首页 > 最新文献

Proceedings of the National Academy of Sciences of the United States of America最新文献

英文 中文
Reply to Van der Stigchel et al.: Empirical evidence that AI survey contamination is real and substantial. 回复Van der stichel等人:人工智能调查污染的经验证据是真实和实质性的。
IF 9.1 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-02-24 Epub Date: 2026-02-18 DOI: 10.1073/pnas.2537420123
Sean J Westwood, Samuel Frederick
{"title":"Reply to Van der Stigchel et al.: Empirical evidence that AI survey contamination is real and substantial.","authors":"Sean J Westwood, Samuel Frederick","doi":"10.1073/pnas.2537420123","DOIUrl":"https://doi.org/10.1073/pnas.2537420123","url":null,"abstract":"","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"123 8","pages":"e2537420123"},"PeriodicalIF":9.1,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146220841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Km-scale coupled simulation and model-observation SST trend discrepancy. 千米尺度耦合模拟与模式观测海温趋势差异。
IF 9.1 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-02-24 Epub Date: 2026-02-19 DOI: 10.1073/pnas.2522161123
Sarah M Kang, Dian A Putrasahan, Noel G Brizuela, Helmuth Haak, Jürgen Kröger, Jochem Marotzke, Bjorn Stevens, Jin-Song von Storch

The spatial pattern of sea surface temperature (SST) change in the tropical Pacific plays a central role in shaping global climate through its influence on atmospheric circulation, rainfall, and extreme weather. Accurately simulating this pattern is critical for reliable near-term climate projections, yet persistent discrepancies between models and observations remain. While global warming is unequivocal, satellite-era observations reveal pronounced cooling in the southeastern tropical Pacific and Southern Ocean, contrary to the warming simulated by most CMIP models. These discrepancies raise concerns about the reliability of current models in projecting near-term regional climate change. Here, we present the historical simulation with the ICON coupled model at a 5 km ocean and 10 km atmosphere grid-spacing. ICON successfully reproduces the observed SST trends, including cooling in both the Southern Ocean and the southeastern tropical Pacific. Its fidelity is enabled by the direct representation of eddy heat transport across the Antarctic Circumpolar fronts and realistic stratocumulus cloud feedbacks in the subtropical southeast Pacific. These findings highlight the importance of fine spatial resolution in capturing the mechanisms of heat uptake in the eddy-rich Southern Ocean. Our results suggest a pathway for resolving long-standing biases in historical simulations and improving confidence in near-term climate projections.

热带太平洋海温变化的空间格局通过对大气环流、降雨和极端天气的影响对全球气候的形成起着核心作用。准确模拟这种模式对于可靠的近期气候预测至关重要,然而模式和观测之间仍然存在持续的差异。虽然全球变暖是毫无疑问的,但卫星时代的观测显示,热带太平洋东南部和南大洋明显变冷,这与大多数CMIP模式模拟的变暖相反。这些差异引起了人们对当前模式在预测近期区域气候变化方面的可靠性的担忧。本文采用ICON耦合模式进行了5 km海洋和10 km大气格距的历史模拟。ICON成功地再现了观测到的海温趋势,包括南大洋和热带东南太平洋的冷却。通过直接呈现南极环极锋的涡旋热输送和副热带东南太平洋真实的层积云云反馈,使其保真度得以实现。这些发现强调了精细空间分辨率在捕捉涡旋丰富的南大洋热吸收机制方面的重要性。我们的研究结果为解决历史模拟中长期存在的偏差和提高近期气候预测的可信度提供了一条途径。
{"title":"Km-scale coupled simulation and model-observation SST trend discrepancy.","authors":"Sarah M Kang, Dian A Putrasahan, Noel G Brizuela, Helmuth Haak, Jürgen Kröger, Jochem Marotzke, Bjorn Stevens, Jin-Song von Storch","doi":"10.1073/pnas.2522161123","DOIUrl":"https://doi.org/10.1073/pnas.2522161123","url":null,"abstract":"<p><p>The spatial pattern of sea surface temperature (SST) change in the tropical Pacific plays a central role in shaping global climate through its influence on atmospheric circulation, rainfall, and extreme weather. Accurately simulating this pattern is critical for reliable near-term climate projections, yet persistent discrepancies between models and observations remain. While global warming is unequivocal, satellite-era observations reveal pronounced cooling in the southeastern tropical Pacific and Southern Ocean, contrary to the warming simulated by most CMIP models. These discrepancies raise concerns about the reliability of current models in projecting near-term regional climate change. Here, we present the historical simulation with the ICON coupled model at a 5 km ocean and 10 km atmosphere grid-spacing. ICON successfully reproduces the observed SST trends, including cooling in both the Southern Ocean and the southeastern tropical Pacific. Its fidelity is enabled by the direct representation of eddy heat transport across the Antarctic Circumpolar fronts and realistic stratocumulus cloud feedbacks in the subtropical southeast Pacific. These findings highlight the importance of fine spatial resolution in capturing the mechanisms of heat uptake in the eddy-rich Southern Ocean. Our results suggest a pathway for resolving long-standing biases in historical simulations and improving confidence in near-term climate projections.