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Transcription-coupled repair - mechanisms of action, regulation, and associated human disorders. 转录偶联修复-作用机制，调节，和相关的人类疾病。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-20 DOI: 10.1002/1873-3468.15073
Yuka Nakazawa, Yasuyoshi Oka, Tomoko Matsunaga, Tomoo Ogi
{"title":"Transcription-coupled repair - mechanisms of action, regulation, and associated human disorders.","authors":"Yuka Nakazawa, Yasuyoshi Oka, Tomoko Matsunaga, Tomoo Ogi","doi":"10.1002/1873-3468.15073","DOIUrl":"https://doi.org/10.1002/1873-3468.15073","url":null,"abstract":"<p><p>The transcription-coupled repair (TCR) pathway resolves transcription-blocking DNA lesions to maintain cellular function and prevent transcriptional arrest. Stalled RNA polymerase II (RNAPII) triggers repair mechanisms, including RNAPII ubiquitination, which recruit UVSSA and TFIIH. Defects in TCR-associated genes cause disorders like Cockayne syndrome, UV-sensitive syndrome, xeroderma pigmentosum, and recently defined AMeDS. TCR safeguards transcription, linking its failure to neurodegeneration and disease phenotypes.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863881","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
Temperature adaptation of yeast phospholipid molecular species at the acyl chain positional level. 酵母磷脂分子物种在酰基链位置水平上的温度适应性。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-13 DOI: 10.1002/1873-3468.15060
Celine Kelso, Alan T Maccarone, Anton I P M de Kroon, Todd W Mitchell, Mike F Renne
{"title":"Temperature adaptation of yeast phospholipid molecular species at the acyl chain positional level.","authors":"Celine Kelso, Alan T Maccarone, Anton I P M de Kroon, Todd W Mitchell, Mike F Renne","doi":"10.1002/1873-3468.15060","DOIUrl":"https://doi.org/10.1002/1873-3468.15060","url":null,"abstract":"<p><p>Yeast is a poikilothermic organism and adapts its lipid composition to the environmental temperature to maintain membrane physical properties. Studies addressing temperature-dependent adaptation of the lipidome have described changes in the phospholipid composition at the level of sum composition (e.g. PC 32:1) and molecular composition (e.g. PC 16:0_16:1). However, there is little information at the level of positional isomers (e.g. PC 16:0/16:1 versus PC 16:1/16:0). Here, we used collision- and ozone-induced dissociation (CID/OzID) mass spectrometry to investigate homeoviscous adaptation of PC, PE and PS to determine the phospholipid acyl chains at the sn-1 and sn-2 position. Our data establish the sn-molecular species composition of PC, PE and PS in the lipidome of yeast cultured at different temperatures.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823966","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
RETRACTION: Theaflavins retard human breast cancer cell migration by inhibiting NF-κB via p53-ROS cross-talk. 返回：茶黄素通过 p53-ROS 交叉对话抑制 NF-κB 从而延缓人类乳腺癌细胞的迁移。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-13 DOI: 10.1002/1873-3468.15076
{"title":"RETRACTION: Theaflavins retard human breast cancer cell migration by inhibiting NF-κB via p53-ROS cross-talk.","authors":"","doi":"10.1002/1873-3468.15076","DOIUrl":"https://doi.org/10.1002/1873-3468.15076","url":null,"abstract":"<p><strong>Retraction: </strong>A. Adhikary, S. Mohanty, L. Lahiry, D. S. Hossain, S. Chakraborty and T. Das, \"Theaflavins Retard Human Breast Cancer Cell Migration by Inhibiting NF-κB via p53-ROS Cross-talk,\" FEBS Letters 584, no. 1 (2010): 7-14, https://doi.org/10.1016/j.febslet.2009.10.081. The above article, published online on 31 October 2009 in Wiley Online Library (wileyonlinelibrary.com), has been published by agreement between the journal Editor-in-Chief, Michael Brunner; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed due to partial duplication of micrographs observed in Figure 2C and the unexpected similarity of curves presented in 3C. Additionally, the blot against histone H1 in figure 4D (bottom-left panel) is a stretched duplication of the blot against alpha-actin in figure 3F (right-hand panel). Further, duplications have been observed between the MCF-7 p53 bands presented in Figures 1D and the p53 bands in Figure 3F; the alpha actin bands shown in Figure 3F and the Histone H1 bands in Figure 4D; and the alpha actin bands presented in Figures 3E and 4D. The authors provided some supporting data and an explanation, but the editors found them unsatisfactory. Due to the extent and nature of these concerns, the editors consider the results and conclusions of this article to be invalid. The authors disagree with the retraction.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823962","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
Suppression of amber stop codons impairs pathogenicity in Salmonella. 琥珀色终止密码子的抑制削弱了沙门氏菌的致病性。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-12 DOI: 10.1002/1873-3468.15075
Zhihui Lyu, Cierra Wilson, Prajita Paul, Jiqiang Ling
