Acta biochimica et biophysica Sinica最新文献

Presenilin 1 is located in the mitochondrial inner inner membrane and regulates mitochondrial cristae junction protein arrangement and cristae formation in HEK293 cells. 早老素1位于线粒体内膜，在HEK293细胞中调控线粒体嵴连接蛋白的排列和嵴的形成。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-04-25 DOI: 10.3724/abbs.2026064

Pan You, Pengjin Zhu, Hui Yu, Luwen Wang, Bo Su

{"title":"Presenilin 1 is located in the mitochondrial inner inner membrane and regulates mitochondrial cristae junction protein arrangement and cristae formation in HEK293 cells.","authors":"Pan You, Pengjin Zhu, Hui Yu, Luwen Wang, Bo Su","doi":"10.3724/abbs.2026064","DOIUrl":"https://doi.org/10.3724/abbs.2026064","url":null,"abstract":"Presenilin 1 (PS1), a key pathogenic factor in familial Alzheimer's disease, is implicated in the regulation of mitochondrial functions, yet its precise sub-mitochondrial localization and underlying mechanisms remain poorly understood. In this study, we generate PS1-knockout cell lines to investigate the role of PS1 in mitochondrial structure and function. Our results indicate that PS1 is directly localized in the mitochondrial inner membrane. PS1 deficiency leads to reduced ATP production, impaired mitochondrial respiration capacity, decreased mitochondrial membrane potential, disrupted Ca 2+ homeostasis, and elevated ROS accumulation. Moreover, loss of PS1 leads to abnormal mitochondrial cristae structure. Further analysis reveals that PS1 interacts with mitochondrial inner membrane proteins. Its absence promotes ATAD3A oligomerization and disrupts its arrangement at mitochondrial cristae junctions, leading to expansion of the mitochondria-associated membrane and instability of mitochondrial DNA. Our findings demonstrate that PS1 acts as a central regulator of mitochondrial cristae morphogenesis by modulating protein interaction networks at cristae junctions, thereby illuminating fundamental molecular mechanisms contributing to mitochondrial dysfunction in Alzheimer's disease.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Paclitaxel induces neurotoxicity via activating ferroptosis by suppressing Nrf2/SLC7A11/GSH/GPX4 signaling. 紫杉醇通过抑制Nrf2/SLC7A11/GSH/GPX4信号通路激活铁下垂诱导神经毒性。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-04-25 DOI: 10.3724/abbs.2026068

Jiaqi Yu, Weifeng Xu, Dongmeng Liu, Xiaoli Feng, Chenglong Zheng, Xiaodan Li, Jiaolin Bao, Sulan Luo, Ren-Bo Ding

引用次数: 0

Scaffold compound T4015 attenuates pulmonary fibrosis via suppressing JAK/STAT and NF-κB signaling. 支架化合物T4015通过抑制JAK/STAT和NF-κB信号通路减轻肺纤维化。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-04-25 DOI: 10.3724/abbs.2026035

Minghui Zhang, Hang Xu, Shan Liu, Xiaohan Xu, Jiayi Yin, Xinxin Zhang, Xiaonan Zhang, Xiaoping Yang, Xiaochun Liu, Bin Yin, Mingming Zhou, Lewei Wang, Meng Zhang, Huiying Liu, Wenqing Jiang, Qiaoling Song, Jinbo Yang

{"title":"Scaffold compound T4015 attenuates pulmonary fibrosis via suppressing JAK/STAT and NF-κB signaling.","authors":"Minghui Zhang, Hang Xu, Shan Liu, Xiaohan Xu, Jiayi Yin, Xinxin Zhang, Xiaonan Zhang, Xiaoping Yang, Xiaochun Liu, Bin Yin, Mingming Zhou, Lewei Wang, Meng Zhang, Huiying Liu, Wenqing Jiang, Qiaoling Song, Jinbo Yang","doi":"10.3724/abbs.2026035","DOIUrl":"https://doi.org/10.3724/abbs.2026035","url":null,"abstract":"Pulmonary fibrosis (PF) is a life-threatening interstitial lung disease characterized by scarring and inflammation in lung tissues. Aberrant activation of the JAK/STAT and NF-κB signaling pathways is critical in initiating and sustaining the inflammatory processes that drive fibrotic progression. In this study, we identify a novel small-molecule compound, T4015, a 4-indolyl-2-phenylaminopyrimidine derivative, as a dual-pathway inhibitor targeting both JAK/STAT and NF-κB signaling. Dual-luciferase reporter assays demonstrate the potent inhibitory activity of T4015 against these pathways. T4015 effectively suppresses the phosphorylation of STAT3, JAK1, and TYK2 induced by IL-6 and IFN-β, while suppressing LPS-induced NF-κB activation in macrophages. Transcriptome sequencing and pathway enrichment analyses further confirm that T4015 downregulates multiple inflammation-related signaling cascades, including the JAK/STAT, NF-κB, TNF, IL-17, and Toll-like receptor pathways. In a mouse model of bleomycin-induced PF, T4015 treatment significantly improves survival, attenuates collagen deposition, and reduces the expression of pro-inflammatory and profibrotic markers such as IL-6, CCL2, and COL1. Molecular docking and target prediction analyses suggest that T4015 exhibits strong binding affinity for multiple kinases within the JAK/STAT and NF-κB networks, including JAK1, TYK2, JAK2, JAK3, RIPK1, IRAK1/4, TAB1, and ZAP70. Collectively, these results highlight T4015 as a promising therapeutic candidate for PF through its simultaneous inhibition of the JAK/STAT and NF-κB signaling pathways.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