</p>","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"123 8","pages":"e2522161123"},"PeriodicalIF":9.1,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146228334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Valuing wildfire smoke-related mortality benefits from climate mitigation. 评估与野火烟雾有关的死亡率从气候减缓中获益。
IF 9.1 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-02-24 Epub Date: 2026-02-19 DOI: 10.1073/pnas.2533772123
Minghao Qiu, Christopher W Callahan, Iván Higuera-Mendieta, Lisa Rennels, Bryan Parthum, Noah S Diffenbaugh, Marshall Burke

Human-induced climate change has increased wildfire risks, associated air pollution, and health damages in North America. Despite its large potential for damage, climate-induced wildfire smoke is rarely incorporated in estimates of the societal costs of climate change. We develop an integrated framework to estimate air pollution from climate-induced wildfire smoke (fine particulate matter, PM2.5) and the associated mortality damage in the United States across different trajectories of greenhouse gas emissions and global mean surface temperature. Our framework accounts for fire-vegetation feedbacks by empirically estimating the effects of past fires on future burn probability. Under 3 °C of global warming (relative to 1850-1900), we estimate that smoke exposure will lead to 64,000 deaths annually in the United States (95% CI: 33,500 to 112,300; calculated using historical population), a 60% increase above estimated annual smoke deaths during 2011-2020. Limiting global warming to 2 °C reduces smoke-related mortality by 14% (8,900 deaths per year) relative to our estimate for 3 °C. For every additional tonne of CO2 emissions in 2025, we calculate a net present value of monetized damage (i.e., a partial social cost of carbon) of $11.2 (95%CI: [Formula: see text]$1.1 to $41.6; 2020USD) due to climate-induced wildfire smoke mortality in the United States. Incorporating wildfire smoke damages into existing nonwildfire damage estimates increases the US domestic social cost of carbon by 74%, substantially increasing the expected benefits of greenhouse gas mitigation within the United States.

在北美,人为引起的气候变化增加了野火风险、相关的空气污染和健康损害。尽管气候引起的野火烟雾具有巨大的破坏潜力,但它很少被纳入对气候变化社会成本的估计。我们开发了一个综合框架来评估气候引起的野火烟雾(细颗粒物、PM2.5)造成的空气污染以及美国不同温室气体排放和全球平均地表温度轨迹下相关的死亡率损害。我们的框架通过经验估计过去火灾对未来燃烧概率的影响来解释火灾-植被反馈。在全球变暖3°C的情况下(相对于1850-1900年),我们估计烟雾暴露将导致美国每年64,000人死亡(95% CI: 33,500至112,300;使用历史人口计算),比2011-2020年期间估计的每年烟雾死亡人数增加60%。将全球变暖限制在2°C,与我们估计的3°C相比,可使与吸烟有关的死亡率减少14%(每年8900人死亡)。对于2025年每增加一吨二氧化碳排放,我们计算出美国因气候引起的野火烟雾死亡而造成的货币化损失(即碳的部分社会成本)的净现值为11.2美元(95%置信区间:[公式:见文本]1.1至41.6美元;2020USD)。将野火烟雾损害纳入现有的非野火损害估计,将使美国国内的碳社会成本增加74%,大大提高了美国国内温室气体减排的预期效益。
{"title":"Valuing wildfire smoke-related mortality benefits from climate mitigation.","authors":"Minghao Qiu, Christopher W Callahan, Iván Higuera-Mendieta, Lisa Rennels, Bryan Parthum, Noah S Diffenbaugh, Marshall Burke","doi":"10.1073/pnas.2533772123","DOIUrl":"https://doi.org/10.1073/pnas.2533772123","url":null,"abstract":"<p><p>Human-induced climate change has increased wildfire risks, associated air pollution, and health damages in North America. Despite its large potential for damage, climate-induced wildfire smoke is rarely incorporated in estimates of the societal costs of climate change. We develop an integrated framework to estimate air pollution from climate-induced wildfire smoke (fine particulate matter, PM<sub>2.5</sub>) and the associated mortality damage in the United States across different trajectories of greenhouse gas emissions and global mean surface temperature. Our framework accounts for fire-vegetation feedbacks by empirically estimating the effects of past fires on future burn probability. Under 3 °C of global warming (relative to 1850-1900), we estimate that smoke exposure will lead to 64,000 deaths annually in the United States (95% CI: 33,500 to 112,300; calculated using historical population), a 60% increase above estimated annual smoke deaths during 2011-2020. Limiting global warming to 2 °C reduces smoke-related mortality by 14% (8,900 deaths per year) relative to our estimate for 3 °C. For every additional tonne of CO<sub>2</sub> emissions in 2025, we calculate a net present value of monetized damage (i.e., a partial social cost of carbon) of $11.2 (95%CI: [Formula: see text]$1.1 to $41.6; 2020USD) due to climate-induced wildfire smoke mortality in the United States. Incorporating wildfire smoke damages into existing nonwildfire damage estimates increases the US domestic social cost of carbon by 74%, substantially increasing the expected benefits of greenhouse gas mitigation within the United States.