Journal of Molecular Biology最新文献_第8页

IsoTools 2.0: Software for Comprehensive Analysis of Long-read Transcriptome Sequencing Data. IsoTools 2.0：用于全面分析长读转录组测序数据的软件。

IF 4.7 2区生物学

Journal of Molecular Biology Pub Date : 2025-02-26 DOI: 10.1016/j.jmb.2025.169049

Yalan Bi, Tom Lukas Lankenau, Matthias Lienhard, Ralf Herwig

{"title":"IsoTools 2.0: Software for Comprehensive Analysis of Long-read Transcriptome Sequencing Data.","authors":"Yalan Bi, Tom Lukas Lankenau, Matthias Lienhard, Ralf Herwig","doi":"10.1016/j.jmb.2025.169049","DOIUrl":"10.1016/j.jmb.2025.169049","url":null,"abstract":"<p><p>Direct, single molecule measurement of RNA by long-read transcriptome sequencing (LRTS) enables the reliable detection of transcripts and alternative splicing events, thus contributing to the identification of splicing mechanisms, improvement of current gene models, as well as to the prediction of more reliable protein isoforms. LRTS data comes from either PacBio's single-molecule real time sequencing or from Oxford Nanopore's nanopore sequencing. Previously, we developed IsoTools, a software originally designed for processing and analyzing PacBio data. IsoTools copes with the complexity of LRTS data and offers multiple functionality for transcript identification and quantification as well as the analysis of differential isoform usage and local differential splicing events. Here, we report an update of the software, IsoTools 2.0, and demonstrate its additional performance on Oxford Nanopore data from multiple experimental protocols. We present the IsoTools 2.0 workflow, highlighting novel functionalities with respect to reliable transcript detection as well as transcription start site prediction. Additionally, we show novel metrics for structural description and quantification of gene model variability based on the gene's transcripts. We demonstrate the performance of IsoTools 2.0 on a variety of experimental protocols for library construction from a recent LRTS challenge. We show that IsoTools 2.0 is able to cope with the inherent complexity of LRTS data and that the workflow generates meaningful hypotheses on biomarkers for alternative splicing. The software is available from https://github.com/HerwigLab/IsoTools2/.</p>","PeriodicalId":369,"journal":{"name":"Journal of Molecular Biology","volume":" ","pages":"169049"},"PeriodicalIF":4.7,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Off-pathway oligomers of α-synuclein and Aβ inhibit secondary nucleation of α-synuclein amyloid fibrils α-突触核蛋白和Aβ的通路低聚物抑制α-突触核蛋白淀粉样原纤维的二次成核。

IF 4.7 2区生物学

Journal of Molecular Biology Pub Date : 2025-02-25 DOI: 10.1016/j.jmb.2025.169048

Marie P. Schützmann , Wolfgang Hoyer

{"title":"Off-pathway oligomers of α-synuclein and Aβ inhibit secondary nucleation of α-synuclein amyloid fibrils","authors":"Marie P. Schützmann , Wolfgang Hoyer","doi":"10.1016/j.jmb.2025.169048","DOIUrl":"10.1016/j.jmb.2025.169048","url":null,"abstract":"<div><div><span><math><mrow><mi>α</mi></mrow></math></span>-Synuclein (<span><math><mrow><mi>α</mi></mrow></math></span>Syn) is a key culprit in the pathogenesis of synucleinopathies such as Parkinson’s Disease (PD), in which it forms not only insoluble aggregates called amyloid fibrils but also smaller, likely more detrimental species termed oligomers. This property is shared with other amyloidogenic proteins such as the Alzheimer’s Disease-associated amyloid-<span><math><mrow><mi>β</mi></mrow></math></span> (A<span><math><mrow><mi>β</mi></mrow></math></span>). We previously found an intriguing interplay between off-pathway A<span><math><mrow><mi>β</mi></mrow></math></span> oligomers and A<span><math><mrow><mi>β</mi></mrow></math></span> fibrils, in which the oligomers interfere with fibril formation via inhibition of secondary nucleation by blocking secondary nucleation sites on the fibril surface. Here, using ThT aggregation kinetics and atomic force microscopy (AFM), we tested if the same interplay applies to <span><math><mrow><mi>α</mi></mrow></math></span>Syn fibrils. Both homotypic (i.e. <span><math><mrow><mi>α</mi></mrow></math></span>Syn) and heterotypic (i.e. A<span><math><mrow><mi>β</mi></mrow></math></span>) off-pathway oligomers inhibited <span><math><mrow><mi>α</mi></mrow></math></span>Syn aggregation in kinetic assays of secondary nucleation. Initially soluble, kinetically trapped A<span><math><mrow><mi>β</mi></mrow></math></span> oligomers co-precipitated with <span><math><mrow><mi>α</mi></mrow></math></span>Syn(1–108) fibrils. The resulting co-assemblies were imaged as clusters of curvilinear oligomers by AFM. The results indicate that off-pathway oligomers have a general tendency to bind amyloid fibril surfaces, also in the absence of sequence homology between fibril and oligomer. The interplay between off-pathway oligomers and amyloid fibrils adds another level of complexity to the homo- and hetero-assembly processes of amyloidogenic proteins.</div></div>","PeriodicalId":369,"journal":{"name":"Journal of Molecular Biology","volume":"437 10","pages":"Article 169048"},"PeriodicalIF":4.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Pioneer in Molecular Biology: Conformational Ensembles in Molecular Recognition, Allostery, and Cell Function 分子生物学先驱：分子识别、变构和细胞功能中的构象集成。

