首页 > 最新文献

Cell Communication and Signaling最新文献

英文 中文
SLC25A35 enhances fatty acid oxidation and mitochondrial biogenesis to promote the carcinogenesis and progression of hepatocellular carcinoma by upregulating PGC-1α. SLC25A35 通过上调 PGC-1α 促进脂肪酸氧化和线粒体生物生成,从而促进肝细胞癌的发生和发展。
IF 8.2 2区 生物学 Q1 CELL BIOLOGY Pub Date : 2025-03-10 DOI: 10.1186/s12964-025-02109-y
Heng-Chao Yu, Lu Bai, Liang Jin, Yu-Jia Zhang, Zi-Han Xi, De-Sheng Wang

Mitochondria dysfunction has been closely linked to a wide spectrum of human cancers, whereas the molecular basis has yet to be fully understood. SLC25A35 belongs to the SLC25 family of mitochondrial carrier proteins. However, the role of SLC25A35 in mitochondrial metabolism reprogramming, development and progression in human cancers remains unclear. Here, we found that SLC25A35 markedly reprogramed mitochondrial metabolism, characterized by increased oxygen consumption rate and ATP production and decreased ROS level, via enhancing fatty acid oxidation (FAO). Meanwhile, SLC25A35 also enhanced mitochondrial biogenesis characterized by increased mitochondrial mass and DNA content. Mechanistic studies revealed that SLC25A35 facilitated FAO and mitochondrial biogenesis through upregulating peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) via increasing acetyl-CoA-mediated acetylation of PGC-1α. Clinically, SLC25A35 was highly expressed in HCC and correlated with adverse patients' survival. Functionally, SLC25A35 promoted the proliferation and metastasis of HCC cells both in vitro and in vivo, as well as the carcinogenesis in a DEN-induced HCC mice model. Moreover, we found that SLC25A35 upregulation is caused, at least in part, by decreased miR-663a in HCC cells. Together, our results suggest a crucial oncogenic role of SLC25A35 in HCC by reprogramming mitochondrial metabolism and suggest SLC25A35 as a potential therapeutic target for the treatment of HCC.

{"title":"SLC25A35 enhances fatty acid oxidation and mitochondrial biogenesis to promote the carcinogenesis and progression of hepatocellular carcinoma by upregulating PGC-1α.","authors":"Heng-Chao Yu, Lu Bai, Liang Jin, Yu-Jia Zhang, Zi-Han Xi, De-Sheng Wang","doi":"10.1186/s12964-025-02109-y","DOIUrl":"10.1186/s12964-025-02109-y","url":null,"abstract":"<p><p>Mitochondria dysfunction has been closely linked to a wide spectrum of human cancers, whereas the molecular basis has yet to be fully understood. SLC25A35 belongs to the SLC25 family of mitochondrial carrier proteins. However, the role of SLC25A35 in mitochondrial metabolism reprogramming, development and progression in human cancers remains unclear. Here, we found that SLC25A35 markedly reprogramed mitochondrial metabolism, characterized by increased oxygen consumption rate and ATP production and decreased ROS level, via enhancing fatty acid oxidation (FAO). Meanwhile, SLC25A35 also enhanced mitochondrial biogenesis characterized by increased mitochondrial mass and DNA content. Mechanistic studies revealed that SLC25A35 facilitated FAO and mitochondrial biogenesis through upregulating peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) via increasing acetyl-CoA-mediated acetylation of PGC-1α. Clinically, SLC25A35 was highly expressed in HCC and correlated with adverse patients' survival. Functionally, SLC25A35 promoted the proliferation and metastasis of HCC cells both in vitro and in vivo, as well as the carcinogenesis in a DEN-induced HCC mice model. Moreover, we found that SLC25A35 upregulation is caused, at least in part, by decreased miR-663a in HCC cells. Together, our results suggest a crucial oncogenic role of SLC25A35 in HCC by reprogramming mitochondrial metabolism and suggest SLC25A35 as a potential therapeutic target for the treatment of HCC.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"130"},"PeriodicalIF":8.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11895242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
IL-1β stimulates ADAMTS9 expression and contributes to preterm prelabor rupture of membranes.
IF 8.2 2区 生物学 Q1 CELL BIOLOGY Pub Date : 2025-03-08 DOI: 10.1186/s12964-025-02120-3
Jiasong Cao, Yixin Wang, Qimei Lin, Shuqi Wang, Yongmei Shen, Lei Zhang, Wen Li, Ling Chen, Chunliu Liu, Shihan Yao, Ling Shuai, Xu Chen, Zongjin Li, Ying Chang

Background: Preterm prelabor rupture of membranes (pPROM) is a leading cause of neonatal morbidity and mortality. While intra-amniotic infection is a well-established driver of pPROM, the role of sterile intra-amniotic inflammation remains unclear. Recent evidence suggests that interleukin-1 beta (IL-1β) promotes extracellular matrix (ECM) remodeling via downstream effectors, a disintegrin-like and metalloproteinase domain with thrombospondin type 1 motif 9 (ADAMTS9), while protein O-fucosyltransferase 2 (POFUT2) facilitates its O-fucosylation and secretion, amplifying ECM degradation. This study investigates how IL-1β-triggered nuclear factor kappa-B (NF-κB) activation promotes ADAMTS9 and POFUT2 expression, ultimately driving fetal membrane ECM remodeling and weakening in pPROM without signs of intra-amniotic infection.