E3 ubiquitin ligase COP1-mediated GSK3β degradation activates β-catenin signaling to facilitate colorectal cancer cell proliferation. E3泛素连接酶cop1介导的GSK3β降解激活β-catenin信号通路促进结直肠癌细胞增殖。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-04-17 DOI: 10.3724/abbs.2026023

Dakui Luo, Kangjunjie Wang, Yufei Yang, Qingguo Li, Xinxiang Li

引用次数: 0

Small chemical molecule CPP promotes angiogenesis in surgically created severe lower limb ischemia and diabetes-induced limb vascular reduction models. 小化学分子CPP促进手术建立的严重下肢缺血和糖尿病诱导的肢体血管减少模型中的血管生成。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-04-16 DOI: 10.3724/abbs.2026039

Xinyu Dong, Yangyang Zhang, Congyao Zhao, Xiaomeng Yan, Xiaohui Chi, Xinyu Xie, BaoXiang Zhao, Jian Zhang, Li Wang, Junying Miao, Zhaomin Lin

引用次数: 0

Distinct miR319a identified from Persicaria chinensis mediates cross-kingdom suppression of cervical cancer by targeting ITGA3. 从桃干中分离到的miR319a通过靶向ITGA3介导宫颈癌的跨界抑制。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-04-13 DOI: 10.3724/abbs.2026010

Yueyue Yan, Dan Bai, Lei Li, Leimei Xu, Hua Yang, Yuhui Wang, Han Feng, Lan Zhu

{"title":"Distinct miR319a identified from Persicaria chinensis mediates cross-kingdom suppression of cervical cancer by targeting ITGA3.","authors":"Yueyue Yan, Dan Bai, Lei Li, Leimei Xu, Hua Yang, Yuhui Wang, Han Feng, Lan Zhu","doi":"10.3724/abbs.2026010","DOIUrl":"10.3724/abbs.2026010","url":null,"abstract":"Persicaria chinensis, a well-known traditional Chinese medicinal herb that is both edible and medicinal, has been widely acknowledged for its therapeutic effects, such as anti-inflammatory, antioxidant, and antitumor activities. However, the role of miRNAs from this plant in the cross-kingdom regulation of human diseases has not been investigated. In this study, we analyze the miRNA expression profile of P. chinensis using high-throughput sequencing and identify a total of 673 miRNAs, including 422 novel miRNAs that are unique to this plant and 251 conserved miRNAs. Among the conserved miRNAs, pch-miR319a is found to be the most abundant. Moreover, food-oriented pch-miR319a accumulates in the uterus and tumors and exhibits a rich repertoire of target genes within cancer-related pathways, demonstrating significant cross-kingdom regulatory potential. Utilizing the dual-luciferase reporter gene assay, we demonstrate that pch-miR319a from P. chinensis targets the Itga3 gene, which is associated with cervical cancer progression. Overexpression of pch-miR319a significantly decreases the viability, migration, and induces apoptosis of HeLa cervical cancer cells in vitro. Moreover, in a syngeneic mouse tumor model of cervical cancer, treatment with pch-miR319a effectively inhibits tumor growth and downregulates the expressions of ITGA3 and the proliferation marker Ki-67. Our study highlights the potential of pch-miR319a from P. chinensis as a novel therapeutic agent for cervical cancer by targeting ITGA3 and provides new insights into the cross-kingdom regulatory mechanisms of plant miRNAs in human diseases.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147687614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MerTK inhibition by UNC569 triggers DNA damage and JNK/p38 MAPK cascade-driven apoptosis in pancreatic cancer. UNC569抑制MerTK可触发胰腺癌DNA损伤和JNK/p38 MAPK级联驱动的细胞凋亡。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-04-07 DOI: 10.3724/abbs.2026048