IF 4.7 2区生物学

Journal of Molecular Biology Pub Date : 2025-02-25 DOI: 10.1016/j.jmb.2025.169044

Ruth Nussinov

{"title":"Pioneer in Molecular Biology: Conformational Ensembles in Molecular Recognition, Allostery, and Cell Function","authors":"Ruth Nussinov","doi":"10.1016/j.jmb.2025.169044","DOIUrl":"10.1016/j.jmb.2025.169044","url":null,"abstract":"<div><div>In 1978, for my PhD, I developed the efficient <em>O</em>(<em>n</em><sup>3</sup>) dynamic programming algorithm for the-then open problem of RNA secondary structure prediction. This algorithm, now dubbed the “Nussinov algorithm”, “Nussinov plots”, and “Nussinov diagrams”, is still taught across Europe and the U.S. As sequences started coming out in the 1980s, I started seeking genome-encoded functional signals, later becoming a bioinformatics trend. In the early 1990s I transited to proteins, co-developing a powerful computer vision-based docking algorithm. In the late 1990s, I proposed the foundational role of conformational ensembles in molecular recognition and allostery. At the time, conformational ensembles and free energy landscapes were viewed as physical properties of proteins but were not associated with function. The classical view of molecular recognition and binding was based on <em>only two conformations</em> captured by crystallography: <em>open</em> and <em>closed</em>. I proposed that all conformational states preexist. Proteins always have not one folded form—nor two—but <em>many</em> folded forms. Thus, rather than inducing fit, binding can work by shifting the ensembles between states, and this shifting, or redistributing the ensembles to maintain equilibrium, is the origin of the allosteric effect and protein, thus cell, function. This transformative paradigm impacted community views in allosteric drug design, catalysis, and regulation. Dynamic conformational ensemble shifts are now acknowledged as the origin of recognition, allostery, and signaling, underscoring that conformational ensembles<em>—not proteins—</em>are the workhorses of the cell, pioneering the fundamental idea that dynamic ensembles are the driving force behind cellular processes. Nussinov was recognized as pioneer in molecular biology by <em>JMB</em>.</div></div>","PeriodicalId":369,"journal":{"name":"Journal of Molecular Biology","volume":"437 11","pages":"Article 169044"},"PeriodicalIF":4.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Unexpected Richness of the Bacterial Small RNA World 细菌小RNA世界的意外丰富性。

IF 4.7 2区生物学

Journal of Molecular Biology Pub Date : 2025-02-25 DOI: 10.1016/j.jmb.2025.169045