Methods: A nested case-control study included maternal serum and fetal membrane samples from 60 pregnant women (34 pPROM, 26 full-term births [FTB]). ELISA measured serum levels of IL-1β and ADAMTS9, and their correlations were analyzed. Mechanistic studies utilized primary human amniotic epithelial cells (hAECs) and fetal membrane-decidua explants with IL-1β treatment. The role of NF-κB was explored using chromatin immunoprecipitation (ChIP) and luciferase assays to assess NF-κB binding to the promoters of ADAMTS9 and POFUT2. A murine model of sterile intra-amniotic inflammation under ultrasound-guided IL-1β injection was used to validate in vitro findings and assess pregnancy outcomes.

Results: Serum IL-1β and ADAMTS9 levels at 16 weeks of gestation were significantly higher in pPROM cases compared to FTB controls (P < 0.001). A combined model of these biomarkers demonstrated high predictive accuracy for pPROM (AUC = 0.83). Mechanistically, IL-1β activated NF-κB, leading to its binding to the promoters of ADAMTS9 and POFUT2. NF-κB activation promoted ADAMTS9 expression, while POFUT2 enhanced its secretion. Together, these processes drove versican degradation and ECM weakening. Intra-amniotic administration of IL-1β in mice induced fetal membrane weakening, preterm birth, and adverse neonatal outcomes, which were mitigated by the NF-κB inhibitor BAY 11-7082 treatment.

Conclusion: Maternal serum ADAMTS9 levels at mid-gestation are promising non-invasive biomarkers for pPROM risk stratification. Mechanistically, IL-1β-induced NF-κB activation promotes ADAMTS9 expression and POFUT2-dependent secretion, contributing to fetal membrane weakening. These findings provide new insights into the role and potential therapeutic target for sterile intra-amniotic inflammation in pPROM.

{"title":"IL-1β stimulates ADAMTS9 expression and contributes to preterm prelabor rupture of membranes.","authors":"Jiasong Cao, Yixin Wang, Qimei Lin, Shuqi Wang, Yongmei Shen, Lei Zhang, Wen Li, Ling Chen, Chunliu Liu, Shihan Yao, Ling Shuai, Xu Chen, Zongjin Li, Ying Chang","doi":"10.1186/s12964-025-02120-3","DOIUrl":"10.1186/s12964-025-02120-3","url":null,"abstract":"<p><strong>Background: </strong>Preterm prelabor rupture of membranes (pPROM) is a leading cause of neonatal morbidity and mortality. While intra-amniotic infection is a well-established driver of pPROM, the role of sterile intra-amniotic inflammation remains unclear. Recent evidence suggests that interleukin-1 beta (IL-1β) promotes extracellular matrix (ECM) remodeling via downstream effectors, a disintegrin-like and metalloproteinase domain with thrombospondin type 1 motif 9 (ADAMTS9), while protein O-fucosyltransferase 2 (POFUT2) facilitates its O-fucosylation and secretion, amplifying ECM degradation. This study investigates how IL-1β-triggered nuclear factor kappa-B (NF-κB) activation promotes ADAMTS9 and POFUT2 expression, ultimately driving fetal membrane ECM remodeling and weakening in pPROM without signs of intra-amniotic infection.</p><p><strong>Methods: </strong>A nested case-control study included maternal serum and fetal membrane samples from 60 pregnant women (34 pPROM, 26 full-term births [FTB]). ELISA measured serum levels of IL-1β and ADAMTS9, and their correlations were analyzed. Mechanistic studies utilized primary human amniotic epithelial cells (hAECs) and fetal membrane-decidua explants with IL-1β treatment. The role of NF-κB was explored using chromatin immunoprecipitation (ChIP) and luciferase assays to assess NF-κB binding to the promoters of ADAMTS9 and POFUT2. A murine model of sterile intra-amniotic inflammation under ultrasound-guided IL-1β injection was used to validate in vitro findings and assess pregnancy outcomes.</p><p><strong>Results: </strong>Serum IL-1β and ADAMTS9 levels at 16 weeks of gestation were significantly higher in pPROM cases compared to FTB controls (P < 0.001). A combined model of these biomarkers demonstrated high predictive accuracy for pPROM (AUC = 0.83). Mechanistically, IL-1β activated NF-κB, leading to its binding to the promoters of ADAMTS9 and POFUT2. NF-κB activation promoted ADAMTS9 expression, while POFUT2 enhanced its secretion. Together, these processes drove versican degradation and ECM weakening. Intra-amniotic administration of IL-1β in mice induced fetal membrane weakening, preterm birth, and adverse neonatal outcomes, which were mitigated by the NF-κB inhibitor BAY 11-7082 treatment.</p><p><strong>Conclusion: </strong>Maternal serum ADAMTS9 levels at mid-gestation are promising non-invasive biomarkers for pPROM risk stratification. Mechanistically, IL-1β-induced NF-κB activation promotes ADAMTS9 expression and POFUT2-dependent secretion, contributing to fetal membrane weakening. These findings provide new insights into the role and potential therapeutic target for sterile intra-amniotic inflammation in pPROM.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"127"},"PeriodicalIF":8.2,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Specific sDMA modifications on the RGG/RG motif of METTL14 regulate its function in AML.
IF 8.2 2区 生物学 Q1 CELL BIOLOGY Pub Date : 2025-03-08 DOI: 10.1186/s12964-025-02130-1
Yulun Zhong, Rou Zhang, Lingzi Lu, Huijian Tan, Yuyu You, Yang Mao, Yanqiu Yuan

Background: Protein arginine methylations are crucial post-translational modifications (PTMs) in eukaryotes, playing a significant regulatory role in diverse biological processes. Here, we present our investigation into the detailed arginine methylation pattern of the C-terminal RG-rich region of METTL14, a key component of the m6A RNA methylation machinery, and its functional implications in biology and disease.