</p>","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"123 8","pages":"e2533772123"},"PeriodicalIF":9.1,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146228490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Seeing the forest through the trees: Harmonizing infection-associated chronic illnesses research. 透过树木看森林:协调与感染有关的慢性疾病研究。
IF 9.1 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-02-24 Epub Date: 2026-02-18 DOI: 10.1073/pnas.2600628123
Adrian F Hernandez, Betty Diamond, Julie Liao, Andrew N March, Kent E Kester
{"title":"Seeing the forest through the trees: Harmonizing infection-associated chronic illnesses research.","authors":"Adrian F Hernandez, Betty Diamond, Julie Liao, Andrew N March, Kent E Kester","doi":"10.1073/pnas.2600628123","DOIUrl":"https://doi.org/10.1073/pnas.2600628123","url":null,"abstract":"","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"123 8","pages":"e2600628123"},"PeriodicalIF":9.1,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146220829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
TROP2-targeted NIR-II fluorescence imaging for visualizing surgical margins and metastatic sentinel lymph nodes in breast cancers. trop2靶向NIR-II荧光成像用于乳腺癌手术边缘和转移前哨淋巴结的可视化。
IF 9.1 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-02-24 Epub Date: 2026-02-19 DOI: 10.1073/pnas.2519420123
Kang-Liang Lou, Jing-Wen Bai, Hong-Tan Liu, Lin-Ling Lin, Cheng-Xi Li, Yi-Yang Gao, Sheng-Jie Lin, Yi-Fei Pei, Xiao-Long Wei, Yi-Xin Chen, Yi-Yin Tang, Hong-Yu Chen, Zhi-Yao Li, Rong Guo, Shi-Cong Tang, Chuan-Liu Wu, Guo-Jun Zhang

In early breast cancer surgery (EBC), free margins significantly decrease local recurrence in breast-conserving surgery (BCS), while metastatic status of sentinel lymph node (SLN) impacts axillary management. However, intraoperative visualization of margins and metastatic SLNs (mSLNs) remains challenging. Here, we report a second-window near-infrared (NIR-II) fluorescence probe by conjugating ICG to TROP2-targeting cyclic peptide (TTP-ICG). Our results showed that TTP-ICG specifically binds to TROP2-expressing cells in vitro and identifies TROP2-positive tumors in vivo. In addition, TTP-ICG enabled efficient intraoperative evaluation of surgical margins and visualization of mSLNs at a submillimeter level in preclinical models. Additionally, we optimized the rapid incubation imaging method (RIIM) by shortening the procedure to less than 8 min, illustrating TTP-ICG's high performance in distinguishing malignant from normal tissues/fibroadenoma lesions as well as detecting metastatic lymph nodes in a cohort of 59 patients. Thus, this TROP2-targeting probe demonstrates its significance for fluorescence imaging-guided surgery with dual applicability in EBC, providing translational potential for further clinical decision-making.

在早期乳腺癌手术(EBC)中,游离切缘显著降低保乳手术(BCS)的局部复发率,而前哨淋巴结(SLN)的转移状态影响腋窝治疗。然而,术中边缘和转移性sln (msln)的可视化仍然具有挑战性。在这里,我们报道了一种第二窗口近红外(NIR-II)荧光探针,通过将ICG偶联到trop2靶向环肽(TTP-ICG)上。我们的研究结果表明,TTP-ICG在体外特异性结合表达trop2的细胞,并在体内识别trop2阳性肿瘤。此外,TTP-ICG能够在临床前模型中对手术边缘进行有效的术中评估,并在亚毫米水平上显示msln。此外,我们优化了快速培养成像方法(RIIM),将过程缩短到不到8分钟,说明了TTP-ICG在区分正常组织/纤维腺瘤病变以及检测转移性淋巴结方面的高性能。因此,该trop2靶向探针在EBC的荧光成像引导手术中具有双重适用性,为进一步的临床决策提供了转化潜力。