Gisela Storz

{"title":"Unexpected Richness of the Bacterial Small RNA World","authors":"Gisela Storz","doi":"10.1016/j.jmb.2025.169045","DOIUrl":"10.1016/j.jmb.2025.169045","url":null,"abstract":"<div><div>I stumbled onto a small RNA (sRNA) induced by oxidative stress when I did the “wrong” northern blot experiment as a second-year graduate student. I was so intrigued by the very strong induction of the 109 nt OxyS RNA that I kept working to elucidate its function while carrying out other projects. Over a decade after developing the first OxyS northern, I was able to document that the RNA acts as a regulator. This finding together with concurrent observations about the 91 nt DsrA RNA by Susan Gottesman’s group led to the realization that regulatory sRNAs were far more prevalent in bacteria than initially imagined. I do not think we could have anticipated how integral sRNAs are to regulatory networks in bacteria and how much we would learn about the mechanisms by which these sRNAs regulate gene expression, most commonly through limited base pairing with target mRNAs, chaperoned by the Hfq protein. Our work was greatly facilitated by the collegiality in the bacterial sRNA field and the regular discussions and collaborations between my group and the Gottesman group. Susan and I are both writing overviews but have agreed to emphasize different aspects of the investigation into bacterial sRNAs with the intent that our articles are read in parallel.</div></div>","PeriodicalId":369,"journal":{"name":"Journal of Molecular Biology","volume":"437 11","pages":"Article 169045"},"PeriodicalIF":4.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

TGT Damages its Substrate tRNAs by the Formation of Abasic Sites in the Anticodon Loop. TGT通过反密码子环中基本位点的形成破坏其底物trna。

IF 4.7 2区生物学

Journal of Molecular Biology Pub Date : 2025-02-25 DOI: 10.1016/j.jmb.2025.169000

Kevin Kopietz, Kasturi Raorane, Wei Guo, Florian Flegler, Valérie Bourguignon, Quentin Thuillier, Lea-Marie Kilz, Marlies Weber, Virginie Marchand, Klaus Reuter, Francesca Tuorto, Mark Helm, Yuri Motorin

{"title":"TGT Damages its Substrate tRNAs by the Formation of Abasic Sites in the Anticodon Loop.","authors":"Kevin Kopietz, Kasturi Raorane, Wei Guo, Florian Flegler, Valérie Bourguignon, Quentin Thuillier, Lea-Marie Kilz, Marlies Weber, Virginie Marchand, Klaus Reuter, Francesca Tuorto, Mark Helm, Yuri Motorin","doi":"10.1016/j.jmb.2025.169000","DOIUrl":"https://doi.org/10.1016/j.jmb.2025.169000","url":null,"abstract":"<p><p>RNA modification is a well-recognized way for gene expression regulation in a living cell. Natural enzymatic RNA modifications have been characterized for decades. Recently, additional mechanisms, more related to RNA damage, have emerged, which do not involve targeted enzymatic activity but nonetheless alter the chemical structure of nucleosides. Aberrantly modified RNA may also appear due to incomplete or erroneous enzymatic reactions. We demonstrate that tRNA-guanine transglycosylase (TGT) in bacteria and eukaryotes accidentally leaves RNA abasic sites (rAP) in the anticodon loop of substrate tRNAs. The formation of an rAP site is a part of the TGT catalytic mechanism, involving the cleavage of the N-glycosidic bond, and the formation of a covalent enzyme-tRNA adduct. The phenomenon of rAP site formation is readily detectable for tRNA<sup>Tyr</sup>(GUA) in bacteria and tRNA<sup>Asp</sup>(GUC) in eukaryotes and is amplified when the supply for preQ<sub>1</sub> in bacteria is compromised. The TGT-mediated accumulation of rAP sites in tRNAs is strongly induced upon stress, and most prominent upon oxidative stress in bacteria. Polysome profiling in bacteria points out the partial exclusion of rAP-containing tRNAs from the translating ribosome fraction, prompting a consideration of these tRNA species as \"damaged\" and most likely non-functional. The exploratory analysis of rAP tRNA(GUN) sites in mice demonstrates a substantial variability among different tissues, with the highest accumulation of damaged tRNA observed in the brain, the lung and the spleen. Altogether, these results uncover a unique molecular mechanism of RNA modification that, via a presumably erroneous reaction, diminishes RNA function rather than enhancing it.</p>","PeriodicalId":369,"journal":{"name":"Journal of Molecular Biology","volume":" ","pages":"169000"},"PeriodicalIF":4.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

SAMD12 as a Master Regulator of MAP4Ks by Decoupling Kinases From the CNKSR2 Scaffold SAMD12通过与CNKSR2支架解耦激酶作为MAP4Ks的主调控因子。

IF 4.7 2区生物学

Journal of Molecular Biology Pub Date : 2025-02-24 DOI: 10.1016/j.jmb.2025.169034

Wen Pan , Zhijie Lin , Shiwen Chen , Jiahui Li , Yu Wang , Keyu Chen , Mingjie Zhang