Methods: Using ETD-based mass spectrometry and in vitro enzyme reactions, we uncover a specific arginine methylation pattern on METTL14. RNA methyltransferase activity assays were used to assess the impact of sDMA on METTL3:METTL14 complex activity. RNA immunoprecipitation was used to evaluate mRNA-m6A reader interactions. MeRIP-seq analysis was used to study the genome-wide effect of METTL14 sDMA on m6A modification in acute myeloid leukemia cells.

Results: We demonstrate that PRMT5 catalyzes the site-specific symmetric dimethylation at R425 and R445 within the extensively methylated RGG/RG motifs of METTL14. We show a positive regulatory role of symmetric dimethylarginines (sDMA) in the catalytic efficiency of the METTL3:METTL14 complex and m6A-specific gene expression in HEK293T and acute myeloid leukemia cells, potentially through the action of m6A reader protein YTHDF1. In addition, the combined inhibition of METTL3 and PRMT5 further reduces the expression of several m6A substrate genes essential for AML proliferation, suggesting a potential therapeutic strategy for AML treatment.

Conclusions: The study confirms the coexistence of sDMA and aDMA modifications on METTL14's RGG/RG motifs, with sDMA at R425 and R445 enhancing METTL3:METTL14's catalytic efficacy and regulating gene expression through m6A deposition in cancer cells.

{"title":"Specific sDMA modifications on the RGG/RG motif of METTL14 regulate its function in AML.","authors":"Yulun Zhong, Rou Zhang, Lingzi Lu, Huijian Tan, Yuyu You, Yang Mao, Yanqiu Yuan","doi":"10.1186/s12964-025-02130-1","DOIUrl":"10.1186/s12964-025-02130-1","url":null,"abstract":"<p><strong>Background: </strong>Protein arginine methylations are crucial post-translational modifications (PTMs) in eukaryotes, playing a significant regulatory role in diverse biological processes. Here, we present our investigation into the detailed arginine methylation pattern of the C-terminal RG-rich region of METTL14, a key component of the m6A RNA methylation machinery, and its functional implications in biology and disease.</p><p><strong>Methods: </strong>Using ETD-based mass spectrometry and in vitro enzyme reactions, we uncover a specific arginine methylation pattern on METTL14. RNA methyltransferase activity assays were used to assess the impact of sDMA on METTL3:METTL14 complex activity. RNA immunoprecipitation was used to evaluate mRNA-m6A reader interactions. MeRIP-seq analysis was used to study the genome-wide effect of METTL14 sDMA on m6A modification in acute myeloid leukemia cells.</p><p><strong>Results: </strong>We demonstrate that PRMT5 catalyzes the site-specific symmetric dimethylation at R425 and R445 within the extensively methylated RGG/RG motifs of METTL14. We show a positive regulatory role of symmetric dimethylarginines (sDMA) in the catalytic efficiency of the METTL3:METTL14 complex and m6A-specific gene expression in HEK293T and acute myeloid leukemia cells, potentially through the action of m6A reader protein YTHDF1. In addition, the combined inhibition of METTL3 and PRMT5 further reduces the expression of several m6A substrate genes essential for AML proliferation, suggesting a potential therapeutic strategy for AML treatment.</p><p><strong>Conclusions: </strong>The study confirms the coexistence of sDMA and aDMA modifications on METTL14's RGG/RG motifs, with sDMA at R425 and R445 enhancing METTL3:METTL14's catalytic efficacy and regulating gene expression through m6A deposition in cancer cells.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"126"},"PeriodicalIF":8.2,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143587731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction: Targeting the ERK1/2 and p38 MAPK pathways attenuates Golgi tethering factor golgin-97 depletion-induced cancer progression in breast cancer.
IF 8.2 2区 生物学 Q1 CELL BIOLOGY Pub Date : 2025-03-07 DOI: 10.1186/s12964-025-02119-w
Yu-Chin Liu, Tsung-Jen Lin, Kowit-Yu Chong, Guan-Ying Chen, Chia-Yu Kuo, Yi-Yun Lin, Chia-Wei Chang, Ting-Feng Hsiao, Chih-Liang Wang, Yo-Chen Shih, Chia-Jung Yu
{"title":"Correction: Targeting the ERK1/2 and p38 MAPK pathways attenuates Golgi tethering factor golgin-97 depletion-induced cancer progression in breast cancer.","authors":"Yu-Chin Liu, Tsung-Jen Lin, Kowit-Yu Chong, Guan-Ying Chen, Chia-Yu Kuo, Yi-Yun Lin, Chia-Wei Chang, Ting-Feng Hsiao, Chih-Liang Wang, Yo-Chen Shih, Chia-Jung Yu","doi":"10.1186/s12964-025-02119-w","DOIUrl":"10.1186/s12964-025-02119-w","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"123"},"PeriodicalIF":8.2,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11887253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Extracellular vesicular delivery of ceramides from pulmonary macrophages to endothelial cells facilitates chronic obstructive pulmonary disease.
IF 8.2 2区 生物学 Q1 CELL BIOLOGY Pub Date : 2025-03-07 DOI: 10.1186/s12964-025-02125-y
Qiqing Huang, Tutu Kang, Shaoran Shen, Lele Liu, Lili Zhang, Xiaoli Zou, Jianqing Wu