{"title":"TROP2-targeted NIR-II fluorescence imaging for visualizing surgical margins and metastatic sentinel lymph nodes in breast cancers.","authors":"Kang-Liang Lou, Jing-Wen Bai, Hong-Tan Liu, Lin-Ling Lin, Cheng-Xi Li, Yi-Yang Gao, Sheng-Jie Lin, Yi-Fei Pei, Xiao-Long Wei, Yi-Xin Chen, Yi-Yin Tang, Hong-Yu Chen, Zhi-Yao Li, Rong Guo, Shi-Cong Tang, Chuan-Liu Wu, Guo-Jun Zhang","doi":"10.1073/pnas.2519420123","DOIUrl":"https://doi.org/10.1073/pnas.2519420123","url":null,"abstract":"<p><p>In early breast cancer surgery (EBC), free margins significantly decrease local recurrence in breast-conserving surgery (BCS), while metastatic status of sentinel lymph node (SLN) impacts axillary management. However, intraoperative visualization of margins and metastatic SLNs (mSLNs) remains challenging. Here, we report a second-window near-infrared (NIR-II) fluorescence probe by conjugating ICG to TROP2-targeting cyclic peptide (TTP-ICG). Our results showed that TTP-ICG specifically binds to TROP2-expressing cells in vitro and identifies TROP2-positive tumors in vivo. In addition, TTP-ICG enabled efficient intraoperative evaluation of surgical margins and visualization of mSLNs at a submillimeter level in preclinical models. Additionally, we optimized the rapid incubation imaging method (RIIM) by shortening the procedure to less than 8 min, illustrating TTP-ICG's high performance in distinguishing malignant from normal tissues/fibroadenoma lesions as well as detecting metastatic lymph nodes in a cohort of 59 patients. Thus, this TROP2-targeting probe demonstrates its significance for fluorescence imaging-guided surgery with dual applicability in EBC, providing translational potential for further clinical decision-making.</p>","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"123 8","pages":"e2519420123"},"PeriodicalIF":9.1,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146228356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Crohn’s disease–related RNF123 prevents NLRP3 inflammasome assembly by catalyzing unanchored K63-linked ubiquitination on NEK7 克罗恩病相关的RNF123通过催化NEK7上的非锚定k63连接泛素化来阻止NLRP3炎症小体组装
IF 11.1 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-02-20 DOI: 10.1073/pnas.2518759123
Feng Liu, Wanxin Zhuang, Yuan Yang, Wenting Zhao, Siyuan Li, Ziyue Zhang, Yifan Liu, Bingyu Liu, Xiaopeng Qi, Wei Zhao, Lintai Da, Chengjiang Gao
The NLRP3 inflammasome is crucial for host defense against pathogen invasion and is implicated in various inflammatory disorders. The pathogenic association and the involved mechanism between the NLRP3 inflammasome and inflammatory diseases have garnered significant attention. Here, we demonstrate that Crohn’s disease–associated SNP RNF123-R854H aggravates colitis in vivo through the NLRP3-dependent pathway. Deficiency of RNF123 also aggravates dextran sodium sulfate-induced colitis, LPS (lipopolysaccharide)-induced endotoxemia, and Alum-induced peritonitis and enhances host defense against bacterial infection via the NLRP3-dependent pathway in vivo and promotes the NLRP3 inflammasome activation in cells. We establish RNF123 as a regulator for the NLRP3 inflammasome, highlighting its implication in the NLRP3 inflammasome-driven inflammatory diseases. Mechanistically, RNF123 catalyzes unanchored K63-linked ubiquitination of NEK7, thereby preventing NEK7-mediated dissociation of the inactive cage-like NLRP3 aggregates and the subsequent NLRP3 inflammasome assembly. Additionally, we prove that K63-linked polyubiquitin chains can be specifically captured by NEK7 in vitro and inhibit the NEK7-licensed NLRP3 inflammasome assembly. We propose that NEK7-captured unanchored K63-polyubiquitin chains serve as a key determinant for the NLRP3 inflammasome activation, acting as a molecular brake to limit the excessive NLRP3 inflammasome activation and preserve immune homeostasis. Our work yields mechanistic insights into the NLRP3 inflammasome regulation and its pathogenic link to inflammatory disease.
NLRP3炎性小体对宿主防御病原体入侵至关重要,并与各种炎症疾病有关。NLRP3炎性小体与炎症性疾病的致病关系及其相关机制已引起人们的广泛关注。在这里,我们证明了克罗恩病相关的SNP RNF123-R854H通过nlrp3依赖途径在体内加重结肠炎。RNF123缺乏还会加重葡聚糖硫酸钠诱导的结肠炎、脂多糖诱导的内毒素血症和铝诱导的腹膜炎,并在体内通过NLRP3依赖途径增强宿主对细菌感染的防御能力,促进细胞中NLRP3炎性体的激活。我们建立了RNF123作为NLRP3炎症小体的调节因子,强调其在NLRP3炎症小体驱动的炎症性疾病中的意义。机制上,RNF123催化非锚定的k63连接的NEK7泛素化,从而阻止NEK7介导的无活性笼状NLRP3聚集体的解离和随后的NLRP3炎性体组装。此外,我们证明了k63连接的多泛素链可以在体外被NEK7特异性捕获,并抑制NEK7许可的NLRP3炎症小体组装。我们认为nek7捕获的非锚定的k63 -多泛素链是NLRP3炎性体激活的关键决定因素,作为限制NLRP3炎性体过度激活和保持免疫稳态的分子制动器。我们的工作为NLRP3炎性小体调控及其与炎症性疾病的致病联系提供了机制见解。
