Protein & Cell蛋白质与细胞
Protein & Cell(英文缩写 PROTEIN CELL),ISSN 1674-800X,eISSN 1674-8018,中文译名:蛋白质与细胞 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 | 15.328 | Q1 |
| 2022 | 21.100 | Q1 |
| 2023 | 13.600 | Q1 |
| 2024 | 12.800 | Q1 |
| 2025 | 18.200 | Q1 |
Protein & Cell 最新收录文献
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1. Mosaic Loss of the Y Chromosome: Mechanisms and Diseases.
1. Y染色体嵌合缺失：机制与疾病PMID:日期:2026-10-01Mosaic loss of the Y chromosome (mLOY) is a male‑specific somatic loss of the Y chromosome that is predominantly observed in peripheral blood leukocytes, but can also be found in other tissue types. It represents one of the most common male-specific somatic mutations, particularly prevalent in aging individuals. Accumulating evidence shows that mLOY markedly increases the incidence, progression, and adverse prognosis of multiple diseases, including, but not limited to, myocardial fibrosis, lung and bladder cancers, and Alzheimer's disease. Mechanistically, for extrinsic effects of mLOY, hematopoietic mLOY affect other cell populations, thereby promoting disease initiation and progression. From an intrinsic effects, mLOY within cells reprograms autosomal gene expression and reshapes interactions with the immune microenvironment, jointly driving malignant evolution. In this review, we summarize the current understanding of both intrinsic and extrinsic mLOY effects on immune regulation and disease pathogenesis, highlighting its multifaceted roles across cancer, cardiovascular disorders, infections, and other mLOY-associated conditions.
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2. Human intestinal organoid models: Advancing Inflammatory Bowel Disease Research.
2. 人类肠道类器官模型：推动炎症性肠病研究PMID:日期:2026-09-30The incidence of inflammatory bowel disease (IBD), which affects the health of millions of people worldwide, is increasing. The etiology and pathogenesis of IBD are complex, and well-established in vitro models that closely mimic disease development and progression in humans are currently lacking. This has hindered in-depth analyses of disease mechanisms and the development of effective therapeutic targets. Recently, emerging organoid technology, particularly the establishment of patient-derived intestinal organoid systems, has seemingly invigorated IBD research. This article combines recent research progress to discuss the maintenance of intestinal epithelial homeostasis, summarize the strategies of gut organoid construction, provide an overview of the main current applications of intestinal organoid models in IBD research and possible therapies, and discuss the prospects and limitations of organoid technology. It is intended to serve as a foundational resource for both established and emerging scholars in this discipline. Moreover, this work may offer a reference for clinicians in selecting personalized strategies for treating patients with refractory IBD, informing the advancement of precision medicine.
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3. NDRG2 orchestrates structural and functional adaptation for cardioprotection during mammalian hibernation.
3. NDRG2在哺乳动物冬眠期间协调结构和功能适应以实现心脏保护PMID:日期:2026-09-23Cold stress severely challenges the cardiovascular system under distinct physiological contexts: environmental cold exposure, systemic hypothermia, and donor heart cold preservation. Yet, hibernating mammals remarkably tolerate these extremes without evident injury, offering ideal models to decipher cardiac cold adaptation. Here, we induced hibernation in Syrian hamsters, a mammalian hibernator, under controlled cold stress (4 °C ambient, ∼5 °C body temperature). Notably, torpid Syrian hamsters exhibited reversible cardiac hypertrophy, a process verified to represent physiological rather than pathological remodeling that enhances cardiac cold resilience. We further identified NDRG2 as a key effector, and its overexpression in non-hibernating mice recapitulated this adaptive phenotype, promoting physiological cardiac hypertrophy, attenuating pathological remodeling, and improving cardiac cold tolerance. Mechanistically, NDRG2 orchestrates a fatty acid metabolic program to mitigate cold-induced cardiac injury during hibernation. Collectively, our work identifies the NDRG2-fatty acid axis as a central mechanism integrating structural, metabolic, and functional adaptation to cold stress, providing unique insights into cardioprotection.
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4. An internationally circulating chikungunya virus lineage with distinct mutational signatures was associated with the 2025 outbreak in China.
4. 一个具有独特突变特征的国际流行基孔肯雅病毒谱系与2025年中国的疫情暴发相关PMID:日期:2026-09-17该文献暂无摘要。
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5. Evolution of debate on the human adult hippocampal neurogenesis.
5. 人类成年海马神经发生争论的演变PMID:日期:2026-09-15该文献暂无摘要。
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6. An H2A.Z-dependent epigenetic checkpoint in macrophages couples genetic risk to microbial metabolite signaling.
