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AAA+ protein unfoldases-the Moirai of the proteome. AAA+蛋白展开——蛋白质组的Moirai。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-05-07 DOI: 10.1002/1873-3468.70348
Stavros Azinas, Marta Carroni
{"title":"AAA+ protein unfoldases-the Moirai of the proteome.","authors":"Stavros Azinas, Marta Carroni","doi":"10.1002/1873-3468.70348","DOIUrl":"https://doi.org/10.1002/1873-3468.70348","url":null,"abstract":"<p><p>AAA+ ATPases safeguard proteostasis by harnessing ATP hydrolysis to unfold misfolded or damaged proteins. Depending on their specific structural motifs and partners, they either channel substrates to peptidases for degradation or disentangle aggregates for refolding. This conserved mechanism across all life domains relies on the conversion of chemical energy into mechanical force. Although structural, biochemical and single-molecule studies have provided valuable insights into ATP-driven unfolding, the precise threading mechanism remains unresolved. This review synthesises current knowledge on three classes of AAA+ unfoldases: (a) self-contained proteases with both ATPase and peptidase domains, (b) ATPases cooperating with separate peptidases and (c) ATPases dedicated to disaggregation and refolding without proteolysis. We discuss existing models, underline technological limitations and outline experimental approaches to address these challenges. Gaining a clearer picture of substrate threading will enhance our grasp of basic protein quality control and also enable modulation of proteostasis in eukaryotic cells, relevant to neurodegenerative diseases and antibiotic targeting of bacterial unfoldases. Like the mythological Moirai, AAA+ enzymes govern the fate of proteins, though their exact decision-making and handling of their protein substrates remains elusive.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835838","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
pH-mediated activation of the lysosomal arginine sensor SLC38A9. ph介导的溶酶体精氨酸传感器SLC38A9的激活。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-05-03 DOI: 10.1002/1873-3468.70352
Xuelang Mu, Ampon Sae Her, Tamir Gonen
{"title":"pH-mediated activation of the lysosomal arginine sensor SLC38A9.","authors":"Xuelang Mu, Ampon Sae Her, Tamir Gonen","doi":"10.1002/1873-3468.70352","DOIUrl":"https://doi.org/10.1002/1873-3468.70352","url":null,"abstract":"<p><p>Cells rely on metabolic control; the mechanistic target of rapamycin complex 1 (mTORC1) senses nutrient availability, particularly amino acids. Lysosomes maintain amino acid homeostasis through recycling. SLC38A9, a lysosomal amino acid transporter, functions as a critical sensor in the mTORC1 pathway. Here, we investigate how pH regulates SLC38A9 activity. We show that arginine uptake is pH-dependent, with His544 residue serving as the pH sensor. Mutating His544 abolishes pH dependence without impairing overall transport, indicating His544 influences transport through protonation/deprotonation, instead of involving in the substrate binding. We propose a working model for pH-induced activation, through comparing two determined SLC38A9 structures at different pH. These findings reveal how local ionic shifts regulate lysosomal transporters and fine-tune SLC38A9 function to control mTORC1 signaling.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812618","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
Unique SNPs in the promoter of the peptide transporter gene PTR2 increase its expression in the Saccharomyces cerevisiae sake strain. 肽转运基因PTR2启动子中独特的snp增加了其在酿酒酵母菌株中的表达。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-05-01 DOI: 10.1002/1873-3468.70349
Nanami Nakagawa, Kenji Kitamura
{"title":"Unique SNPs in the promoter of the peptide transporter gene PTR2 increase its expression in the Saccharomyces cerevisiae sake strain.","authors":"Nanami Nakagawa, Kenji Kitamura","doi":"10.1002/1873-3468.70349","DOIUrl":"https://doi.org/10.1002/1873-3468.70349","url":null,"abstract":"<p><p>Although the mechanism of action of the tripeptide-like herbicide bialaphos is well understood, its cellular uptake process remains elusive. We report that a peptide transporter mediates its uptake in Saccharomyces cerevisiae. The Japanese sake yeast strain Kyokai 7 (K7) was supersensitive to bialaphos compared to S288C. Disruption of PTR2, which encodes a peptide transporter, alleviated bialaphos sensitivity in K7. PTR2 mRNA and protein levels were higher in K7 than in S288C. Higher expression levels were observed in the S288C strain when Ptr2 was expressed using the K7-derived genomic promoter of PTR2. We identified single-nucleotide polymorphisms (SNPs) in the PTR2 promoter responsible for the increased expression levels. One of the critical SNPs was specifically found in sake strains of K7-lineage.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812692","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: Down-Regulation of Adenine Nucleotide Translocase 3 and Its Role in Camptothecin-Induced Apoptosis in Human Hepatoma QGY7703 Cells. 撤回：腺嘌呤核苷酸转位酶3的下调及其在喜树碱诱导的人肝癌QGY7703细胞凋亡中的作用。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-04-29 DOI: 10.1002/1873-3468.70354
