MOLECULES AND CELLS分子与细胞
MOLECULES AND CELLS(英文缩写 MOL CELLS),ISSN 1016-8478,eISSN 0219-1032,中文译名:分子与细胞 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 | 4.250 | Q2 |
| 2022 | 3.800 | Q2 |
| 2023 | 3.700 | Q2 |
| 2024 | 6.500 | Q1 |
| 2025 | 8.200 | Q1 |
MOLECULES AND CELLS 最新收录文献
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1. Updated guide to RNA quantification by RNA sequencing and reverse transcription-qPCR.
PMID:日期:2026-09-04RNA sequencing (RNA-seq) and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) are widely used for RNA quantification. RNA species with distinct structural and biogenetic features require specific computational and experimental approaches. Here, we provide an updated MiniResource that extends our previous guides to RNA-seq analysis and RT-qPCR-based RNA quantification. We introduce available tools and key considerations for analyzing circular RNAs, double-stranded RNAs, ribosomal RNAs, and transfer RNAs. This guide will help researchers choose appropriate methods for RNA species-specific quantification.
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2. Epigenetic priming and locus-specific demethylation enhance cell-death susceptibility in liver cancer.
2. 表观遗传启动和位点特异性去甲基化增强肝癌的细胞死亡易感性PMID:日期:2026-08-19Liver cancer treatment with epigenetic drugs remains challenging because demethylating agents such as 5-azacytidine (5-AZA) induce genome-wide toxicity and may activate oncogenes. We hypothesized that a low, nontoxic dose of 5-AZA could prime liver cancer cells by partially relaxing chromatin at selected loci to restore silenced cell-death regulators. HepG2 cells treated with 2 μM 5-AZA underwent ATAC-seq and RNA-seq to identify genes with promoter opening and increased expression. Among ten candidates, BFL-1 and SQOR were prioritized for roles in cell death and redox control. Forced expression of either gene increased sensitivity to TNF-α/cycloheximide (CHX) and sorafenib, both of which elevated mitochondrial reactive oxygen species. To establish causality in a physiological context, we used CRISPR-dCas9-TET1 to demethylate CpG-rich promoter regions of BFL-1 or SQOR. Locus-specific editing sensitized cells to TNF-α/CHX more rapidly than conventional overexpression and reproduced the heightened death response elicited by low-dose 5-AZA without baseline toxicity. Analysis of the cancer cell line encyclopedia and The Cancer Genome Atlas datasets showed consistent BFL-1 downregulation in liver cancer, variable SQOR expression across cancers, and positive correlations of both genes with tumor-suppression markers and immune-cell infiltration. These results indicate that targeted reactivation of BFL-1 and SQOR increases cell-death susceptibility in liver cancer cells. Integrating low-dose pharmacologic priming with precise epigenetic editing may preserve genome-wide methylation while restoring cell-death competence, providing proof-of-concept for locus-specific epigenetic therapy in liver cancer.
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3. Photoreceptors as central hubs of developmental plasticity and environmental adaptation.
PMID:日期:2026-08-19Plant photoreceptors are well known for their roles in light-dependent developmental processes such as photomorphogenesis, shade avoidance, and circadian regulation. These canonical functions involve light perception through specific receptors, including phytochromes and cryptochromes, and downstream transcriptional reprogramming mainly in the context of early seedling growth. Beyond their classical roles, recent studies have revealed that photoreceptors also act as integrators of diverse environmental signals, contributing to abiotic stress adaptation, root development, and vascular differentiation. Notably, these non-canonical functions involve direct protein-protein interactions, post-translational modifications, and hormonal crosstalk, enabling photoreceptors to respond to environmental cues beyond light. Moreover, photoreceptor activity has been detected in tissues with limited or no light exposure, such as roots and adult vascular tissues, where they contribute to developmental and stress-responsive processes. In selected cases, particularly for phyB, non-light stress-related signals have been reported to modulate photoreceptor stability or subnuclear organization, suggesting that the functional repertoire of photoreceptors may extend beyond traditional photoperception. This review summarizes emerging insights into the non-canonical functions of photoreceptors in abiotic stress adaptation and root and vascular development, with particular focus on light-independent signaling, root-local photoreceptor activity, and non-cell autonomous light signaling. By integrating recent findings, we aim to provide a broader perspective on how photoreceptors serve as central regulators of plant plasticity in response to both light and non-light environmental factors, spanning from early to adult developmental programs.
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4. Excessive disulfide bonds in lamin A/C contribute to premature human aging.