{"title":"SAMD12 as a Master Regulator of MAP4Ks by Decoupling Kinases From the CNKSR2 Scaffold","authors":"Wen Pan , Zhijie Lin , Shiwen Chen , Jiahui Li , Yu Wang , Keyu Chen , Mingjie Zhang","doi":"10.1016/j.jmb.2025.169034","DOIUrl":"10.1016/j.jmb.2025.169034","url":null,"abstract":"<div><div>The MAP4K member TNIK and the multi-domain scaffold protein CNKSR2, both of which are clustered at neuronal synapses, interact with each other and are closely associated with neurodevelopmental disorders, although the mechanism underlying their interaction is unclear. In this study, we characterized the interaction mechanisms between MAP4K kinases (MAP4K4, MINK1 and TNIK) and the CNKSR1/2/3 scaffold proteins, and discovered that SAMD12, a familial adult myoclonic epilepsy disease gene product, or its close homolog SAMD10, binds to CNKSR1/2/3 with exceptionally strong affinities and can quantitatively displace MAP4K from CNKSR1/2/3 scaffolds. Additionally, we demonstrated that CNKSR2 acts as both a scaffold and an activator of TNIK during neuronal synapse development. Ectopic expression of SAMD12 can effectively alter synapse development, likely by inhibiting TNIK activity through the dissociation of the kinase from CNKSR2. Our findings may have broad implications on the roles of MAP4Ks and CNKSR1/2/3 in the nervous system and in other tissues under physiological and pathophysiological processes.</div></div>","PeriodicalId":369,"journal":{"name":"Journal of Molecular Biology","volume":"437 9","pages":"Article 169034"},"PeriodicalIF":4.7,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Timestamp calibration for time-series single cell RNA-seq expression data 时间序列单细胞RNA-seq表达数据的时间戳校准。

IF 4.7 2区生物学

Journal of Molecular Biology Pub Date : 2025-02-24 DOI: 10.1016/j.jmb.2025.169021

Xiran Chen , Sha Lin , Xiaofeng Chen , Weikai Li , Yifei Li

{"title":"Timestamp calibration for time-series single cell RNA-seq expression data","authors":"Xiran Chen , Sha Lin , Xiaofeng Chen , Weikai Li , Yifei Li","doi":"10.1016/j.jmb.2025.169021","DOIUrl":"10.1016/j.jmb.2025.169021","url":null,"abstract":"<div><div>Timestamp automatic annotation (TAA) is a crucial procedure for analyzing time-series scRNA-seq data, as they unveil dynamic biological developments and cell regeneration processes. However, current TAA methods heavily rely on manual timestamps, often overlooking their reliability. This oversight can significantly degrade the performance of timestamp automatic annotation due to noisy timestamps. Nevertheless, the current approach for addressing this issue tends to select less critical cleaned samples for timestamp calibration. To tackle this challenge, we have developed a novel timestamp calibration model called ScPace for handling noisy labeled time-series scRNA-seq data. This approach incorporates a latent variable indicator within a base classifier instead of probability sampling to detect noisy samples effectively. To validate our proposed method, we conducted experiments on both simulated and real time-series scRNA-seq datasets. Cross validation experiments with different artificial mislabeling rates demonstrate that ScPace outperforms previous approaches. Furthermore, after calibrating the timestamps of the original time-series scRNA-seq data using our method, we performed supervised pseudotime analysis, revealing that ScPace enhances its performance significantly. These findings suggest that ScPace is an effective tool for timestamp calibration by enabling reclassification and deletion of detected noisy labeled samples while maintaining robustness across diverse ranges of time-series scRNA-seq datasets. The source code is available at https://github.com/OPUS-Lightphenexx/ScPace.</div></div>","PeriodicalId":369,"journal":{"name":"Journal of Molecular Biology","volume":"437 9","pages":"Article 169021"},"PeriodicalIF":4.7,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Investigation of Domain Interaction in the Apolipoprotein E Isoforms by HDX-MS 载脂蛋白E同型结构域相互作用的HDX-MS研究。

IF 4.7 2区生物学

Journal of Molecular Biology Pub Date : 2025-02-24 DOI: 10.1016/j.jmb.2025.169036

