Nucleus细胞核
Nucleus(英文缩写 NUCLEUS-PHILA),ISSN 1949-1034,eISSN 1949-1042,中文译名:细胞核 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：2025-11-01 至 2026-10-31，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 | 4.590 | Q3 |
| 2022 | 3.700 | Q3 |
| 2023 | 2.700 | Q3 |
| 2024 | 4.500 | Q2 |
| 2025 | 5.500 | Q2 |
Nucleus 最新收录文献
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1. Redundant mispair excision mechanisms in eukaryotic DNA mismatch repair.
PMID:日期:2026-10-04DNA mismatch repair (MMR) corrects DNA replication errors, some forms of chemical damage to DNA bases, and acts in processes such as heteroduplex rejection, triplet repeat expansion, antibody maturation and cytotoxicity of alkylating agents. During MMR, the newly synthesized DNA strand containing the error must be removed and resynthesized to prevent mutations. In bacteria, this strand is displaced by the UvrD DNA helicase. In eukaryotes, this strand is excised by redundant pathways. In the first excision pathway identified, Msh2-Msh6 (or Msh2-Msh3) and/or Mlh1-Pms1 (human MLH1-PMS2) recruit Exo1 to 5' nicks, and 5'-to-3' excision by Exo1 excises the daughter strand containing the mispair to generate a single-stranded gap. The Mlh1-Pms1 endonuclease also mediates excision through extensive nicking of the daughter strand to generate single-stranded gaps. In coupled strand-displacement synthesis coordinated by Msh2-Msh6 (or Msh2-Msh3), DNA polymerase delta and Rad27 (human FEN1)-mediated 5' flap cleavage excise the mispair and resynthesize the daughter strand. Resynthesis in the Exo1- and Mlh1-Pms1-mediated pathways can be performed by both DNA polymerase delta and epsilon, and in all excision pathways the nicked product can be sealed by DNA ligase. Genetic analysis in suggests that these three pathways correspond to all or at least the major excision pathways; however, other factors such as Fan1, Artemis, Mre11, Dna2, Fun30, and the RSC complex have been implicated in eukaryotic MMR but are less well understood. The roles of excision and its redundant pathways have also been less well characterized for other processes involving MMR proteins.
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2. Telomeres in mitosis: organization and dynamics.
PMID:日期:2026-09-18Telomeres are specialized chromosomal structures that protect chromosome ends and maintain genome stability. Their organization depends on telomeric DNA repeats, the shelterin complex, accessory factors, and telomerase. While telomere structure and maintenance have been characterized, their dynamics during mammalian mitosis remain incompletely understood. Mitosis involves profound cellular reorganization, including chromatin condensation, spindle formation, and nuclear membrane disassembly and reassembly. Emerging evidence suggests that telomeres participate in these processes and may contribute to proper chromosome segregation and post-mitotic chromatin organization. Studies indicate that telomeric proteins such as TRF1 and TNKS1 interact with centrosomes and spindle components, while telomeres also interface with chromatin and nuclear membrane reassembly factors, including BAF1, LAP2α, and the ESCRT machinery during late mitosis. Defects in these processes or interactions can lead to telomere dysfunction and genomic instability. Understanding telomere dynamics during mitosis is therefore critical for elucidating mechanisms underlying aging, laminopathies, and other telomere-related human diseases.
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3. Benchmarking three simple DNA staining-based image metrics for live-cell tracking of chromatin organization.
PMID:日期:2026-09-12Quantifying chromatin-state dynamics in living cells remains challenging, in part because most methods require fixation or cell lysis. Here, we introduce two simple DNA image-derived metrics - Diffuse Signal Index (DSI)and 1-Gini - and benchmark them against the coefficient of variation (CV) as fixation-free readouts of chromatin reorganization. Leveraging the pronounced compact-to-decompact chromatin transition of NETosis, we show that all three metrics track progressive chromatin reorganization, with DSI providing the strongest trajectory-level discrimination between NETing and non-NETing cells. All three metrics also correlate with ATAC-see-based chromatin accessibility measurement in fixed cells, supporting their biological interpretability. In dividing cells, the metrics capture mitotic chromatin compaction and post-mitotic decompaction, demonstrating applicability in diverse biological processes. Together, these results provide a practical framework for extracting readouts of chromatin reorganization from routine live-cell DNA staining. We also provide NucMetrics, an open-source ImageJ/Fiji macro toolset for easily computing CV, DSI and 1-Gini.
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4. Nuclear mechanobiology: a brief history and five unresolved questions.
4. 核力学生物学：简史与五个未解之谜PMID:日期:2026-08-24该文献暂无摘要。
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5. A homozygous lamin B receptor variant resulting in Pelger-Huët anomaly without skeletal dysplasia.
