FEBS Letters最新文献_第3页

Chelatase activity of magnesium dechelatase associated with chlorophyll degradation. 与叶绿素降解相关的镁脱羧酶的螯合酶活性。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2025-06-17 DOI: 10.1002/1873-3468.70094

Soma Sato, Mitsuaki Hirose, Hitoshi Tamiaki, Hisashi Ito

引用次数: 0

Circulating histones as clinical biomarkers in critically ill conditions. 循环组蛋白在危重患者中的临床生物标志物作用。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2025-06-17 DOI: 10.1002/1873-3468.70093

José Luis García-Gimenez, Juan Carlos Ruiz-Rodríguez, Ricard Ferrer, Raquel Durá, Antonio Artigas, Iván Bajaña, David Bolado López de Andujar, Irene Cánovas-Cervera, Adrián Ceccato, Luis Chiscano-Camón, Elena Climent-Martinez, Georgia García Fernández, Gemma Goma, Verónica Monforte, Beatriz Quevedo-Sánchez, Adolf Ruiz-Sanmartín, Antonio Sierra-Rivera, Nieves Carbonell Monleón

{"title":"Circulating histones as clinical biomarkers in critically ill conditions.","authors":"José Luis García-Gimenez, Juan Carlos Ruiz-Rodríguez, Ricard Ferrer, Raquel Durá, Antonio Artigas, Iván Bajaña, David Bolado López de Andujar, Irene Cánovas-Cervera, Adrián Ceccato, Luis Chiscano-Camón, Elena Climent-Martinez, Georgia García Fernández, Gemma Goma, Verónica Monforte, Beatriz Quevedo-Sánchez, Adolf Ruiz-Sanmartín, Antonio Sierra-Rivera, Nieves Carbonell Monleón","doi":"10.1002/1873-3468.70093","DOIUrl":"https://doi.org/10.1002/1873-3468.70093","url":null,"abstract":"Extracellular histones, primarily nuclear proteins involved in chromatin organization, have emerged as key mediators in pathological processes in critically ill patients. When released into circulation due to cell death mechanisms such as NETosis, histones act as damage-associated molecular patterns (DAMPs), contributing to excessive inflammation, endothelial dysfunction, immune response dysregulation, coagulation activation, cell death, and multi-organ damage. Increasing evidence supports their role in the pathophysiology of sepsis, acute lung injury, cardiac injury, pancreatitis, and other life-threatening conditions. Given their strong association with disease severity and prognosis, circulating histones have gained attention as potential clinical biomarkers for early diagnosis, prognosis, and therapeutic monitoring in critically ill patients. This review discusses the biological roles of extracellular histones, their potential as biomarkers, different approaches to measure them, and emerging therapeutic strategies aimed at neutralizing or removing circulating histones to improve patient outcomes in severe medical conditions. Impact statement This review highlights extracellular histones as key mediators and biomarkers in sepsis, proposing their use in diagnosis, prognosis, and treatment monitoring. Integrating quantitative proteomics for the detection of circulating histones may enhance patient stratification and guide therapeutic strategies, advancing personalized medicine in critical care.","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316232","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

Genomic modifiers of neurological resilience in a Niemann-Pick C family. Niemann-Pick C家族神经弹性的基因组修饰因子。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2025-06-12 DOI: 10.1002/1873-3468.70091

Macarena Las Heras, Benjamín Szenfeld, Valeria Olguín, Juan Carlos Rubilar, Juan Francisco Calderón, Yanireth Jimenez, Silvana Zanlungo, Emanuele Buratti, Andrea Dardis, Francisco A Cubillos, Andrés D Klein

{"title":"Genomic modifiers of neurological resilience in a Niemann-Pick C family.","authors":"Macarena Las Heras, Benjamín Szenfeld, Valeria Olguín, Juan Carlos Rubilar, Juan Francisco Calderón, Yanireth Jimenez, Silvana Zanlungo, Emanuele Buratti, Andrea Dardis, Francisco A Cubillos, Andrés D Klein","doi":"10.1002/1873-3468.70091","DOIUrl":"https://doi.org/10.1002/1873-3468.70091","url":null,"abstract":"Niemann-Pick type C (NPC) disease, caused by NPC1 or NPC2 variants, disrupts cholesterol and glycolipid trafficking, leading to diverse clinical manifestations. To understand the genetic basis of neurological resilience, we analyzed an NPC family with variable phenotypes, identifying loss-of-function variants in CCDC115, SLC4A5, DEPDC5, ETFDH, SNRNP200, and DOCK1 that co-segregated with milder neurological involvement. Using yeast models, we successfully predicted NPC-like severity based on orthologous gene variants. RNA-seq revealed a positive correlation between mitochondrial transcripts and cellular fitness. Modeling NPC in yeast lacking the SLC4A5 ortholog, bor1, enhanced cellular fitness, improved mitochondrial function, and reduced sterol accumulation. Our findings identify potential modifiers and biomarkers of NPC severity, highlighting mitochondrial pathways and SLC4A5 as a therapeutic target. Impact statement Niemann-Pick type C (NPC) disease is a progressive neurovisceral lysosomal storage disorder. Here, we identified genomic modifiers of neurological resilience in an NPC family, with SLC4A5 emerging as a key biomarker and therapeutic target. Additionally, our study highlighted mitochondrial transcripts and metabolites as potential biomarkers of severity.","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144283072","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