{"title":"The Crohn’s disease–related RNF123 prevents NLRP3 inflammasome assembly by catalyzing unanchored K63-linked ubiquitination on NEK7","authors":"Feng Liu, Wanxin Zhuang, Yuan Yang, Wenting Zhao, Siyuan Li, Ziyue Zhang, Yifan Liu, Bingyu Liu, Xiaopeng Qi, Wei Zhao, Lintai Da, Chengjiang Gao","doi":"10.1073/pnas.2518759123","DOIUrl":"https://doi.org/10.1073/pnas.2518759123","url":null,"abstract":"The NLRP3 inflammasome is crucial for host defense against pathogen invasion and is implicated in various inflammatory disorders. The pathogenic association and the involved mechanism between the NLRP3 inflammasome and inflammatory diseases have garnered significant attention. Here, we demonstrate that Crohn’s disease–associated SNP RNF123-R854H aggravates colitis in vivo through the NLRP3-dependent pathway. Deficiency of RNF123 also aggravates dextran sodium sulfate-induced colitis, LPS (lipopolysaccharide)-induced endotoxemia, and Alum-induced peritonitis and enhances host defense against bacterial infection via the NLRP3-dependent pathway in vivo and promotes the NLRP3 inflammasome activation in cells. We establish RNF123 as a regulator for the NLRP3 inflammasome, highlighting its implication in the NLRP3 inflammasome-driven inflammatory diseases. Mechanistically, RNF123 catalyzes unanchored K63-linked ubiquitination of NEK7, thereby preventing NEK7-mediated dissociation of the inactive cage-like NLRP3 aggregates and the subsequent NLRP3 inflammasome assembly. Additionally, we prove that K63-linked polyubiquitin chains can be specifically captured by NEK7 in vitro and inhibit the NEK7-licensed NLRP3 inflammasome assembly. We propose that NEK7-captured unanchored K63-polyubiquitin chains serve as a key determinant for the NLRP3 inflammasome activation, acting as a molecular brake to limit the excessive NLRP3 inflammasome activation and preserve immune homeostasis. Our work yields mechanistic insights into the NLRP3 inflammasome regulation and its pathogenic link to inflammatory disease.","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"107 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146231166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Human lncRNA RMRP interacts with DEAD-box helicases and modulates mitochondrial function 人类lncRNA RMRP与DEAD-box解旋酶相互作用并调节线粒体功能
IF 11.1 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-02-20 DOI: 10.1073/pnas.2522583123
Higor Sette Pereira, Jason Luddu, Govardhan Reddy Veerareddygari, Shridhar Kiran Sanghvi, Priyanshi B. Patel, Zachary E. Robinson, M. Quadir Siddiqui, Harpreet Singh, Trushar R. Patel
The human long noncoding RNA (lncRNA) RMRP , initially identified as part of the RNase MRP complex, is linked to various human diseases. However, its structural flexibility and broader cellular roles are not well understood. Here, we offer a comprehensive analysis of RMRP ’s structure in solution, its interactions with human proteins, and its mitochondrial functions. Using small-angle X-ray scattering (SAXS), we show that RMRP adopts different Mg 2+ -dependent shapes, shifting from an extended Y-shaped form to a more compact one as Mg 2+ levels increase. We identified and characterized interactions between RMRP and the DEAD-box RNA helicases DDX5 and DDX3X, with DDX5 binding strongly and exhibiting ATP-dependent helicase activity on RMRP , while DDX3X mainly acts as an expression regulator. Both helicases are crucial for the proper mitochondrial localization of RMRP , working within a complex regulatory network. Functionally, reducing RMRP levels disrupts mitochondrial stability, leading to membrane depolarization and an increase in reactive oxygen species, without affecting cell growth. Mechanistically, RMRP specifically controls nuclear-encoded mitochondrial proteins involved in cristae structure (DNAJC11) and respiratory chain function (NDUFS8). Our results position RMRP as a structurally adaptable lncRNA that collaborates with RNA helicases to preserve mitochondrial health through specific gene regulation. These insights provide perspectives on RMRP ’s biology and the molecular mechanisms underlying RMRP -related disorders, which could inform future therapies for conditions resulting from RMRP dysfunction.
人类长链非编码RNA (lncRNA) RMRP,最初被鉴定为RNase MRP复合体的一部分,与多种人类疾病有关。然而,其结构灵活性和更广泛的细胞作用尚未得到很好的理解。在此,我们对RMRP在溶液中的结构、与人类蛋白质的相互作用及其线粒体功能进行了全面的分析。利用小角度x射线散射(SAXS),我们发现RMRP采用不同的Mg 2+依赖形状,随着Mg 2+水平的增加,从扩展的y形形状转变为更紧凑的形状。我们鉴定并表征了RMRP与DEAD-box RNA解旋酶DDX5和DDX3X之间的相互作用,DDX5与RMRP结合强烈,并表现出atp依赖性解旋酶活性,而DDX3X主要作为表达调节剂。这两种解旋酶对RMRP的线粒体定位至关重要,在复杂的调控网络中起作用。在功能上,降低RMRP水平会破坏线粒体稳定性,导致膜去极化和活性氧增加,而不影响细胞生长。在机制上,RMRP特异性控制核编码的线粒体蛋白参与嵴结构(DNAJC11)和呼吸链功能(NDUFS8)。我们的研究结果将RMRP定位为一种结构适应性强的lncRNA,它与RNA解旋酶合作,通过特定的基因调控来保护线粒体的健康。这些见解为RMRP的生物学和RMRP相关疾病的分子机制提供了新的视角,可以为未来治疗由RMRP功能障碍引起的疾病提供信息。