PMID:日期:2026-08-17Nuclear lamins provide structural integrity to the nuclear envelope through coiled-coil dimer meshworks. Lamin A contains a C-terminal immunoglobulin (Ig)-like domain and a cysteine-rich unstructured tail, whereas lamin C lacks the latter, retaining only 1 cysteine within the Ig-like domain. Mutations R435C and R471C in the Ig-like domain are linked to progeroid syndromes, fatal disorders characterized by premature aging. Here, we elucidate a pathogenic mechanism driven by aberrant disulfide cross-linking. We found that the R435C mutation, but not R471C, facilitates successive disulfide bond formation between Ig-like domains in vitro using purified recombinant proteins, causing nuclear deformation in lamin C-overexpressing cells. In lamin A-overexpressing cells, both R435C and R471C mutations induce additional intermolecular disulfide bonds involving the lamin A-specific cysteine residues in the C-terminal tail. Importantly, we demonstrate that glutathione and its precursor, N-acetyl cysteine, can disrupt these aberrant bonds. Using Caenorhabditis elegans as an in vivo model, we show that the orthologous cysteine mutation causes progeria phenotypes, which are suppressed by antioxidant treatment. These findings identify aberrant disulfide cross-linking as a key driver of progeria and suggest antioxidant therapies as a potential treatment strategy. Our study offers broader implications for vertebrate aging, suggesting that oxidative stress-mediated changes in lamin architecture are a conserved mechanism contributing to the loss of nuclear structural integrity and age-dependent nuclear aberration.
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5. USP15 mutation associated with autism spectrum disorder alters progenitor fate and neuronal maturation in human brain organoids.
5. 与自闭症谱系障碍相关的USP15突变改变了人脑类器官中的祖细胞命运和神经元成熟PMID:日期:2026-07-29De novo variants in the ubiquitin-proteasome pathway are linked to autism spectrum disorder (ASD), yet their functional impact on neurodevelopment remains poorly understood. We investigated USP15, a deubiquitinating enzyme with rare damaging variants identified in individuals with ASD, using isogenic human iPSC-derived brain organoids and single-cell transcriptomics. USP15 mutant organoids showed genotype-dependent, progenitor-centered alterations during corticogenesis. Heterozygous organoids modeling haploinsufficiency displayed a shift toward later pseudotime states together with altered maturation and synaptic organization of deep-layer neurons. In contrast, homozygous organoids showed broader phenotypes, including mitotic suppression, aberrant HOX gene expression, and stress-response activation. Regulon analysis showed reduced activity of progenitor-associated regulons, including SOX2, NR2F1, and NR2F2, in heterozygous organoids, whereas homozygous organoids exhibited broader changes in transcriptional regulatory networks. Furthermore, USP15 mutant-associated gene expression patterns were significantly enriched for established ASD risk genes. Comparison with the mouse brain perturbation atlas showed that the transcriptional signature of the USP15 mutant showed notable overlap with those of Fezf2 and Foxp1 mutants, key regulators of deep-layer projection neuron identity. These findings characterize genotype-dependent neurodevelopmental phenotypes associated with reduced USP15 dosage and provide a human neural framework for investigating ASD-relevant developmental mechanisms in the context of a rare ubiquitin-pathway variant.
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6. Oxidative Stress Drives Liver Failure During In Vivo Partial Reprogramming.
PMID:日期:2026-06-04In vivo reprogramming using the Yamanaka factors (OCT4, SOX2, KLF4, and c-MYC; OSKM) enables tissue regeneration but raises major safety concerns when factor expression is sustained. Here, using a doxycycline-inducible OSKM mouse model, we show that prolonged systemic OSKM induction causes early lethality associated with hepatocyte dedifferentiation and oxidative stress, in the absence of tumor formation. Single-nucleus RNA sequencing revealed activation of reactive oxygen species (ROS), oxidative stress, and NRF2 signaling pathways in hepatocytes. Increased ROS production in hepatocytes, together with the higher resistance of female mice and sex-dependent differences in antioxidant response programs, implicates oxidative stress as a primary driver of mortality during sustained OSKM expression. Importantly, antioxidant treatment with N-acetylcysteine (NAC) alleviated oxidative stress and significantly improved survival without impairing reprogramming-associated cellular plasticity. These findings establish oxidative stress as a key driver of liver failure during sustained in vivo reprogramming and provide a mechanistic rationale for cyclic induction strategies.
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7. scpp5 regulates tooth development and injury-induced repair in zebrafish through mineralization and Wnt/β-catenin signaling.