{"title":"Suppression of amber stop codons impairs pathogenicity in Salmonella.","authors":"Zhihui Lyu, Cierra Wilson, Prajita Paul, Jiqiang Ling","doi":"10.1002/1873-3468.15075","DOIUrl":"10.1002/1873-3468.15075","url":null,"abstract":"<p><p>Translation terminates at UAG (amber), UGA (opal), and UAA (ochre) stop codons. In nature, readthrough of stop codons can be substantially enhanced by suppressor tRNAs. Stop-codon suppression also provides powerful tools in synthetic biology and disease treatment. How stop-codon suppression affects bacterial pathogenesis is poorly understood. Here, we show that suppression of UAG codons, but not UGA or UAA codons, attenuates expression of Salmonella Pathogenicity Island 1 (SPI-1) genes, which are required for virulence. Consistently, amber suppression abolishes Salmonella infection of macrophages. Systematic genetic and biochemical analyses further show that amber suppression decreases the activity, but not the level, of the master SPI-1 regulator HilD. Our work thus demonstrates an unexpected selectivity of stop codons in regulating Salmonella virulence.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817562","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 immunological interface: dendritic cells as key regulators in metabolic dysfunction-associated steatotic liver disease. 免疫界面：树突状细胞作为代谢功能障碍相关脂肪变性肝病的关键调节因子。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-12 DOI: 10.1002/1873-3468.15072
Camilla Klaimi, WanTing Kong, Camille Blériot, Joel T Haas
{"title":"The immunological interface: dendritic cells as key regulators in metabolic dysfunction-associated steatotic liver disease.","authors":"Camilla Klaimi, WanTing Kong, Camille Blériot, Joel T Haas","doi":"10.1002/1873-3468.15072","DOIUrl":"https://doi.org/10.1002/1873-3468.15072","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) refers to a broad spectrum of conditions associating fat accumulation in the liver (steatosis) with varying degrees of inflammation (hepatitis) and fibrosis, which can progress to cirrhosis and potentially cancer (hepatocellular carcinoma). The first stages of these diseases are reversible and the immune system, together with metabolic factors (obesity, insulin resistance, Western diet, etc.), can influence the disease trajectory leading to progression or regression. Dendritic cells are professional antigen-presenting cells that constantly sense environmental stimuli and orchestrate immune responses. Herein, we discuss the existing literature on the heterogeneity of dendritic cell lineages, states, and functions, to provide a comprehensive overview of how liver dendritic cells influence the onset and evolution of MASLD.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817567","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
Transcriptional regulation of basophil-specific protease genes by C/EBPα, GATA2, TGF-β signaling, and epigenetic mechanisms. C/EBPα、GATA2、TGF-β信号通路和表观遗传机制对嗜碱性粒细胞特异性蛋白酶基因的转录调控
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-11 DOI: 10.1002/1873-3468.15069
Ryotaro Tojima, Kazuki Nagata, Naoto Ito, Kenta Ishii, Takahiro Arai, Tomoka Ito, Kazumi Kasakura, Chiharu Nishiyama
{"title":"Transcriptional regulation of basophil-specific protease genes by C/EBPα, GATA2, TGF-β signaling, and epigenetic mechanisms.","authors":"Ryotaro Tojima, Kazuki Nagata, Naoto Ito, Kenta Ishii, Takahiro Arai, Tomoka Ito, Kazumi Kasakura, Chiharu Nishiyama","doi":"10.1002/1873-3468.15069","DOIUrl":"https://doi.org/10.1002/1873-3468.15069","url":null,"abstract":"<p><p>Basophils and mast cells (MCs) play an important role in immune responses against allergens and parasitic infection. To elucidate the mechanisms that determine the commitment between basophils and mast cell (MCs), transcription factors and epigenetic modifications regulating the gene expression of basophil-specific enzymes, Mcpt8 and Mcpt11, were analyzed using bone marrow-derived (BM) cells containing basophils and MCs. Knockdown (KD) and overexpression experiments revealed that the transcription factor C/EBPα positively regulated the gene expression of Mcpt8 and Prss34 (encoding Mcpt11). Cebpa, Mcpt8, and Prss34 mRNAs levels were upregulated by histone deacetylases and downregulated by DNA methyltransferases. Gata2 KD significantly reduced the mRNA levels of Mcpt8 and Prss34, while TGF-β treatment increased those of Mcpt8 and Prss34. These results show that basophil-specific protease genes were transactivated by C/EBPα, GATA2, and TGF-β signaling and modified with epigenetic regulation.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806514","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
Covalent labeling of the Arabidopsis plasma membrane H+-ATPase reveals 3D conformational changes involving the C-terminal regulatory domain. 拟南芥质膜H+- atp酶的共价标记揭示了涉及c端调控域的三维构象变化。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-03 DOI: 10.1002/1873-3468.15067
Matthew R Blackburn, Thao T Nguyen, Sophia E Patton, Jordan M Bartosiak, Michael R Sussman