{"title":"Human lncRNA RMRP interacts with DEAD-box helicases and modulates mitochondrial function","authors":"Higor Sette Pereira, Jason Luddu, Govardhan Reddy Veerareddygari, Shridhar Kiran Sanghvi, Priyanshi B. Patel, Zachary E. Robinson, M. Quadir Siddiqui, Harpreet Singh, Trushar R. Patel","doi":"10.1073/pnas.2522583123","DOIUrl":"https://doi.org/10.1073/pnas.2522583123","url":null,"abstract":"The human long noncoding RNA (lncRNA) <jats:italic toggle=\"yes\">RMRP</jats:italic> , initially identified as part of the RNase MRP complex, is linked to various human diseases. However, its structural flexibility and broader cellular roles are not well understood. Here, we offer a comprehensive analysis of <jats:italic toggle=\"yes\">RMRP</jats:italic> ’s structure in solution, its interactions with human proteins, and its mitochondrial functions. Using small-angle X-ray scattering (SAXS), we show that <jats:italic toggle=\"yes\">RMRP</jats:italic> adopts different Mg <jats:sup>2+</jats:sup> -dependent shapes, shifting from an extended Y-shaped form to a more compact one as Mg <jats:sup>2+</jats:sup> levels increase. We identified and characterized interactions between <jats:italic toggle=\"yes\">RMRP</jats:italic> and the DEAD-box RNA helicases DDX5 and DDX3X, with DDX5 binding strongly and exhibiting ATP-dependent helicase activity on <jats:italic toggle=\"yes\">RMRP</jats:italic> , while DDX3X mainly acts as an expression regulator. Both helicases are crucial for the proper mitochondrial localization of <jats:italic toggle=\"yes\">RMRP</jats:italic> , working within a complex regulatory network. Functionally, reducing <jats:italic toggle=\"yes\">RMRP</jats:italic> levels disrupts mitochondrial stability, leading to membrane depolarization and an increase in reactive oxygen species, without affecting cell growth. Mechanistically, <jats:italic toggle=\"yes\">RMRP</jats:italic> specifically controls nuclear-encoded mitochondrial proteins involved in cristae structure (DNAJC11) and respiratory chain function (NDUFS8). Our results position <jats:italic toggle=\"yes\">RMRP</jats:italic> as a structurally adaptable lncRNA that collaborates with RNA helicases to preserve mitochondrial health through specific gene regulation. These insights provide perspectives on <jats:italic toggle=\"yes\">RMRP</jats:italic> ’s biology and the molecular mechanisms underlying <jats:italic toggle=\"yes\">RMRP</jats:italic> -related disorders, which could inform future therapies for conditions resulting from <jats:italic toggle=\"yes\">RMRP</jats:italic> dysfunction.","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"10 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146231050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Aging-associated differences in mammary tumor–initiating populations and immune evasion pathways in breast cancer 乳腺癌中乳腺肿瘤启动人群和免疫逃避途径的衰老相关差异
IF 11.1 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-02-20 DOI: 10.1073/pnas.2523254123
Pengze Yan, Triet Bui, Ernesto Rojas Jimenez, Yanan Kuang, Shidong Xu, Cloud P. Paweletz, Hodaya Haimov, Menachem Sklartz, Ofir Cohen, Sandra S. McAllister, Kornelia Polyak
Aging is a major risk factor for breast cancer, yet how it shapes tumor development, molecular phenotype, and immune evasion remains incompletely understood. Deciphering how aging influences cancer evolution is critical for improving risk assessment, prevention, and treatment. Here, using a N-nitroso-N-methylurea (NMU)-induced rat mammary tumor model that recapitulates key features of human breast cancer, we integrated bulk and single-cell transcriptomics, whole-exome sequencing, and histopathological analysis to dissect age-associated differences in mammary tumorigenesis. We found that the age at NMU exposure critically influences tumor incidence, mutational burden, molecular subtype, and the tumor immune microenvironment. Tumors arising in aged rats originated from aging luminal progenitor-like cells, exhibited increased genomic instability, reduced immune cell infiltration, and impaired antigen presentation linked to loss of heterozygosity at chromosome (Chr) 20p. The age-associated epithelial and immune changes we identified were conserved in human breast cancers, where the loss of the homologous Chr 6p region correlated with reduced lymphocyte infiltration and shorter relapse-free survival. These findings reveal that aging profoundly affects tumor-initiating cell populations and promotes immune evasion through chromosomal instability-driven defects in antigen presentation. Our work provides a molecular basis for understanding disease onset and progression that may impact efficacy of immunotherapy in older breast cancer patients.