5. 一种纯合的层粘连蛋白B受体变体，导致Pelger Huët异常，但没有骨骼发育不良PMID:日期:2026-08-20[中文摘要] 层粘连蛋白B受体（lamin B receptor，LBR）是一种内核膜蛋白，具有影响中性粒细胞核分叶的结构功能，以及作为甾醇还原酶的酶学功能。杂合变异导致核分叶减少（Pelger-Huët异常），而纯合致病性变异则导致一系列系统性畸形，甚至严重的骨骼畸形和产前死亡。早在1981年，已有报道一例纯合Pelger-Huët先证者，其表现为中性粒细胞核呈卵圆形，但无特殊临床症状。随后研究表明LBR量减少，可能由调控性变异所致。我们现已重新分析该先证者的DNA，证实存在纯合错义变异（NM_002296.4）：c.1445T > G；p.V482G。然而，进一步的分子检测未发现任何调控性变异。对该错义变异进行了进一步研究：其影响一个进化上高度保守的氨基酸，该氨基酸与内核膜直接接触，但对LBR甾醇还原酶活性无直接影响。迄今为止，尚未在任何研究中检测到纯合缬氨酸至甘氨酸的替换。因此，我们得出结论：该变异对LBR的结构功能具有显著影响，但对其酶学功能无临床相关影响。
[英文摘要] The lamin B receptor (LBR) is an inner nuclear membrane protein with a structural function affecting nuclear segmentation in neutrophils and an enzymatic function as a sterol reductase. Heterozygous variants cause nuclear hyposegmentation (Pelger-Huët anomaly), while homozygous pathogenic variants cause a spectrum of systemic malformations up to severe skeletal deformities and prenatal death. Already in 1981, a homozygous Pelger-Huët proband with ovoid neutrophil nuclei but without special clinical symptoms has been reported. Later it was shown that the amount of LBR was reduced, perhaps due to a regulatory variant. We have now re-analyzed the proband´s DNA and confirmed the existence of a homozygous missense variant (NM_002296.4): c.1445T > G; p.V482G. However, further molecular testing did not reveal any regulatory variant. The missense variant was further investigated: It affects an evolutionary highly conserved amino acid, which is in direct contact with the inner nuclear membrane, but has no direct influence on the LBR sterol reductase activity. A homozygous valine to glycine substitution has not been detected in any study so far. Therefore, we conclude that this variant has a significant effect on the structural function of LBR but no clinically relevant effect on its enzymatic function.
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7. More than SAM: mechanisms of action of the Polycomb group protein polyhomeotic.
7. 超越SAM：多梳-group蛋白polyhomeotic的作用机制PMID:日期:2026-08-04[中文摘要] 多梳组（PcG）系统调控不同物种的发育转变和细胞状态。两个主要的PcG复合物，即多梳抑制复合物1和2（PRC1、PRC2），调控转录并通过染色质形成表观遗传记忆。Polyhomeotic（Ph）是一个重要的PRC1亚基，但受到的关注相对较少，这可能是因为它既不参与组蛋白翻译后修饰（PTM）的沉积也不参与其识别。相反，Ph通过其标志性的聚合性不育α基序（SAM）调控染色质架构。本文综述了Ph及哺乳动物polyhomeotic样蛋白（PHC）的生物化学与功能。我们描述了SAM聚合的作用以及不依赖聚合的SAM必要功能的证据。本文还探讨了Ph的进化起源，以及无序区和有序区可能协同进化以维持但改变Ph功能的可能性。最后，我们将动物中SAM的功能与植物PcG蛋白中新发现的聚合活性进行了类比，后者可能反映了趋同进化。
[英文摘要] The Polycomb Group (PcG) system controls developmental transitions and cell states across species. Two main PcG complexes, Polycomb Repressive Complexes 1 and 2 (PRC1, PRC2), regulate transcription and form epigenetic memory through chromatin. Polyhomeotic (Ph) is an essential PRC1 subunit that has received relatively little attention, perhaps because it is not implicated in either depositing or recognizing histone post-translational modifications (PTMs). Instead, Ph regulates chromatin architecture through its hallmark polymerizing sterile alpha motif (SAM). Here we review the biochemistry and function of Ph and mammalian polyhomeotic-like proteins (PHCs). We describe the role of SAM polymerization and evidence for essential polymerization-independent SAM functions. The evolutionary origins of Ph and possible co-evolution of disordered and ordered regions to maintain but modify Ph function are considered. Finally, we draw parallels between SAM function in animals and a recently discovered polymerization activity in a plant PcG protein that may reflect convergent evolution.
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8. The nuclear pore complex as a spatial organizing hub for high-risk DNA lesions.
8. 核孔复合体作为高风险DNA损伤的空间组织中枢PMID:日期:2026-07-30The nuclear pore complex (NPC) is best known for nucleocytoplasmic transport, but growing evidence implicates nucleoporins and NPC-associated environments in genome maintenance. Here, we discuss the NPC as a spatial organizer of hazardous DNA lesions rather than a passive transport channel. Three functions recur across systems. First, NPC-associated environments can quarantine lesions arising in repetitive DNA, heterochromatin, dysfunctional telomeres, and other high-risk chromatin contexts. Second, nuclear pore association can influence recombination and repair pathway choice. Third, mobile off-pore nucleoporins may act directly at damaged chromatin to stabilize repair-associated chromatin states and restrain harmful RNA-containing intermediates. We distinguish direct mechanistic insight from evidence based on spatial association or genetic perturbation and highlight unresolved questions about NPC heterogeneity, lesion mobility, and protective versus mutagenic repair. This view positions nucleoporins as conditional regulators of genome stability.