Meng Guo, Junwan Lu, Yue Sun, Lan Wang, Wen Li, Peizhen Wang, Yao Deng, Zhijie Tan, Hanbin Chen, Yang Hu, Bin Lu, Rongrong Wang

{"title":"MerTK inhibition by UNC569 triggers DNA damage and JNK/p38 MAPK cascade-driven apoptosis in pancreatic cancer.","authors":"Meng Guo, Junwan Lu, Yue Sun, Lan Wang, Wen Li, Peizhen Wang, Yao Deng, Zhijie Tan, Hanbin Chen, Yang Hu, Bin Lu, Rongrong Wang","doi":"10.3724/abbs.2026048","DOIUrl":"https://doi.org/10.3724/abbs.2026048","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is a malignancy with increasing mortality rates and remains a major clinical challenge due to its aggressive progression and limited therapeutic options. Therefore, the identification of early biomarkers and the development of effective targeted therapies are critically needed. MerTK, a receptor tyrosine kinase aberrantly expressed in various cancers, can be selectively inhibited by UNC569, a small-molecule antagonist with demonstrated efficacy in hematologic malignancies. This study shows that UNC569 potently suppresses PDAC cell proliferation and clonogenic growth, inhibits migration and invasion by attenuating epithelial-mesenchymal transition, and enhances the sensitivity of PDAC cells to Gemcitabine while promoting apoptosis. Mechanistically, UNC569 induces DNA damage-mediated G2/M phase arrest and activates JNK/p38 mitogen-activated protein kinase-dependent apoptotic signaling. Collectively, these results establish MerTK as a promising therapeutic target in PDAC and highlight the translational potential of UNC569 as a dual-pathway inhibitor for PDAC treatment.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147621435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tanshinones from Salvia miltiorrhiza alleviate ulcerative colitis via reprogramming the gut microbiota-metabolite axis. 丹参酮从丹参缓解溃疡性结肠炎通过重编程肠道微生物代谢轴。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-03-31 DOI: 10.3724/abbs.2026054

Zhe Liu, Chan Hui, Guochao Zhang, Haicheng Yang, Yi Wang, Yaqian Shi, Chao Wang, Yanfei Liu, Xia Gao, Yuting Wen

{"title":"Tanshinones from Salvia miltiorrhiza alleviate ulcerative colitis via reprogramming the gut microbiota-metabolite axis.","authors":"Zhe Liu, Chan Hui, Guochao Zhang, Haicheng Yang, Yi Wang, Yaqian Shi, Chao Wang, Yanfei Liu, Xia Gao, Yuting Wen","doi":"10.3724/abbs.2026054","DOIUrl":"https://doi.org/10.3724/abbs.2026054","url":null,"abstract":"The anti-inflammatory properties of the traditional herb Salvia miltiorrhiza Bunge are well-established, yet its precise mechanism of action in ulcerative colitis (UC) remains unclear. Herein, we evaluate the therapeutic potential of four major tanshinones-tanshinone IIA (Tan IIA), miltirone, neocryptotanshinone, and dihydrotanshinone I-in a murine dextran sulfate sodium (DSS)-induced colitis model. Our results show that tanshinones effectively alleviate disease severity, suppress systemic and local inflammation, and restore intestinal barrier integrity. Integrated multi-omics analysis reveals that the therapeutic efficacy originates from a comprehensive reprogramming of the gut microbiota-metabolite axis. Specifically, tanshinones reverse colitis-associated dysbiosis and rectify metabolic disturbances in linoleic acid metabolism, bile acid biosynthesis, and amino acid utilization. Correlation network analysis identifies key functional modules linking beneficial microbes ( e. g., Akkermansia) to anti-inflammatory lipid mediators and associating pathobionts ( e . g., Desulfovibrio) with disrupted bile acid metabolism. Notably, supplementation with Akkermansia muciniphila synergizes with Tan IIA to amplify barrier restoration and metabolic normalization. Our findings establish that tanshinones ameliorate UC through microbiota-driven metabolic reprogramming, wherein the restructured microbial community actively shapes a therapeutic metabolic output. This work elucidates a metabolite-mediated mechanism of action and positions tanshinones as promising microbiome-targeting therapeutics for inflammatory bowel disease.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147589289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

circ_0006156 promotes esophageal squamous cell carcinoma progression via activation of the TGFβ/Smad pathway. circ_0006156通过激活TGFβ/Smad通路促进食管鳞状细胞癌的进展。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-03-27 DOI: 10.3724/abbs.2026049