Background: Ceramides are known for their harmful, cell-autonomous effects in cigarette smoke (CS)-triggered chronic obstructive pulmonary disease (COPD), yet their potential role as intercellular signals in COPD pathogenesis remains unclear. This study aims to investigate whether ceramides act as cell-nonautonomous mediators of COPD development by transmitting metabolic stress from pulmonary macrophages to endothelial cells (ECs), compromising endothelial function and thereby orchestrating the pulmonary inflammation.

Methods: We analyzed single-cell RNA sequencing data from human lung tissues and bulk RNA sequencing data from alveolar macrophages (AMs) in COPD patients to investigate the transcriptomic profiles of ceramide biosynthesis enzymes. The expression changes of several key enzymes were validated in human lung sections, AMs isolated from CS-exposed mice, and cigarette smoke extract (CSE)-treated macrophages. Ceramide levels in macrophages and their extracellular vesicles (EVs) were quantified using mass spectroscopy lipidomics. EVs were further characterized by transmission electron microscopy and nanoparticle tracking analysis. The uptake of macrophage-derived EVs by ECs and their effects on endothelial barriers were evaluated in vitro using a co-culture system and in vivo using a CS-exposed COPD mouse model.

Results: CS exposure upregulated enzymes involved in de novo ceramide biosynthesis in pulmonary macrophages, increasing levels of long- and very long-chain ceramides. These ceramides were packaged into EVs and delivered to ECs, where they disrupted gap junctions, increased endothelial permeability, and impaired EC migration. Silencing these enzymes involved in de novo ceramide biosynthesis in pulmonary macrophages could block this metabolic communication between macrophages and ECs mediated by EV-delivered ceramides, protecting EC function from CS exposure. When intratracheally administered to CS-exposed mice, these ceramide-rich macrophage-derived EVs exacerbated COPD by facilitating endothelial barrier disruption.

Conclusion: Our study uncovered a novel mechanism in COPD pathogenesis, where pulmonary macrophages propagate CS-induced metabolic stress to ECs via ceramide-laden EVs, leading to endothelial barrier dysfunction. This intercellular pathway represents a potential target for therapeutic intervention in COPD.

{"title":"Extracellular vesicular delivery of ceramides from pulmonary macrophages to endothelial cells facilitates chronic obstructive pulmonary disease.","authors":"Qiqing Huang, Tutu Kang, Shaoran Shen, Lele Liu, Lili Zhang, Xiaoli Zou, Jianqing Wu","doi":"10.1186/s12964-025-02125-y","DOIUrl":"10.1186/s12964-025-02125-y","url":null,"abstract":"<p><strong>Background: </strong>Ceramides are known for their harmful, cell-autonomous effects in cigarette smoke (CS)-triggered chronic obstructive pulmonary disease (COPD), yet their potential role as intercellular signals in COPD pathogenesis remains unclear. This study aims to investigate whether ceramides act as cell-nonautonomous mediators of COPD development by transmitting metabolic stress from pulmonary macrophages to endothelial cells (ECs), compromising endothelial function and thereby orchestrating the pulmonary inflammation.</p><p><strong>Methods: </strong>We analyzed single-cell RNA sequencing data from human lung tissues and bulk RNA sequencing data from alveolar macrophages (AMs) in COPD patients to investigate the transcriptomic profiles of ceramide biosynthesis enzymes. The expression changes of several key enzymes were validated in human lung sections, AMs isolated from CS-exposed mice, and cigarette smoke extract (CSE)-treated macrophages. Ceramide levels in macrophages and their extracellular vesicles (EVs) were quantified using mass spectroscopy lipidomics. EVs were further characterized by transmission electron microscopy and nanoparticle tracking analysis. The uptake of macrophage-derived EVs by ECs and their effects on endothelial barriers were evaluated in vitro using a co-culture system and in vivo using a CS-exposed COPD mouse model.</p><p><strong>Results: </strong>CS exposure upregulated enzymes involved in de novo ceramide biosynthesis in pulmonary macrophages, increasing levels of long- and very long-chain ceramides. These ceramides were packaged into EVs and delivered to ECs, where they disrupted gap junctions, increased endothelial permeability, and impaired EC migration. Silencing these enzymes involved in de novo ceramide biosynthesis in pulmonary macrophages could block this metabolic communication between macrophages and ECs mediated by EV-delivered ceramides, protecting EC function from CS exposure. When intratracheally administered to CS-exposed mice, these ceramide-rich macrophage-derived EVs exacerbated COPD by facilitating endothelial barrier disruption.</p><p><strong>Conclusion: </strong>Our study uncovered a novel mechanism in COPD pathogenesis, where pulmonary macrophages propagate CS-induced metabolic stress to ECs via ceramide-laden EVs, leading to endothelial barrier dysfunction. This intercellular pathway represents a potential target for therapeutic intervention in COPD.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"124"},"PeriodicalIF":8.2,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11887234/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
From mechanisms to medicine: Ferroptosis as a Therapeutic target in liver disorders.
IF 8.2 2区 生物学 Q1 CELL BIOLOGY Pub Date : 2025-03-07 DOI: 10.1186/s12964-025-02121-2
Yuqi He, Yumeng Lin, Jinfeng Song, Mingzhu Song, Xiaoxia Nie, Hong Sun, Changyun Xu, Zhongyu Han, Juan Cai