{"title":"RETRACTION: Down-Regulation of Adenine Nucleotide Translocase 3 and Its Role in Camptothecin-Induced Apoptosis in Human Hepatoma QGY7703 Cells.","authors":"","doi":"10.1002/1873-3468.70354","DOIUrl":"https://doi.org/10.1002/1873-3468.70354","url":null,"abstract":"<p><strong>Retraction: </strong>Z. Hu , X. Guo , Q. Yu , L. Qiu , J. Li , K. Ying , C. Guo and J. Zhang , \"Down-Regulation of Adenine Nucleotide Translocase 3 and Its Role in Camptothecin-Induced Apoptosis in Human Hepatoma QGY7703 Cells,\" FEBS Letters 583, no. 2 (2009): 383-388, https://doi.org/10.1016/j.febslet.2008.12.029. The above article, published online on 25 December 2008 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Michael Brunner; the Federation of European Biochemical Societies; and John Wiley & Sons Ltd. The retraction has been agreed upon following concerns raised by a third party. An investigation identified several unexpected similarities between the FACS 6h and 12h panels shown in Figure 1A. Duplication of the β-actin bands between Figures 2 and 3A, and between Figures 2 and 4A, was also identified. Due to the time that has elapsed since publication, the authors were unable to provide any original data and stated that the duplications resulted from unintentional errors. In light of these issues, the editors consider the results and conclusions to be unreliable.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766658","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
Organizing the interface-Plasma membrane architecture and receptor dynamics in virus-cell interactions. 组织病毒-细胞相互作用中的界面-质膜结构和受体动力学。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-04-27 DOI: 10.1002/1873-3468.70347
Jan Schlegel, Christian Sieben
{"title":"Organizing the interface-Plasma membrane architecture and receptor dynamics in virus-cell interactions.","authors":"Jan Schlegel, Christian Sieben","doi":"10.1002/1873-3468.70347","DOIUrl":"https://doi.org/10.1002/1873-3468.70347","url":null,"abstract":"<p><p>Plasma membranes are organized into dynamic nanoscale domains that regulate lipid and protein distribution, diffusion, and receptor availability. Because viruses act on similar length scales, this organization shapes early infection steps, including attachment, membrane exploration, receptor engagement, and entry. This review summarizes how pre-existing receptor nanoplatforms promote viral capture and how virus binding can remodel plasma membrane nanoarchitecture. Using influenza A virus and human immunodeficiency virus 1 as examples, we discuss how multivalent, low-affinity glycoprotein-glycan interactions exploit clustered attachment factors to increase avidity and tune receptor dynamics. We also address transbilayer lipid asymmetry and how its perturbation-particularly phosphatidylserine exposure and apoptotic mimicry-is exploited by enveloped viruses.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766743","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 ubiquitin ligase RNF115 is required for the clearance of damaged lysosomes. 泛素连接酶RNF115是清除受损溶酶体所必需的。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-04-24 DOI: 10.1002/1873-3468.70346
Sae Nakanaga, Toshiki Takahashi, Akiko Kuma, Hiroyuki Kawahara
{"title":"The ubiquitin ligase RNF115 is required for the clearance of damaged lysosomes.","authors":"Sae Nakanaga, Toshiki Takahashi, Akiko Kuma, Hiroyuki Kawahara","doi":"10.1002/1873-3468.70346","DOIUrl":"https://doi.org/10.1002/1873-3468.70346","url":null,"abstract":"<p><p>Lysosomes play a critical role in the quality control of cellular organelles. However, lysosomal membranes can be damaged under a variety of conditions, leading to the onset of various diseases. Damaged lysosomes are selectively cleared via a ubiquitin-dependent mechanism, but the molecular mechanisms underlying this process have not been adequately elucidated. In this study, we found that RNF115 is a lysosomal damage-responsive ubiquitin ligase that undergoes massive translocation from the cytosol to the p62/SQSTM1-positive puncta around ruptured lysosomes. In accordance with the changes in its distribution, the depletion of RNF115 delayed the removal of Gal3 from damaged lysosomes during the restoration process following lysosomal damage. These observations suggest that RNF115 is responsible for the clearance of damaged lysosomes.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766686","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
Investigating human pregnancy with trophoblast organoids. 利用滋养细胞类器官研究人类妊娠。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-04-24 DOI: 10.1002/1873-3468.70344
Ida Calvi, Margherita Yayoi Turco
{"title":"Investigating human pregnancy with trophoblast organoids.","authors":"Ida Calvi, Margherita Yayoi Turco","doi":"10.1002/1873-3468.70344","DOIUrl":"https://doi.org/10.1002/1873-3468.70344","url":null,"abstract":"<p><p>The placenta plays a vital role in supporting and nourishing the fetus throughout pregnancy, yet the mechanisms governing its development remain poorly understood. Recent advances in 3D human trophoblast organoid systems derived from both primary tissues and stem cells provide physiologically relevant platforms to investigate placental development in both health and disease. This 'In a Nutshell' review highlights how these models are transforming our ability to investigate human placental biology in pregnancy.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766688","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