衰老是乳腺癌的主要危险因素,但它如何影响肿瘤发展、分子表型和免疫逃避仍不完全清楚。破解衰老如何影响癌症进化对于改善风险评估、预防和治疗至关重要。在这里,利用n -亚硝基-n -甲基脲(NMU)诱导的大鼠乳腺肿瘤模型,概括了人类乳腺癌的关键特征,我们整合了大量和单细胞转录组学,全外显子组测序和组织病理学分析,以解剖乳腺肿瘤发生的年龄相关差异。我们发现NMU暴露的年龄对肿瘤发生率、突变负担、分子亚型和肿瘤免疫微环境有重要影响。老年大鼠的肿瘤起源于老化的腔内祖细胞样细胞,表现出基因组不稳定性增加、免疫细胞浸润减少以及与染色体(Chr) 20p杂合性丧失相关的抗原呈递受损。我们发现的与年龄相关的上皮和免疫变化在人类乳腺癌中是保守的,其中同源Chr 6p区域的缺失与淋巴细胞浸润减少和无复发生存期缩短相关。这些发现表明,衰老深刻地影响肿瘤启动细胞群,并通过染色体不稳定驱动的抗原呈递缺陷促进免疫逃避。我们的工作为了解可能影响老年乳腺癌患者免疫治疗疗效的疾病发生和进展提供了分子基础。
{"title":"Aging-associated differences in mammary tumor–initiating populations and immune evasion pathways in breast cancer","authors":"Pengze Yan, Triet Bui, Ernesto Rojas Jimenez, Yanan Kuang, Shidong Xu, Cloud P. Paweletz, Hodaya Haimov, Menachem Sklartz, Ofir Cohen, Sandra S. McAllister, Kornelia Polyak","doi":"10.1073/pnas.2523254123","DOIUrl":"https://doi.org/10.1073/pnas.2523254123","url":null,"abstract":"Aging is a major risk factor for breast cancer, yet how it shapes tumor development, molecular phenotype, and immune evasion remains incompletely understood. Deciphering how aging influences cancer evolution is critical for improving risk assessment, prevention, and treatment. Here, using a N-nitroso-N-methylurea (NMU)-induced rat mammary tumor model that recapitulates key features of human breast cancer, we integrated bulk and single-cell transcriptomics, whole-exome sequencing, and histopathological analysis to dissect age-associated differences in mammary tumorigenesis. We found that the age at NMU exposure critically influences tumor incidence, mutational burden, molecular subtype, and the tumor immune microenvironment. Tumors arising in aged rats originated from aging luminal progenitor-like cells, exhibited increased genomic instability, reduced immune cell infiltration, and impaired antigen presentation linked to loss of heterozygosity at chromosome (Chr) 20p. The age-associated epithelial and immune changes we identified were conserved in human breast cancers, where the loss of the homologous Chr 6p region correlated with reduced lymphocyte infiltration and shorter relapse-free survival. These findings reveal that aging profoundly affects tumor-initiating cell populations and promotes immune evasion through chromosomal instability-driven defects in antigen presentation. Our work provides a molecular basis for understanding disease onset and progression that may impact efficacy of immunotherapy in older breast cancer patients.","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"96 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146231049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A Meier–Gorlin syndrome mutation impairs the loading of the MCM2–7 complex during DNA replication initiation 在DNA复制起始过程中,Meier-Gorlin综合征突变会损害MCM2-7复合物的负载
IF 11.1 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-02-20 DOI: 10.1073/pnas.2526022123
Yusong Liu, Mengquan Yang, Ping Lu, Haishan Gao, Maozhou He, Yitao Wang, Ao Qi, Ting Cao, Qiuqin Zhang, Shutao Qi, Yigong Shi, Hongtao Yu
Chromatin loading of the hexameric replicative helicase MCM2–7 complex requires coordinated interactions with the origin recognition complex (ORC), CDC6, and CDT1. MCM2–7 not bound to DNA forms a single hexamer (SH) with an open DNA entry gate between MCM2 and MCM5. Two MCM2–7 SHs can be loaded sequentially to form the double hexamer (DH) that encircles the DNA duplex. Activated MCM2–7 then unwinds DNA and initiates DNA replication. Our cryoelectron microscopy analyses show that a fraction of human MCM2–7 without DNA exists as DH. Unexpectedly, we find that the MCM3 winged helix domain (WHD) docks on MCM2 in both DNA-free DH and SH, creating a safety latch across the DNA entry gate to block DNA entry into the central channel. The safety latch can be opened by ORC-CDC6 binding. Perturbing this latch by structure-based or disease-related mutations of MCM3 causes replication defects and DNA damage checkpoint activation. Shortening the MCM3 linker between the helicase domain and WHD alleviates the cell cycle defects of the latch-strengthening mutation. Our findings uncover a regulated step in MCM2–7 loading with implications for human diseases.