PMID:日期:2026-09-15Inflammatory gene programs must be precisely controlled to maintain immune homeostasis, yet the chromatin mechanisms enforcing transcriptional shutdown remain unclear. Here we show that the histone variant H2A.Z is evicted from pro-inflammatory loci upon acute macrophage activation and re-deposited during resolution. Myeloid-specific H2a.z deletion in mice causes unrestrained inflammatory transcription, arrested macrophage maturation, exacerbates colitis and dysbiosis, depleting butyrate-producing bacteria. Consistently, gut short-chain fatty acids, particularly butyrate, promote H2A.Z deposition through histone acylation, and butyrate's anti-inflammatory effects require H2A.Z. Strikingly, human inflammatory bowel disease (IBD)-associated risk variants are linked to reduced expression of GAS41 and TIP60, which form a reader-writer module that senses acylation mark to direct H2A.Z deposition. Diminished GAS41/TIP60 expression in patient tissues correlates with IBD progression and poor response to anti-TNF therapy. Thus, H2A.Z deposition functions as an acylation-dependent epigenetic checkpoint that couples macrophage differentiation to inflammatory resolution, integrating host genetics and microbial metabolites to calibrate immune responses.
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7. Guanine promotes acute lung injury by repressing H3K27me3 in sepsis.
PMID:日期:2026-09-03Sepsis is systemic inflammation with high mortality, accompanied by multi-organ failure including acute respiratory distress syndrome. Extracellular vesicles (EVs) encapsulating bioactive cargoes, mediate cell-cell communication to exert systemic regulation. However, whether and how host lung tissue responds quickly to plasma bacterial infection through EVs in sepsis is poorly understood. Here, we identify that peripheral blood macrophages secrete more exosomal G6PD protein to induce lung injury by rewiring purine metabolism during sepsis. Guanine accumulation reduces H3K27 trimethylation and subsequently induces Nos2, Ccl6 and Il6 expression by suppressing de novo EZH2 synthesis. Macrophage-specific Rab27a or G6pd knockout mice had low exosomal G6PD protein in serum, and failed to exert lung injury upon bacterial infection. Beyond, targeting macrophage-derived G6PD by G6PD inhibitors or engineered EVs delivering si-G6pd relieves lung injury in septic mice. In summary, our findings reveal that circulating G6PD promotes lung injury by rewiring purine metabolism and remodeling the epigenetic profile in sepsis, shedding light on the critical role of EVs as a pro-inflammatory signal and targeting G6PD for future sepsis diagnosis and treatment.
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8. Molecular virulence mechanism of phospholipase C from Pseudomonas aeruginosa.
8. 铜绿假单胞菌磷脂酶C的分子毒力机制PMID:日期:2026-09-01该文献暂无摘要。
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9. Correction to: Multi-omics analysis reveals comprehensive aberrant protein and phosphorylation characteristics in breast cancer and paired metastatic lymph nodes.
9. 更正：多组学分析揭示乳腺癌及配对转移淋巴结中全面的异常蛋白质和磷酸化特征PMID:日期:2026-08-28该文献暂无摘要。
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10. LMNA R527C pathogenic variant causes an inflammation-driven segmental progeroid syndrome via triggering DNA-sensing pathways.
10. LMNA R527C致病性变体通过触发DNA传感途径引起炎症驱动的节段性早衰综合征PMID:日期:2026-08-25Homozygous pathogenic variants in Ig-like domain of LMNA cause severe segmental progeroid syndromes. Unlike typical HGPS, it remains elusive how these pathogenic variants cause segmental progeroid syndromes. We here reported that affected individuals with LMNAR527C/R527C pathogenic variant developed an atypical segmental progeroid syndrome characterized by autoimmune features. Mesenchymal stem cells (MSCs) derived from these affected individuals exhibited significant inflammation and cellular senescence. In mice, LmnaR527C/R527C pathogenic variant triggered chronic interferon signaling, exacerbated aging-related pathologies, and even induced thymic lymphomas following ionizing radiation. In addition, this pathogenic variant increased susceptibility to inflammation induced by a high-fat diet or LCMV infection. R527C pathogenic variant disrupted the interaction between Lamin A and DNA-binding proteins, causing abnormal protein aggregation and hyperactivation of the cGAS-STING. Importantly, blocking DNA sensing pathways suppressed inflammation, rescued senescence in affected individual-derived MSCs, and alleviated premature aging in LmnaR527C/R527C mice. These findings establish a homozygous LMNA pathogenic variant as a key driver of inflammation-driven segmental progeroid syndrome and highlight DNA sensing pathways as promising therapeutic targets.