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9. XPO1-dependent nuclear export regulates NS3 localization and promotes DENV-2 replication through mitochondrial remodeling and interferon suppression.
9. XPO1依赖的核输出调控NS3定位，并通过线粒体重塑和干扰素抑制促进DENV-2复制PMID:日期:2026-07-28Nucleocytoplasmic transport is essential for cellular homeostasis and is frequently exploited by viruses during infection. Although dengue virus (DENV) non-structural protein 3 (NS3) undergoes nuclear trafficking, the role of nuclear export pathways in its localization and in viral replication remains poorly understood. Here, we show that pharmacological inhibition of exportin 1 (XPO1) promotes the accumulation of DENV-2 NS3 in both the nucleus and mitochondria of infected Huh-7 cells. XPO1 inhibition also induces mitochondrial morphological alterations resembling those observed during DENV infection. Moreover, blockade of nuclear export enhances DENV-2 replication in interferon-stimulated cells by reducing type I interferon production, suggesting the establishment of a pro-viral cellular environment. Our findings reveal that XPO1-mediated nuclear export contributes to the regulation of NS3 localization and links nuclear export to mitochondrial remodeling and suppression of antiviral signaling during DENV infection.
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10. Repair and misrepair of telomeric DNA in dynamic interactions with PML nuclear bodies and lamin B1 in doxorubicin-treated cancer cells.
10. 阿霉素处理的癌细胞中端粒DNA在与PML核体和核纤层蛋白B1动态相互作用中的修复与错误修复PMID:日期:2026-07-23[中文摘要] 在上皮性肿瘤中，端粒由端粒酶维持；然而，在多柔比星（DOX）处理的MDA-MB-231乳腺癌细胞系中，我们发现在细胞生长恢复之前，端粒酶（TERT）出现了短暂抑制。细胞在晚S-G2/M期蓄积、有丝分裂滑移、八倍体化以及核纤层蛋白B1（LMNB1）减少与该反应同时发生。在11-12%的细胞中观察到端粒聚集和以端粒保护蛋白（TRF2）为标志的ALT样过程，与DNA双链断裂（γH2AX）及重组酶RAD51共定位于PML小体。这些现象由PML小体阵列预先设定，这些PML小体与减数分裂前期蛋白SPO11和DMC1的焦点近旁共定位。在第3周，细胞去多倍体化并恢复正常周期、端粒酶和丝分裂。在BRAFV600E-SK-MEL-28黑色素瘤细胞经DOX处理后也发现了ALT样小体。然而，在亚致死剂量的DOX处理后，出现了由错误修复的TRF2/γH2AX焦点侧翼排列并串联连接的PML二聚体杆状结构形成。此类PML束绕过经历MOS-微管驱动旋转的细胞核，与外周染色质相互作用并与LMNB1片段交错。此外，LMNB1大量离开核外周，形成核内流，和/或卷曲进入大的核仁周围PML小体。我们将观察结果解释为受损、衰老的癌细胞尝试利用多种机制，借助PML异构体和减数分裂蛋白进行端粒修复。
[英文摘要] Telomeres in epithelial tumors are maintained by telomerase; however, in the MDA-MB-231 breast cancer cell line, treated by doxorubicin (DOX), we found a transient suppression of the telomerase (TERT) before cell growth resumed. Accumulation of cells in late-S-G2/M, mitotic slippage, octaploidy, and decrease of lamin B1 (LMNB1) coincided with this response. The telomere clustering and ALT-like process marked by the telomere shelterin (TRF2) colocalised in PML bodies with DNA DSBs (γH2AX) and recombinase RAD51 were observed in 11-12% of cells. They were preset by arrays of PML-bodies juxta-colocalized with the foci of meiotic prophase proteins SPO11 and DMC1. On the 3rd week, the cells de-polyploidised and returned to the normal cycle, telomerase, and mitosis. ALT-like bodies were also found in BRAFV600E-SK-MEL-28 DOX-treated melanoma cells. However, after sublethal doses of DOX, the formation of PML dimeric rods flanked and tandemly joined by misrepaired TRF2/γH2AX foci occured. Such PML tracts, circumventing cell nuclei undergoing MOS-microtubule-driven rotation, interacted with peripheral chromatin and intermitted with LMNB1 fragments. Furthermore, LMNB1 massively left the nuclear periphery, forming intranuclear flows, and/or convoluted into large peri-nucleolar PML bodies. We interpret our observations as the attempts by damaged, senescing cancer cells to use several mechanisms exploiting PML isoforms and meiotic proteins for telomere repair.