In recent 10 years, ferroptosis has become a hot research direction in the scientific research community as a new way of cell death. Iron toxicity accumulation and lipotoxicity are unique features. Several studies have found that ferroptosis is involved in the regulation of the hepatic microenvironment and various hepatic metabolisms, thereby mediating the progression of related liver diseases. For example, NRF2 and FSP1, as important regulatory proteins of ferroptosis, are involved in the development of liver tumors and liver failure. In this manuscript, we present the mechanisms involved in ferroptosis, the concern of ferroptosis with the liver microenvironment and the progression of ferroptosis in various liver diseases. In addition, we summarize recent clinical advances in targeted ferroptosis therapy for related diseases. We expect that this manuscript can provide a new perspective for clinical treatment of related diseases.

{"title":"From mechanisms to medicine: Ferroptosis as a Therapeutic target in liver disorders.","authors":"Yuqi He, Yumeng Lin, Jinfeng Song, Mingzhu Song, Xiaoxia Nie, Hong Sun, Changyun Xu, Zhongyu Han, Juan Cai","doi":"10.1186/s12964-025-02121-2","DOIUrl":"10.1186/s12964-025-02121-2","url":null,"abstract":"<p><p>In recent 10 years, ferroptosis has become a hot research direction in the scientific research community as a new way of cell death. Iron toxicity accumulation and lipotoxicity are unique features. Several studies have found that ferroptosis is involved in the regulation of the hepatic microenvironment and various hepatic metabolisms, thereby mediating the progression of related liver diseases. For example, NRF2 and FSP1, as important regulatory proteins of ferroptosis, are involved in the development of liver tumors and liver failure. In this manuscript, we present the mechanisms involved in ferroptosis, the concern of ferroptosis with the liver microenvironment and the progression of ferroptosis in various liver diseases. In addition, we summarize recent clinical advances in targeted ferroptosis therapy for related diseases. We expect that this manuscript can provide a new perspective for clinical treatment of related diseases.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"125"},"PeriodicalIF":8.2,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
TFE3 fusion proteins promote the progression of TFE3 rearranged renal cell carcinoma via enhancing chaperone-mediated lipophagy.
IF 8.2 2区 生物学 Q1 CELL BIOLOGY Pub Date : 2025-03-06 DOI: 10.1186/s12964-025-02117-y
Wenliang Ma, Yi Chen, Guijuan Chen, Lei Yang, Yanwen Lu, Xiang Dong, Dongmei Li, Weidong Gan

Background: TFE3 rearranged renal cell carcinoma (TFE3 rRCC), classified as a distinct entity of RCCs, exhibits aggressive biological behavior and possesses unique metabolic characteristics. In the present study, TFE3 rRCC with high expression of TFE3 fusion proteins was employed to investigate the features of lipid metabolism and its underlying mechanism in cancer progression.

Methods: Fluorescence microscope and flow cytometry were employed to detect lipid droplets (LDs). GPO-PAP method and Oil Red O staining were used to quantify triacylglycerol levels. The data for bioinformatics analysis were sourced from GEO and iProX. The biological roles of TFE3 and LAMP2A were investigated by CCK8 assay, EdU staining, seahorse, transwell assay, colony, and sphere formation assay. The regulatory mechanisms involving TFE3, LAMP2A and Hsc70 were investigated using western blotting, immunohistochemistry, qRT-PCR, luciferase assays, Co-IP techniques, and ChIP analyses.

Results: The level of LDs accumulation in TFE3 rRCC was relatively low, and the knockdown of TFE3 led to an increase in LDs accumulation while inhibiting tumor progression. The underlying mechanism revealed that TFE3 fusion proteins inhibited the biosynthesis of LDs within the endoplasmic reticulum by promoting the degradation of DGAT1 and DGAT2 via autophagy. Furthermore, TFE3 fusion proteins upregulated LAMP2A, thereby enhancing chaperone-mediated autophagy pathways. The process facilitated the degradation of LDs and promoted oxidative metabolism of long-chain fatty acids in mitochondria.

Conclusions: TFE3 fusion proteins facilitated the progression of TFE3 rRCC through enhancing the degradation of LDs via chaperone-mediated lipophagy. LAMP2A could serve as a novel potential prognostic biomarker and therapeutic targets.

