NATURE CELL BIOLOGY自然·细胞生物学
NATURE CELL BIOLOGY(英文缩写 NAT CELL BIOL),ISSN 1465-7392,eISSN 1476-4679,中文译名:自然·细胞生物学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 28.213 | Q1 |
| 2022 | 21.300 | Q1 |
| 2023 | 17.300 | Q1 |
| 2024 | 19.100 | Q1 |
| 2025 | 22.700 | Q1 |
NATURE CELL BIOLOGY 最新收录文献
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1. The dual-enhanced graph learning framework DePass allows paired data integration in single-cell and spatial multiomics.
PMID:日期:2026-09-24Recent sequencing advances have enabled abundant multi-omics data generation for both single-cell and spatial contexts. Integrating such multimodal data is critical for decoding cellular and tissue-level complexity. However, compared with single-modality profiling, multimodal data often exhibit higher levels of noise, and existing methods typically overlook this challenge during integration. Meanwhile, most current approaches are tailored to either single-cell or spatial data, limiting their applicability across data types. Here we present DePass, a scalable graph learning framework for paired data integration in both single-cell and spatial multi-omics. We propose a coupled enhancement-integration architecture that iteratively denoises data and improves integrated embeddings. We systematically benchmarked DePass across 6 modalities, 9 tissue types and 13 experimental platforms, demonstrating superior integration accuracy. In the in-house colorectal cancer data, DePass further uncovered immune niche substructure and spatial tumour heterogeneity at near single-cell resolution. These results establish DePass as a unified and generalizable solution for multi-omics integration across diverse biological contexts.
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2. Taxane-induced conformational changes in the microtubule lattice activate GEF-H1-dependent RhoA signalling.
PMID:日期:2026-09-24Taxanes are widely used chemotherapeutic agents that perturb cell division. They also exert effects during interphase, but the underlying mechanisms are poorly understood. Here we show that taxanes activate RhoA signalling and induce actin remodelling by releasing the RhoA activator GEF-H1 from microtubules. This taxane-induced release of GEF-H1 occurs rapidly, is independent of tubulin post-translational modifications, and can be recapitulated using purified proteins. In vitro reconstitution assays combined with analyses of microtubule structure revealed that microtubule binding by GEF-H1 is inhibited by microtubule-stabilizing ligands that expand the microtubule lattice, such as taxanes and GMPCPP, but not by others, including GTPγS and discodermolide, which stabilize a compacted microtubule lattice. Our findings demonstrate that alterations in microtubule lattice conformation can activate key signalling pathways, offering insights into the mode of action of taxanes and the possible origins of their side effects.
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5. Author Correction: Phase separation of initiation hubs on cargo is a trigger switch for selective autophagy.
PMID:日期:2026-09-23该文献暂无摘要。
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6. Author Correction: CLOCK/BMAL1 interactome uncovers homeodomain factors as tissue regulators.
PMID:日期:2026-09-23该文献暂无摘要。
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10. The Batten disease protein CLN8 is a stereospecific acyltransferase in bis(monoacylglycero)phosphate biosynthesis.
PMID:日期:2026-09-15Loss-of-function mutations in the endoplasmic reticulum membrane protein CLN8 cause Batten disease, a neurodegenerative lysosomal storage disorder. CLN8 acts with the lysosomal enzyme CLN5 to produce bis(monoacylglycero)phosphate (BMP), a signature lysosomal phospholipid with unique S,S stereochemistry. However, the role of CLN8 in this pathway has remained unclear. Here we establish that CLN8 is a glycerophosphoglycerol acyltransferase that catalyses the stereospecific acylation of S,S-glycerophosphoglycerol to generate S,S-lysophosphatidylglycerol, the CLN5 substrate in BMP synthesis. Cryo-electron microscopy structures define the CLN8 active site and support a ping-pong acyl transfer mechanism. Batten disease mutations impair CLN8 enzymatic activity and abolish BMP production in mice. Exogenous S,S-lysophosphatidylglycerol, but not the R,S stereoisomer, restores BMP synthesis in CLN8-deficient cells and mice and improves neurological phenotypes in cln8 mutant zebrafish. These findings define the function of CLN8, explain the biochemical basis of CLN8 Batten disease and establish BMP precursor supplementation as a proof-of-concept therapeutic strategy.