{"title":"Covalent labeling of the Arabidopsis plasma membrane H<sup>+</sup>-ATPase reveals 3D conformational changes involving the C-terminal regulatory domain.","authors":"Matthew R Blackburn, Thao T Nguyen, Sophia E Patton, Jordan M Bartosiak, Michael R Sussman","doi":"10.1002/1873-3468.15067","DOIUrl":"https://doi.org/10.1002/1873-3468.15067","url":null,"abstract":"<p><p>The plasma membrane proton pump is the primary energy transducing, electrogenic ion pump of the plasma membrane in plants and fungi. Compared to its fungal counterpart, the plant plasma membrane proton pump's regulatory C-terminal domain (CTD) contains an additional regulatory segment that links multiple sensory pathways regulating plant cell length through phosphorylation and recruitment of regulatory 14-3-3 proteins. However, a complete structural model of a plant proton pump is lacking. Here, we performed covalent labeling with mass spectrometric analysis (CL-MS) on the Arabidopsis pump AHA2 to identify potential interactions between the CTD and the catalytic domains. Our results suggest that autoinhibition in the plant enzyme is much more structurally complex than in the fungal enzyme.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767610","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
YAP1 modulation of primary cilia-mediated ciliogenesis in 2D and 3D prostate cancer models. YAP1 在二维和三维前列腺癌模型中对原发性纤毛介导的纤毛生成的调节。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-01 Epub Date: 2024-10-18 DOI: 10.1002/1873-3468.15029
Yingbo Guo, Mathilde Dupart, Marie Irondelle, Pascal Peraldi, Frederic Bost, Nathalie M Mazure
{"title":"YAP1 modulation of primary cilia-mediated ciliogenesis in 2D and 3D prostate cancer models.","authors":"Yingbo Guo, Mathilde Dupart, Marie Irondelle, Pascal Peraldi, Frederic Bost, Nathalie M Mazure","doi":"10.1002/1873-3468.15029","DOIUrl":"10.1002/1873-3468.15029","url":null,"abstract":"<p><p>The primary cilium, a non-motile organelle present in most human cells, plays a crucial role in detecting microenvironmental changes and regulating intracellular signaling. Its dysfunction is linked to various diseases, including cancer. We explored the role of ciliated cells in prostate cancer by using Gefitinib and Jasplakinolide compounds to induce ciliated cells in both normal and tumor-like prostate cell lines. We assessed GLI1 and IFT20 expression and investigated YAP1 protein's role, which is implicated in primary cilium regulation. Finally, we examined these compounds in 3D cell models, aiming to simulate in vivo conditions. Our study highlights YAP1 as a potential target for novel genetic models to understand the primary cilium's role in mediating resistance to anticancer treatments.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":"3071-3086"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461349","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 role of Lin28A and Lin28B in cancer beyond Let-7. Lin28A和Lin28B在癌症中的作用超越了Let-7。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-01 Epub Date: 2024-08-16 DOI: 10.1002/1873-3468.15004
Sandra Cotino-Nájera, Enrique García-Villa, Samantha Cruz-Rosales, Patricio Gariglio, José Díaz-Chávez
{"title":"The role of Lin28A and Lin28B in cancer beyond Let-7.","authors":"Sandra Cotino-Nájera, Enrique García-Villa, Samantha Cruz-Rosales, Patricio Gariglio, José Díaz-Chávez","doi":"10.1002/1873-3468.15004","DOIUrl":"10.1002/1873-3468.15004","url":null,"abstract":"<p><p>Lin28A and Lin28B are paralogous RNA-binding proteins that play fundamental roles in development and cancer by regulating the microRNA family of tumor suppressor Let-7. Although Lin28A and Lin28B share some functional similarities with Let-7 inhibitors, they also have distinct expression patterns and biological functions. Increasing evidence indicates that Lin28A and Lin28B differentially impact cancer stem cell properties, epithelial-mesenchymal transition, metabolic reprogramming, and other hallmarks of cancer. Therefore, it is important to understand the overexpression of Lin28A and Lin28B paralogs in specific cancer contexts. In this review, we summarize the main similarities and differences between Lin28A and Lin28B, their implications in different cellular processes, and their role in different types of cancer. In addition, we provide evidence of other specific targets of each lin28 paralog, as well as the lncRNAs and miRNAs that promote or inhibit its expression, and how this impacts cancer development and progression.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":"2963-2979"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11665955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141995589","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
The FEBS 60th anniversary writing contest-blueprints for the scientific society of tomorrow. FEBS 60周年纪念写作比赛-未来科学社会的蓝图。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-01 DOI: 10.1002/1873-3468.15066
Duncan E Wright
{"title":"The FEBS 60th anniversary writing contest-blueprints for the scientific society of tomorrow.","authors":"Duncan E Wright","doi":"10.1002/1873-3468.15066","DOIUrl":"https://doi.org/10.1002/1873-3468.15066","url":null,"abstract":"<p><p>The Federation of European Biochemical Societies (FEBS) celebrated its 60th anniversary in 2024, and FEBS Letters marked the occasion with a writing contest on the future of scientific societies. This editorial introduces the winning article by Yussuf Ali and presents an overview of the predominant themes that emerged during the contest, which included AI, interdisciplinarity, diversity and sustainability.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"598 24","pages":"2943-2945"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881670","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
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