六聚体复制解旋酶MCM2-7复合体的染色质装载需要与起源识别复合体(ORC)、CDC6和CDT1协调相互作用。未与DNA结合的MCM2 - 7在MCM2和MCM5之间形成一个开放的DNA入口门,形成一个单六聚体(SH)。两个MCM2-7 SHs可以依次加载,形成环绕DNA双聚体的双六聚体(DH)。被激活的MCM2-7随后解开DNA并启动DNA复制。我们的低温电镜分析表明,人类MCM2-7中没有DNA的一部分以DH的形式存在。出乎意料的是,我们发现MCM3带翼螺旋结构域(WHD)在无DNA的DH和SH中都停靠在MCM2上,在DNA进入门上形成一个安全锁闩,阻止DNA进入中央通道。安全锁闩可以通过ORC-CDC6结合打开。通过MCM3的基于结构或疾病相关的突变来扰乱这个锁存器会导致复制缺陷和DNA损伤检查点激活。缩短解旋酶结构域与WHD之间的MCM3连接体,减轻了锁存强化突变的细胞周期缺陷。我们的发现揭示了MCM2-7装载过程中的一个调控步骤,对人类疾病具有影响。
{"title":"A Meier–Gorlin syndrome mutation impairs the loading of the MCM2–7 complex during DNA replication initiation","authors":"Yusong Liu, Mengquan Yang, Ping Lu, Haishan Gao, Maozhou He, Yitao Wang, Ao Qi, Ting Cao, Qiuqin Zhang, Shutao Qi, Yigong Shi, Hongtao Yu","doi":"10.1073/pnas.2526022123","DOIUrl":"https://doi.org/10.1073/pnas.2526022123","url":null,"abstract":"Chromatin loading of the hexameric replicative helicase MCM2–7 complex requires coordinated interactions with the origin recognition complex (ORC), CDC6, and CDT1. MCM2–7 not bound to DNA forms a single hexamer (SH) with an open DNA entry gate between MCM2 and MCM5. Two MCM2–7 SHs can be loaded sequentially to form the double hexamer (DH) that encircles the DNA duplex. Activated MCM2–7 then unwinds DNA and initiates DNA replication. Our cryoelectron microscopy analyses show that a fraction of human MCM2–7 without DNA exists as DH. Unexpectedly, we find that the MCM3 winged helix domain (WHD) docks on MCM2 in both DNA-free DH and SH, creating a safety latch across the DNA entry gate to block DNA entry into the central channel. The safety latch can be opened by ORC-CDC6 binding. Perturbing this latch by structure-based or disease-related mutations of MCM3 causes replication defects and DNA damage checkpoint activation. Shortening the MCM3 linker between the helicase domain and WHD alleviates the cell cycle defects of the latch-strengthening mutation. Our findings uncover a regulated step in MCM2–7 loading with implications for human diseases.","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"174 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146231054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Robust input disentanglement through dendritic calcium–mediated action potentials 通过树突钙介导的动作电位实现鲁棒输入解缠
IF 11.1 1区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Pub Date : 2026-02-20 DOI: 10.1073/pnas.2515371123
Sima Hashemi, Shirin Shafiee, Christian Tetzlaff
In daily life, living beings encounter a continuous stream of mixed information, which has to be disentangled by the brain to form proper representations. Using computational modeling, we demonstrate that the interplay between dendritic calcium–mediated action potentials (dCaAPs) with synaptic plasticity and rewiring can enable single neurons to successfully perform this complex task. Compared to other types of dendritic spikes, dCaAPs exhibit a high triggering threshold, large, but graded spike amplitude, with lower amplitudes for stronger synaptic inputs. We show that these properties enable neurons to successfully learn to represent discrete items from a continuous input stream by facilitating the clustering of synapses with temporally correlated presynaptic activities onto the same dendritic branch. In comparison to N-methyl-D-aspartate spikes, dendrites generating dCaAPs can form representations of individual items more efficiently, independent of the temporal order of their presentation during learning—whether randomly, sequentially, as part of a random stream of simultaneously shown input items, or even as items with shared properties. Thus, our results provide further evidence about the critical role of dCaAPs for the computational capabilities of single neurons.
在日常生活中,生物会遇到连续不断的混合信息流,这些信息流必须由大脑进行分解,以形成适当的表征。通过计算模型,我们证明树突钙介导的动作电位(dCaAPs)与突触可塑性和重布线之间的相互作用可以使单个神经元成功地完成这项复杂的任务。与其他类型的树突尖峰相比,dCaAPs具有高触发阈值,大但有梯度的尖峰振幅,当突触输入较强时,其振幅较低。我们表明,这些特性使神经元能够通过促进具有时间相关突触前活动的突触聚类到同一树突分支上,成功地学习从连续输入流中表示离散项目。与n -甲基- d -天冬氨酸峰值相比,生成dcaap的树突可以更有效地形成单个项目的表示,而不依赖于它们在学习过程中呈现的时间顺序——无论是随机的,顺序的,作为同时显示输入项目的随机流的一部分,还是作为具有共享属性的项目。因此,我们的研究结果进一步证明了dcaap对单个神经元计算能力的关键作用。
{"title":"Robust input disentanglement through dendritic calcium–mediated action potentials","authors":"Sima Hashemi, Shirin Shafiee, Christian Tetzlaff","doi":"10.1073/pnas.2515371123","DOIUrl":"https://doi.org/10.1073/pnas.2515371123","url":null,"abstract":"In daily life, living beings encounter a continuous stream of mixed information, which has to be disentangled by the brain to form proper representations. Using computational modeling, we demonstrate that the interplay between dendritic calcium–mediated action potentials (dCaAPs) with synaptic plasticity and rewiring can enable single neurons to successfully perform this complex task. Compared to other types of dendritic spikes, dCaAPs exhibit a high triggering threshold, large, but graded spike amplitude, with lower amplitudes for stronger synaptic inputs. We show that these properties enable neurons to successfully learn to represent discrete items from a continuous input stream by facilitating the clustering of synapses with temporally correlated presynaptic activities onto the same dendritic branch. In comparison to N-methyl-D-aspartate spikes, dendrites generating dCaAPs can form representations of individual items more efficiently, independent of the temporal order of their presentation during learning—whether randomly, sequentially, as part of a random stream of simultaneously shown input items, or even as items with shared properties. Thus, our results provide further evidence about the critical role of dCaAPs for the computational capabilities of single neurons.","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"49 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146231053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Proceedings of the National Academy of Sciences of the United States of America
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1