PMID:日期:2026-06-03A member of the secretory calcium-binding phosphoprotein (SCPP) family, scpp5 is specifically expressed in zebrafish tooth germ. Although preliminary data indicates that scpp5 deficiency impairs tooth mineralization, its molecular mechanism and role in tooth repair remain unclear. In this study, we generated scpp5 knockout and Tg(hsp70l:scpp5-GFP; cryaa:venus) overexpression zebrafish lines. Tooth germ cells were labeled using Tg(dlx2b:Dendra2-NTR), and a tooth injury model was established via the nitroreductase (NTR)/metronidazole (MTZ) system. Loss-of-function studies showed that scpp5 knockout inhibited tooth mineralization and tooth germ cell development during normal development, attenuated Wnt/β-catenin signaling, downregulated calcium efflux channel gene expression, and suppressed both enameloid and dentin matrix-related genes. Rescue of Wnt pathway activity restored calcium efflux channel and dentin matrix gene expression, but not enameloid matrix gene expression. Gain-of-function studies revealed that scpp5 overexpression did not affect normal tooth development, but during repair after injury, it accelerated mineralization and cell regeneration. Mechanistically, scpp5 overexpression during repair activated Wnt/β-catenin signaling, specifically enhancing calcium channel and dentin matrix gene expression, without affecting enameloid matrix gene expression. Collectively, these findings demonstrate that scpp5 promotes tooth mineralization during normal development via Wnt/β-catenin-dependent regulation of both enameloid and dentin matrix genes, whereas during injury repair, scpp5 facilitates regeneration by selectively activating Wnt/β-catenin to drive dentin matrix and calcium channel gene expression, independent of enameloid matrix genes.
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9. Multiple ShKT domain-containing MUL-1 proteins act as redox-responsive modulators of oxidative stress signaling in C. elegans.
9. 含多个ShKT结构域的MUL-1蛋白作为秀丽隐杆线虫中氧化应激信号的红氧响应调节因子PMID:日期:2026-05-21Organismal survival depends on coordinated responses to oxidative stress and DNA damage. Using Caenorhabditis elegans, we investigate mul-1, a robust transcriptional target of ionizing radiation and reactive oxygen species. Although annotated as a mucin, MUcin-Like 1 protein (MUL-1) is a small Stichodactyla helianthus K channel toxin (ShKT) domain-containing protein belonging to an invertebrate expanded family of cysteine-rich proteins. mul-1 is selectively induced by oxidative stress, including ionizing radiation, hydrogen peroxide, Pseudomonas aeruginosa infection, or loss of the peroxiredoxin PeRoxireDoXin-2 (PRDX-2), via the p38 Mitogen-Activated Protein Kinase-cAMP-dependent Transcription Factor (MAPK-ATF-7) pathway in intestinal cells. Loss of mul-1 and its paralogs increases reactive oxygen species accumulation, oxidative stress sensitivity, and C. Elegans P53-like protein (CEP-1)/p53-dependent germ cell apoptosis. Combined deletion of mul-1 paralogs causes constitutive apoptosis, reduced fecundity, and compensatory activation of abnormal DAuer Formation (DAF)-16/FoxO and SKiNhead-1 (SKN-1)/Nuclear factor erythroid 2-related factor 2 (Nrf2) stress response pathways. Together with genetic analysis of SYstemic Stress signaling Mediator 1 (SYSM-1), these findings suggest MUL-1-like ShKT proteins buffer oxidative stress.
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10. Small molecule inhibition of voltage dependent anion channel 1 reroutes mitochondrial metabolite flux.
PMID:日期:2026-05-13Voltage dependent anion channels (VDACs 1, 2 and 3) in the outer mitochondrial membrane control the flux of anions and oxidizable substrates that sustain mitochondrial metabolism. Nicotinamide adenine dinucleotide (NADH) closes VDAC by binding to a pocket, conserved in all isoforms, located in the inner wall of the channel. Previously, we identified the small molecule SC18 that targets the NADH-binding pocket of VDAC1 employing computational analysis. Here, we explored the interaction between SC18 and VDAC1 using high-resolution nuclear magnetic resonance spectroscopy and molecular dynamics simulations. Atomically resolved data precisely confirmed the computational results, showing that SC18 binds to a site on VDAC1 that partially overlaps with the NADH binding pocket. SC18, in the presence of NADH blocked the conductance of VDAC1 reconstituted in lipid bilayers. To determine the metabolic effect of SC18, we combined readouts of mitochondrial metabolism and glycolysis with functional metabolomics and proteomics. Short-term treatment with SC18 inhibited mitochondrial metabolism and adenosine triphosphate production. Treatment over 24 h and 48 h further reduced mitochondrial uptake of pyruvate and glutamine, utilization of tricarboxylic acid cycle intermediates, as well as lipid, DNA and amino acid synthesis. Concomitant with the inhibition of mitochondrial metabolism, cellular uptake of glucose and glutamine increased in parallel with augmented lactate release. These results indicate that compensatory enhanced glycolysis sustains adenosine triphosphate production after impaired mitochondrial function induced by SC18 blockage of VDAC1. Our work sets a mechanistic foundation for VDAC1 inhibition as a novel strategy to target and reprogram cancer metabolism through modulation of the biosynthetic ability of mitochondria.