Diversity and complexity in neural organoids. 神经类器官的多样性和复杂性。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-04-24 DOI: 10.1002/1873-3468.70329
Ilaria Chiaradia, Madeline A Lancaster
{"title":"Diversity and complexity in neural organoids.","authors":"Ilaria Chiaradia, Madeline A Lancaster","doi":"10.1002/1873-3468.70329","DOIUrl":"https://doi.org/10.1002/1873-3468.70329","url":null,"abstract":"<p><p>The complexity of human neurobiology is influenced by its heterogeneity, reflected in both cell type diversity as well as genetic variations between individuals. Neural organoids are 3D developing neural tissues designed to mimic development of the nervous system; however, most currently fail to capture this diversity. Recent advances have focused on increasing complexity through self-organised multi-region organoids, assembloids and chimeroids. Here, we discuss these approaches, as well as the remaining lack of genetic and ethnic diversity in neural organoid research, its impact on the generalizability of findings, and strategies to address this gap. We provide a flowchart to guide the experimenter towards the choice of model and discuss applications of neural organoids that benefit from complexity or reliability.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766747","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
Crystal structures of Klebsiella oxytoca ribitol dehydrogenase in complex with NAD+, d-allose, or d-allulose reveal insight into substrate recognition. 与NAD+， d-allulose或d-allulose复合物的克雷伯菌脱氧核糖醇脱氢酶的晶体结构揭示了对底物识别的见解。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-04-21 DOI: 10.1002/1873-3468.70345
Hiromi Yoshida, Mayu Matsumoto, Naho Yamamoto, Akihide Yoshihara, Ken Izumori, Shigehiro Kamitori
{"title":"Crystal structures of Klebsiella oxytoca ribitol dehydrogenase in complex with NAD<sup>+</sup>, d-allose, or d-allulose reveal insight into substrate recognition.","authors":"Hiromi Yoshida, Mayu Matsumoto, Naho Yamamoto, Akihide Yoshihara, Ken Izumori, Shigehiro Kamitori","doi":"10.1002/1873-3468.70345","DOIUrl":"https://doi.org/10.1002/1873-3468.70345","url":null,"abstract":"<p><p>Recombinant NAD<sup>+</sup>-dependent ribitol dehydrogenase derived from Klebsiella oxytoca (KoRdh) exhibits activity toward both ribitol and allitol. KoRdh catalyzes the NAD<sup>+</sup>-dependent oxidation of allitol to d-allulose and the NADH-dependent reduction of d-allulose to allitol. Notably, the flexible loop of KoRdh undergoes conformational changes upon NAD<sup>+</sup> and substrate binding. To elucidate the flexible loop's role in substrate recognition, we determined the X-ray structures of KoRdh alone and in complexes with NAD<sup>+</sup>, d-allulose, or d-allose. Although d-allose is an aldose and not a substrate of KoRdh, it binds to KoRdh in the pyranose form, revealing the location of the substrate-binding site. Based on these structures, we propose a substrate recognition mechanism for KoRdh. Impact statement This research reveals an insight into a substrate recognition mechanism in the flexible region of ribitol dehydrogenase. Because ribitol dehydrogenase is a member of the short-chain reductases/oxidases (SDR) family, the current study will provide further insight into related enzymes that harbor the flexible region.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766727","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
Senescent cells acquire resistance to cystine deprivation-induced ferroptosis via the PPARα-PDK4-phosphorylated PDH axis. 衰老细胞通过ppar α- pdk4磷酸化的PDH轴获得对胱氨酸剥夺诱导的铁下垂的抗性。
IF 3 4区 生物学
FEBS Letters Pub Date : 2026-04-19 DOI: 10.1002/1873-3468.70332
Shiho Machii, Kazushi Morimoto, Pakawit Lerksaipheng, Mirinthorn Jutanom, Ken-Ichi Yamada
{"title":"Senescent cells acquire resistance to cystine deprivation-induced ferroptosis via the PPARα-PDK4-phosphorylated PDH axis.","authors":"Shiho Machii, Kazushi Morimoto, Pakawit Lerksaipheng, Mirinthorn Jutanom, Ken-Ichi Yamada","doi":"10.1002/1873-3468.70332","DOIUrl":"https://doi.org/10.1002/1873-3468.70332","url":null,"abstract":"<p><p>Cellular senescence, a state of irreversible cell cycle arrest, is implicated in age-related diseases. While it is well known that senescent cells resist apoptosis, studies on their resistance to ferroptosis are limited and not fully understood. Senescent cells remain sensitive to ferroptosis induced by direct inhibition of glutathione peroxidase 4 (GPX4) but resist ferroptosis from cystine starvation, suggesting a role for mitochondrial metabolism. Here, we found that this resistance is mediated by peroxisome proliferator-activated receptor α (PPARα)-dependent upregulation of pyruvate dehydrogenase kinase 4 (PDK4), which inactivates pyruvate dehydrogenase (PDH) and suppresses mitochondria-derived reactive oxygen species, a key driver of ferroptosis. Our findings identify the PPARα-PDK4-PDH axis as a metabolic switch regulating ferroptosis sensitivity in senescent cells and provide insight into the senescence-ferroptosis interaction.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147722212","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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