{"title":"TFE3 fusion proteins promote the progression of TFE3 rearranged renal cell carcinoma via enhancing chaperone-mediated lipophagy.","authors":"Wenliang Ma, Yi Chen, Guijuan Chen, Lei Yang, Yanwen Lu, Xiang Dong, Dongmei Li, Weidong Gan","doi":"10.1186/s12964-025-02117-y","DOIUrl":"10.1186/s12964-025-02117-y","url":null,"abstract":"<p><strong>Background: </strong>TFE3 rearranged renal cell carcinoma (TFE3 rRCC), classified as a distinct entity of RCCs, exhibits aggressive biological behavior and possesses unique metabolic characteristics. In the present study, TFE3 rRCC with high expression of TFE3 fusion proteins was employed to investigate the features of lipid metabolism and its underlying mechanism in cancer progression.</p><p><strong>Methods: </strong>Fluorescence microscope and flow cytometry were employed to detect lipid droplets (LDs). GPO-PAP method and Oil Red O staining were used to quantify triacylglycerol levels. The data for bioinformatics analysis were sourced from GEO and iProX. The biological roles of TFE3 and LAMP2A were investigated by CCK8 assay, EdU staining, seahorse, transwell assay, colony, and sphere formation assay. The regulatory mechanisms involving TFE3, LAMP2A and Hsc70 were investigated using western blotting, immunohistochemistry, qRT-PCR, luciferase assays, Co-IP techniques, and ChIP analyses.</p><p><strong>Results: </strong>The level of LDs accumulation in TFE3 rRCC was relatively low, and the knockdown of TFE3 led to an increase in LDs accumulation while inhibiting tumor progression. The underlying mechanism revealed that TFE3 fusion proteins inhibited the biosynthesis of LDs within the endoplasmic reticulum by promoting the degradation of DGAT1 and DGAT2 via autophagy. Furthermore, TFE3 fusion proteins upregulated LAMP2A, thereby enhancing chaperone-mediated autophagy pathways. The process facilitated the degradation of LDs and promoted oxidative metabolism of long-chain fatty acids in mitochondria.</p><p><strong>Conclusions: </strong>TFE3 fusion proteins facilitated the progression of TFE3 rRCC through enhancing the degradation of LDs via chaperone-mediated lipophagy. LAMP2A could serve as a novel potential prognostic biomarker and therapeutic targets.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"122"},"PeriodicalIF":8.2,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11887198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143574691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Impact of POU3F4 mutation on cochlear development and auditory function.
IF 8.2 2区 生物学 Q1 CELL BIOLOGY Pub Date : 2025-03-05 DOI: 10.1186/s12964-025-02133-y
Jiong Dang, Panpan Bian, Chao Chen, Chi Chen, Wenqi Shan, Luhang Cai, Yong Li, Huan Tan, Baicheng Xu, Minxin Guan, Yufen Guo

Background: Hearing loss, a major public health issue, affects 1.33 per 1,000 live births worldwide. Genetic factors contribute to over half of congenital cases, with X-linked inheritance accounting for 1-5%. POU3F4 mutations are associated with approximately 50% of X-linked non-syndrome hearing loss cases. POU3F4 plays a critical role in cochlear development by regulating otic mesenchyme cell differentiation. The study investigates the impact of a novel POU3F4 p.E294G mutation on cochlear structure and function using cellular and animal model.

Methods: The study utilized immortalized lymphoblastoid cell lines, POU3F4 overexpressed HEK293 cells and generated Pou3f4 knock-in (Pou3f4KI) mice via CRISPR/Cas9 to introduce the p.E294G mutation. Alterations in expression and subcellular localization of POU3F4 were detected at the cellular level. Auditory function was assessed using auditory brainstem response testing. Cochlear structure was analyzed through histology, immunohistochemistry, scanning electron microscopy, and transmission electron microscopy. RNA sequencing, qPCR and Western blot were conducted to evaluate gene expression and mitochondrial function.

Results: The transcription of POU3F4 was abnormal and the expression was normal in lymphoblastoid cell lines. Abnormal nuclear localization of POU3F4 p.E294G was found in overexpressed HEK293 cells. Pou3f4KI mice exhibited cochlear malformations, including modiolus hypoplasia and reduced stria vascularis cell populations. Auditory testing revealed progressive hearing loss. Pou3f4 affect mitochondrial protein expression by affecting the expression of TFAM. Mitochondrial dysfunction was evident, with reduced oxidative phosphorylation (OXPHOS) complex assembly and activity, decreased ATP levels. The level of reactive oxygen species, mitochondrial fission and apoptosis in cochlea were elevated.

Conclusions: The POU3F4 p.E294G resulted in abnormal nuclear localization. Pou3f4 mutant disrupts cochlear development and function, impairs mitochondrial integrity, induces oxidative stress, and promotes apoptosis, leading to progressive hearing loss. The findings enhance the understanding of POU3F4-related hearing loss mechanisms and highlight the importance of early genetic screening and audiological monitoring.