Mycobacterium tuberculosis virulence-associated small RNA MTS1338 is posttranscriptionally regulated by the ribonuclease YbeY 结核分枝杆菌毒力相关小RNA MTS1338受核糖核酸酶YbeY的转录后调控。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2025-06-09 DOI: 10.1002/1873-3468.70089

Reena Nirban, Saumya Singh, Rajkumar Kulandaisamy, Krishna Kishore Inampudi, Tanmay Dutta

引用次数: 0

Validation of single-cell transcriptomic profiles from Illumina and MGI Tech sequencing platforms. 来自Illumina和MGI Tech测序平台的单细胞转录组谱验证。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2025-06-09 DOI: 10.1002/1873-3468.70087

Valerie Vandenbempt, Michael Roach, Monika Mohenska, Kellie Wise, Taopeng Wang, Kate Harvey, Kirk Jensen, Alexander Swarbrick, Jose M Polo, Esteban N Gurzov, Luciano G Martelotto

引用次数: 0

Investigation of oxidative-stress-induced axon beading using photo-oxidation. 利用光氧化技术研究氧化应激诱导的轴突串珠。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2025-06-09 DOI: 10.1002/1873-3468.70074

Deepak Mehta, Pooja Joshi, Pramod Pullarkat

引用次数: 0

Disruption of SETD3-mediated histidine-73 methylation by the BWCFF-associated β-actin G74S mutation. bwcff相关β-肌动蛋白G74S突变破坏setd3介导的组氨酸-73甲基化。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2025-06-09 DOI: 10.1002/1873-3468.70088

Anja Marquardt, Marcus S Münchhoff, Jacqueline Krohn, Philip M Palarz, Manuel H Taft, Johannes N Greve, Nataliya Di Donato, Falk F R Buettner, Dietmar J Manstein

{"title":"Disruption of SETD3-mediated histidine-73 methylation by the BWCFF-associated β-actin G74S mutation.","authors":"Anja Marquardt, Marcus S Münchhoff, Jacqueline Krohn, Philip M Palarz, Manuel H Taft, Johannes N Greve, Nataliya Di Donato, Falk F R Buettner, Dietmar J Manstein","doi":"10.1002/1873-3468.70088","DOIUrl":"https://doi.org/10.1002/1873-3468.70088","url":null,"abstract":"Histidine-73 methylation of β-actin by SETD3 modulates ATPase activity, filament assembly, and protein interactions. The pathogenic G74S mutation in cytoskeletal β-actin, associated with Baraitser-Winter cerebrofrontofacial syndrome (BWCFF), alters the adjacent phosphate sensor loop, disrupting SETD3-mediated methylation. Molecular docking indicates that SETD3 undergoes structural rearrangements to accommodate the mutant β-actin, leading to reduced catalytic efficiency. Enzymatic assays confirm slower turnover of mutant actin peptides, while mass spectrometry reveals decreased histidine-73 methylation in both recombinant mutant β-actin and patient-derived fibroblasts. This perturbance of SETD3-mediated methylation likely generates β-actin pools with distinct methylation states, varying across cell types and developmental stages, thereby impairing cytoskeletal dynamics and contributing to BWCFF pathology. Impact statement This study reveals that the BWCFF-linked G74S mutation in β-actin disrupts SETD3-mediated histidine-73 methylation, impairing a critical post-translational modification. It provides the first direct mechanistic link between a cytoskeletal actinopathy and altered methylation, highlighting potential targets for therapeutic intervention in β-actin-related developmental disorders.","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257666","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

A coiled-coil domain triggers oligomerization of MmpL10, the mycobacterial transporter of trehalose polyphleate precursor 螺旋结构域触发MmpL10寡聚化，这是海藻糖多聚酸前体的分枝杆菌转运体。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2025-06-04 DOI: 10.1002/1873-3468.70085

Julie Couston, Jérôme Feuillard, Aurélie Ancelin, Joséphine Lai-Kee-Him, Konstantin Brodolin, Christian Chalut, Pontus Gourdon, Mickaël Blaise