Zhanpeng Tang, Jian Li, Rongyang Li, Luyuan Ma, Renchang Zhao, Zhenguo Sun, Hui Tian

{"title":"circ_0006156 promotes esophageal squamous cell carcinoma progression via activation of the TGFβ/Smad pathway.","authors":"Zhanpeng Tang, Jian Li, Rongyang Li, Luyuan Ma, Renchang Zhao, Zhenguo Sun, Hui Tian","doi":"10.3724/abbs.2026049","DOIUrl":"https://doi.org/10.3724/abbs.2026049","url":null,"abstract":"Esophageal squamous cell carcinoma (ESCC) represents a common malignancy of the digestive system. Circular RNAs (circRNAs) are a distinct class of single-stranded non-coding RNAs that are essential in the progression of various tumors given that they can act as microRNA (miRNA) sponges in a manner similar to that of mRNAs. In this study, circ_0006156 is screened to be highly expressed in ESCC tissues through high-throughput sequencing and quantitative real-time polymerase chain reaction. Subsequent in vitro and in vivo experiments are conducted to validate its biological functions. Furthermore, the regulatory relationships among circ_0006156, miR-202-5p, and TGFBR1 are investigated using RNA antisense purification, miRNA sequencing, RNA immunoprecipitation, fluorescence in situ hybridization, dual-luciferase reporter assay, and bioinformatics analyses. The results show significant overexpression of circ_0006156 in ESCC tissues, with relatively shorter overall survival observed in patients with high circ_0006156 expression. circ_0006156 is further identified to directly bind to miR-202-5p. miR-202-5p inhibits the proliferation, migration, and invasion of ESCC cells in vitro and partially rescues the effects induced by circ_0006156. Consistent results are reported by subcutaneous xenograft tumor experiments in nude mice. In addition, circ_0006156 is confirmed to act as an endogenous sponge for miR-202-5p, which results in a relieved suppression of its target gene TGFβR1. In summary, circ_0006156 can regulate TGFβR1 expression by sponging miR-202-5p, which may further activate the TGFβ/Smad pathway and promote ESCC progression. Collectively, circ_0006156 functions as a novel oncogenic RNA in ESCC and may serve as a potential tumor marker.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147525283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Structural basis for the FOXM1 DNA binding domain to specific dsDNA substrate. FOXM1 DNA结合域与特定dsDNA底物的结构基础。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-03-27 DOI: 10.3724/abbs.2026036

Mingxuan Sun, Lei Wang, Jing Cui, Liang Zhang, Yunyu Shi, Chao Xu, Wanwan Zhou, Mengqi Lv

{"title":"Structural basis for the FOXM1 DNA binding domain to specific dsDNA substrate.","authors":"Mingxuan Sun, Lei Wang, Jing Cui, Liang Zhang, Yunyu Shi, Chao Xu, Wanwan Zhou, Mengqi Lv","doi":"10.3724/abbs.2026036","DOIUrl":"https://doi.org/10.3724/abbs.2026036","url":null,"abstract":"Forkhead box protein M1 (FOXM1) is a key transcription factor that regulates cell cycle progression and is frequently overexpressed in human cancers, driving tumor proliferation and therapy resistance. FOXM1 recognizes the canonical forkhead response element (FKH motif, RYAAAYA) through its conserved DNA-binding domain (DBD). Here, we report the high-resolution crystal structure of the FOXM1-DBD in complex with a double-stranded DNA substrate containing two FKH motifs. The structure reveals that FOXM1-DBD adopts the canonical winged-helix fold, with the third α-helix (α3) inserted into the DNA major groove to mediate sequence-specific recognition. Within this helix, Asn283, Arg286, and His287 form an essential triad that engages DNA bases through specific hydrogen bonds and hydrophobic interactions. Using structure-guided mutagenesis of key DNA-interacting residues combined with biophysical validation by isothermal titration calorimetry (ITC) and DNA binding assessment via electrophoretic mobility shift assay (EMSA), we confirm the functional importance of these residues and uncover position-dependent tolerance to base substitutions within the FKH motif. Furthermore, we demonstrate that FOXM1 overexpression promotes cell proliferation and upregulates the transcription of target genes in a DBD-dependent manner. Our findings provide a structural basis for understanding the DNA recognition mechanism of FOXM1 and offer mechanistic insights into how FOXM1 selectively binds to its genomic targets to regulate transcription.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147519530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0