{"title":"Impact of POU3F4 mutation on cochlear development and auditory function.","authors":"Jiong Dang, Panpan Bian, Chao Chen, Chi Chen, Wenqi Shan, Luhang Cai, Yong Li, Huan Tan, Baicheng Xu, Minxin Guan, Yufen Guo","doi":"10.1186/s12964-025-02133-y","DOIUrl":"10.1186/s12964-025-02133-y","url":null,"abstract":"<p><strong>Background: </strong>Hearing loss, a major public health issue, affects 1.33 per 1,000 live births worldwide. Genetic factors contribute to over half of congenital cases, with X-linked inheritance accounting for 1-5%. POU3F4 mutations are associated with approximately 50% of X-linked non-syndrome hearing loss cases. POU3F4 plays a critical role in cochlear development by regulating otic mesenchyme cell differentiation. The study investigates the impact of a novel POU3F4 p.E294G mutation on cochlear structure and function using cellular and animal model.</p><p><strong>Methods: </strong>The study utilized immortalized lymphoblastoid cell lines, POU3F4 overexpressed HEK293 cells and generated Pou3f4 knock-in (Pou3f4KI) mice via CRISPR/Cas9 to introduce the p.E294G mutation. Alterations in expression and subcellular localization of POU3F4 were detected at the cellular level. Auditory function was assessed using auditory brainstem response testing. Cochlear structure was analyzed through histology, immunohistochemistry, scanning electron microscopy, and transmission electron microscopy. RNA sequencing, qPCR and Western blot were conducted to evaluate gene expression and mitochondrial function.</p><p><strong>Results: </strong>The transcription of POU3F4 was abnormal and the expression was normal in lymphoblastoid cell lines. Abnormal nuclear localization of POU3F4 p.E294G was found in overexpressed HEK293 cells. Pou3f4KI mice exhibited cochlear malformations, including modiolus hypoplasia and reduced stria vascularis cell populations. Auditory testing revealed progressive hearing loss. Pou3f4 affect mitochondrial protein expression by affecting the expression of TFAM. Mitochondrial dysfunction was evident, with reduced oxidative phosphorylation (OXPHOS) complex assembly and activity, decreased ATP levels. The level of reactive oxygen species, mitochondrial fission and apoptosis in cochlea were elevated.</p><p><strong>Conclusions: </strong>The POU3F4 p.E294G resulted in abnormal nuclear localization. Pou3f4 mutant disrupts cochlear development and function, impairs mitochondrial integrity, induces oxidative stress, and promotes apoptosis, leading to progressive hearing loss. The findings enhance the understanding of POU3F4-related hearing loss mechanisms and highlight the importance of early genetic screening and audiological monitoring.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"121"},"PeriodicalIF":8.2,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11884022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143568999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
CARM1 regulates tubulin autoregulation through PI3KC2α R175 methylation.
IF 8.2 2区 生物学 Q1 CELL BIOLOGY Pub Date : 2025-03-05 DOI: 10.1186/s12964-025-02124-z
Yena Cho, Jee Won Hwang, Mark T Bedford, Dae-Geun Song, Su-Nam Kim, Yong Kee Kim

Tubulin is crucial in several cellular processes, including intracellular organization, organelle transport, motility, and chromosome segregation. Intracellular tubulin concentration is tightly regulated by an autoregulation mechanism, in which excess free tubulin promotes tubulin mRNA degradation. However, the details of how changes in free tubulin levels initiate this autoregulation remain unclear. In this study, we identified coactivator-associated arginine methyltransferase 1 (CARM1)-phosphatidylinositol 3-kinase class 2α (PI3KC2α) axis as a novel regulator of tubulin autoregulation. CARM1 stabilizes PI3KC2α by methylating its R175 residue. Once PI3KC2α is not methylated, it becomes unstable, leading to decreased cellular levels. Loss of PI3KC2α results in the release of tetratricopeptide repeat domain 5 (TTC5), which initiates tubulin autoregulation. Thus, PI3KC2α, along with its CARM1-mediated arginine methylation, regulates the initiation of tubulin autoregulation. Additionally, disruption of the CARM1-PI3KC2α axis decreases intracellular tubulin levels, leading to a synergistic increase in the cytotoxicity of microtubule-targeting agents (MTAs). Taken together, our study demonstrates that the CARM1-PI3KC2α axis is a key regulator of TTC5-mediated tubulin autoregulation and that disrupting this axis enhances the anti-cancer activity of MTAs.

{"title":"CARM1 regulates tubulin autoregulation through PI3KC2α R175 methylation.","authors":"Yena Cho, Jee Won Hwang, Mark T Bedford, Dae-Geun Song, Su-Nam Kim, Yong Kee Kim","doi":"10.1186/s12964-025-02124-z","DOIUrl":"10.1186/s12964-025-02124-z","url":null,"abstract":"<p><p>Tubulin is crucial in several cellular processes, including intracellular organization, organelle transport, motility, and chromosome segregation. Intracellular tubulin concentration is tightly regulated by an autoregulation mechanism, in which excess free tubulin promotes tubulin mRNA degradation. However, the details of how changes in free tubulin levels initiate this autoregulation remain unclear. In this study, we identified coactivator-associated arginine methyltransferase 1 (CARM1)-phosphatidylinositol 3-kinase class 2α (PI3KC2α) axis as a novel regulator of tubulin autoregulation. CARM1 stabilizes PI3KC2α by methylating its R175 residue. Once PI3KC2α is not methylated, it becomes unstable, leading to decreased cellular levels. Loss of PI3KC2α results in the release of tetratricopeptide repeat domain 5 (TTC5), which initiates tubulin autoregulation. Thus, PI3KC2α, along with its CARM1-mediated arginine methylation, regulates the initiation of tubulin autoregulation. Additionally, disruption of the CARM1-PI3KC2α axis decreases intracellular tubulin levels, leading to a synergistic increase in the cytotoxicity of microtubule-targeting agents (MTAs). Taken together, our study demonstrates that the CARM1-PI3KC2α axis is a key regulator of TTC5-mediated tubulin autoregulation and that disrupting this axis enhances the anti-cancer activity of MTAs.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"120"},"PeriodicalIF":8.2,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11884010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143568995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Revealing the role of RAB27 in HER receptor family expression and signaling in melanoma cells.
IF 8.2 2区 生物学 Q1 CELL BIOLOGY Pub Date : 2025-03-04 DOI: 10.1186/s12964-025-02064-8
Katarzyna Horodecka, Liliana Czernek, Łukasz Pęczek, Magdalena Klink

Background: Alterations in signalling pathways fuel the growth and progression of melanoma. Therefore, understanding these processes is essential for developing effective treatment strategies. RAB27A and RAB27B are known to possess oncogenic effects by modulating cancer cell proliferation, invasion and drug resistance in various types of cancer, including melanoma. These proteins are mostly acknowledged as coordinators of the vesicular trafficking, however, their function in cellular signaling is less recognized. Therefore we aimed to investigate the relationship between RAB27 and oncogenic or signalling proteins in melanoma cells.