Sudip Pal, Subhrajyoti Dolai, Deepa S., Kanchan Garai

{"title":"Investigation of Domain Interaction in the Apolipoprotein E Isoforms by HDX-MS","authors":"Sudip Pal, Subhrajyoti Dolai, Deepa S., Kanchan Garai","doi":"10.1016/j.jmb.2025.169036","DOIUrl":"10.1016/j.jmb.2025.169036","url":null,"abstract":"<div><div>Involvement of apoE4 in the pathology of Alzheimer’s disease (AD) is hypothesized to arise from its unique structural properties, most importantly the interactions between the N- and C-terminal domains. However, structural understanding of the domain interaction is still lacking. Here, we use Hydrogen-Deuterium Exchange Mass Spectrometry (HDX-MS) to study domain interactions by measuring the effect of the C-terminal domain (CTD) on the solvent accessibility of the N-terminal domain (NTD) in both apoE3 and apoE4. Our results indicate that the presence of CTD enhances the solvent accessibility of all the four helices in the NTD in apoE4, but only two helices, specifically Helix-1 and 4 in apoE3. Therefore, the allosteric changes in the conformational ensemble of the NTD induced by the CTD is more extensive in apoE4 than in apoE3. Moreover, strong pH dependence suggests role of the salt bridges in the interdomain interactions. Since the NTD harbors the receptor binding region, the destabilizing effect of CTD on it provides a structural basis for the role of interdomain interactions on the pathological functions of apoE4. Furthermore, we propose HDX-MS as a methodology for screening and assessing the efficacy of ‘structure corrector’ molecules targeting apoE4 to mitigate its pathological effects in AD.</div></div>","PeriodicalId":369,"journal":{"name":"Journal of Molecular Biology","volume":"437 10","pages":"Article 169036"},"PeriodicalIF":4.7,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Lysosomal Degradation of ER Client Proteins by ER-phagy and Related Pathways. 溶酶体吞噬内质网客户蛋白的降解及其相关途径。

IF 4.7 2区生物学

Journal of Molecular Biology Pub Date : 2025-02-22 DOI: 10.1016/j.jmb.2025.169035

Carla Salomo-Coll, Natalia Jimenez-Moreno, Simon Wilkinson

引用次数: 0

O-GlcNAcAtlas 4.0: An Updated Protein O-GlcNAcylation Database with Site-specific Quantification. O-GlcNAcAtlas 4.0：一个更新的蛋白质o - glcnac酰化数据库，具有位点特异性定量。

IF 4.7 2区生物学

Journal of Molecular Biology Pub Date : 2025-02-21 DOI: 10.1016/j.jmb.2025.169033

Chunyan Hou, Weiyu Li, Yaoxiang Li, Junfeng Ma

{"title":"O-GlcNAcAtlas 4.0: An Updated Protein O-GlcNAcylation Database with Site-specific Quantification.","authors":"Chunyan Hou, Weiyu Li, Yaoxiang Li, Junfeng Ma","doi":"10.1016/j.jmb.2025.169033","DOIUrl":"10.1016/j.jmb.2025.169033","url":null,"abstract":"<p><p>O-linked β-N-acetylglucosamine (O-GlcNAc) modification (O-GlcNAcylation) is a monosaccharide modification on proteins predominantly inside cells. It is widely appreciated that spatiotemporal protein O-GlcNAcylation regulates a plethora of biological processes. High-throughput analytical techniques, particularly site-specific O-GlcNAc proteomics, have tremendously advanced the profiling of O-GlcNAc proteomes. Recently we established O-GlcNAcAtlas, a highly curated database of O-GlcNAc proteins/peptides/sites from experiments reported in the past forty years. However, a resource for O-GlcNAcylation quantification information is not available yet. Herein, we provide an updated database O-GlcNAcAtlas 4.0 by incorporating information of O-GlcNAcylation quantification. Exhaustive curation of published literature yielded a total of about 5,400 quantification events for 3,130 unique O-GlcNAc sites. The quantification vales were then systematically integrated with the specific O-GlcNAc sites and catalogued in O-GlcNAcAtlas, with key experimental details (including sample sources, conditions and methods) presented. Taken together, we present O-GlcNAcAtlas 4.0, a unique database hosting qualitative and quantitative data of O-GlcNAcylation on proteins. As a comprehensive repository supplemented with protein O-GlcNAcylation dynamics, the updated database will further facilitate related functional investigations by the biomedical community. O-GlcNAcAtlas 4.0 is freely accessible at https://oglcnac.org/atlas/.</p>","PeriodicalId":369,"journal":{"name":"Journal of Molecular Biology","volume":" ","pages":"169033"},"PeriodicalIF":4.7,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143481843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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