgi-damaging reagents, we unravel the mechanism and role of Golgi-LC3 lipidation. Upon DLK1 overexpression, LC3 is lipidated on the Golgi apparatus in an ATG12-ATG5-ATG16L1 complex-dependent manner; a post-Golgi trafficking blockade is the primary cause of this lipidation. During Golgi stress, ATG16L1 is recruited through its interaction with V-ATPase for Golgi-LC3 lipidation. After post-Golgi trafficking inhibition, TFE3, a key regulator of the Golgi stress response, is translocated to the nucleus. Defects in LC3 lipidation disrupt this translocation, leading to an attenuation of the Golgi stress response. Together, our results reveal the mechanism and unexplored function of Golgi-LC3 lipidation in the Golgi stress response.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142245243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decoupled transcript and protein concentrations ensure histone homeostasis in different nutrients. 转录本和蛋白质浓度的脱钩确保了组蛋白在不同营养物质中的平衡。

The EMBO Journal Pub Date : 2024-09-13 DOI: 10.1038/s44318-024-00227-w

Dimitra Chatzitheodoridou,Daniela Bureik,Francesco Padovani,Kalyan V Nadimpalli,Kurt M Schmoller

引用次数: 0

Interaction of chikungunya virus glycoproteins with macrophage factors controls virion production. 基孔肯雅病毒糖蛋白与巨噬细胞因子的相互作用控制着病毒的产生。

The EMBO Journal Pub Date : 2024-09-11 DOI: 10.1038/s44318-024-00193-3

Zhenlan Yao,Sangeetha Ramachandran,Serina Huang,Erin Kim,Yasaman Jami-Alahmadi,Prashant Kaushal,Mehdi Bouhaddou,James A Wohlschlegel,Melody Mh Li

{"title":"Interaction of chikungunya virus glycoproteins with macrophage factors controls virion production.","authors":"Zhenlan Yao,Sangeetha Ramachandran,Serina Huang,Erin Kim,Yasaman Jami-Alahmadi,Prashant Kaushal,Mehdi Bouhaddou,James A Wohlschlegel,Melody Mh Li","doi":"10.1038/s44318-024-00193-3","DOIUrl":"https://doi.org/10.1038/s44318-024-00193-3","url":null,"abstract":"Despite their role as innate sentinels, macrophages can serve as cellular reservoirs of chikungunya virus (CHIKV), a highly-pathogenic arthropod-borne alphavirus that has caused large outbreaks among human populations. Here, with the use of viral chimeras and evolutionary selection analysis, we define CHIKV glycoproteins E1 and E2 as critical for virion production in THP-1 derived human macrophages. Through proteomic analysis and functional validation, we further identify signal peptidase complex subunit 3 (SPCS3) and eukaryotic translation initiation factor 3 subunit K (eIF3k) as E1-binding host proteins with anti-CHIKV activities. We find that E1 residue V220, which has undergone positive selection, is indispensable for CHIKV production in macrophages, as its mutation attenuates E1 interaction with the host restriction factors SPCS3 and eIF3k. Finally, we show that the antiviral activity of eIF3k is translation-independent, and that CHIKV infection promotes eIF3k translocation from the nucleus to the cytoplasm, where it associates with SPCS3. These functions of CHIKV glycoproteins late in the viral life cycle provide a new example of an intracellular evolutionary arms race with host restriction factors, as well as potential targets for therapeutic intervention.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142174789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0