Methods: We generated RAB27A knockout (KO) in SkMel28, A375, and patient-derived DMBC12 melanoma cell lines. Additionally, a double RAB27A/B knockout (dKO) A375 cell line was created. Firstly, we applied the Proteome Profiler array to identify proteins differentially expressed upon RAB27A/B loss. Subsequently, we picked selected specific proteins for a further in-depth analysis using RT-PCR, Western blot, and flow cytometry.

Results: We found that silencing RAB27 markedly decreased the levels of various intracellular proteins linked with proliferation, invasion, angiogenesis, adhesion, or EMT at a cell-line dependent level. Among others, we observed a link between the expression of RAB27 and EGFR, HER2 and HER3. Altered levels of HER receptors disturbed the downstream signaling pathways by reducing the phosphorylation of AKT and ERK1/2 proteins.

Conclusions: Our findings present novel, previously unpublished data on the relationship between HER family receptor expression and potential activity, and the involvement of RAB27 in melanoma cells.

背景:信号通路的改变助长了黑色素瘤的生长和恶化。因此,了解这些过程对于制定有效的治疗策略至关重要。众所周知,RAB27A 和 RAB27B 具有致癌作用,可调节包括黑色素瘤在内的各种癌症的癌细胞增殖、侵袭和耐药性。这些蛋白被认为是囊泡运输的协调者,但它们在细胞信号传导中的功能却鲜为人知。因此,我们旨在研究 RAB27 与黑色素瘤细胞中的致癌蛋白或信号蛋白之间的关系:我们在 SkMel28、A375 和源自患者的 DMBC12 黑色素瘤细胞系中产生了 RAB27A 基因敲除(KO)。此外,我们还创建了RAB27A/B双基因敲除(dKO)的A375细胞系。首先,我们应用蛋白质组剖析器阵列来鉴定 RAB27A/B 缺失时差异表达的蛋白质。随后,我们利用 RT-PCR、Western 印迹和流式细胞术挑选出特定蛋白质进行进一步深入分析:结果:我们发现,在细胞系依赖水平上,沉默 RAB27 会显著降低与增殖、侵袭、血管生成、粘附或 EMT 相关的各种细胞内蛋白的水平。其中,我们观察到 RAB27 的表达与表皮生长因子受体、HER2 和 HER3 之间存在联系。HER受体水平的改变通过减少AKT和ERK1/2蛋白的磷酸化扰乱了下游信号通路:我们的研究结果提供了以前未发表过的新数据,说明了黑色素瘤细胞中 HER 家族受体表达与潜在活性之间的关系以及 RAB27 的参与。
{"title":"Revealing the role of RAB27 in HER receptor family expression and signaling in melanoma cells.","authors":"Katarzyna Horodecka, Liliana Czernek, Łukasz Pęczek, Magdalena Klink","doi":"10.1186/s12964-025-02064-8","DOIUrl":"10.1186/s12964-025-02064-8","url":null,"abstract":"<p><strong>Background: </strong>Alterations in signalling pathways fuel the growth and progression of melanoma. Therefore, understanding these processes is essential for developing effective treatment strategies. RAB27A and RAB27B are known to possess oncogenic effects by modulating cancer cell proliferation, invasion and drug resistance in various types of cancer, including melanoma. These proteins are mostly acknowledged as coordinators of the vesicular trafficking, however, their function in cellular signaling is less recognized. Therefore we aimed to investigate the relationship between RAB27 and oncogenic or signalling proteins in melanoma cells.</p><p><strong>Methods: </strong>We generated RAB27A knockout (KO) in SkMel28, A375, and patient-derived DMBC12 melanoma cell lines. Additionally, a double RAB27A/B knockout (dKO) A375 cell line was created. Firstly, we applied the Proteome Profiler array to identify proteins differentially expressed upon RAB27A/B loss. Subsequently, we picked selected specific proteins for a further in-depth analysis using RT-PCR, Western blot, and flow cytometry.</p><p><strong>Results: </strong>We found that silencing RAB27 markedly decreased the levels of various intracellular proteins linked with proliferation, invasion, angiogenesis, adhesion, or EMT at a cell-line dependent level. Among others, we observed a link between the expression of RAB27 and EGFR, HER2 and HER3. Altered levels of HER receptors disturbed the downstream signaling pathways by reducing the phosphorylation of AKT and ERK1/2 proteins.</p><p><strong>Conclusions: </strong>Our findings present novel, previously unpublished data on the relationship between HER family receptor expression and potential activity, and the involvement of RAB27 in melanoma cells.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"118"},"PeriodicalIF":8.2,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11877929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Cell Communication and Signaling
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:481959085
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