Acta biochimica et biophysica Sinica最新文献

Establishment and evaluation of a stable CHO cell line in which the nanobody PD-L1-Fc gene is precisely targeted into the C12orf35 locus. 将纳米体PD-L1-Fc基因精确定位到C12orf35位点的稳定CHO细胞系的建立和评价

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-10-10 DOI: 10.3724/abbs.2025187

Feng Chang, Chen Zhang, Yu Feng, Wenyun Zheng, Xingyuan Ma

引用次数: 0

The dual role of whole-genome duplication: biological mechanisms, functional consequences, and detection advances. 全基因组复制的双重作用：生物学机制、功能后果和检测进展。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-09-30 DOI: 10.3724/abbs.2025175

Yawei Song, Jiajie Yang, Shuheng Wu, Wei Wu

引用次数: 0

KDM4A regulates microglial polarization after ischemic stroke by regulating SPINK5 signaling. KDM4A通过调控SPINK5信号通路调控缺血性脑卒中后小胶质细胞极化。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-09-26 DOI: 10.3724/abbs.2025132

Xiaoli Min, Lei Xian, Ting Liu, Mengze Wang, Qing Zhao, Jiayi Hu, Rui Jing

{"title":"KDM4A regulates microglial polarization after ischemic stroke by regulating SPINK5 signaling.","authors":"Xiaoli Min, Lei Xian, Ting Liu, Mengze Wang, Qing Zhao, Jiayi Hu, Rui Jing","doi":"10.3724/abbs.2025132","DOIUrl":"https://doi.org/10.3724/abbs.2025132","url":null,"abstract":"Microglia/macrophage polarization is a crucial factor in inflammatory processes following ischemic stroke (IS). This study explores the molecular mechanisms through which lysine-specific histone demethylase 4 (KDM4A) regulates microglial polarization postischemic stroke. IS models are established in vivo via transient middle cerebral artery occlusion (MCAO) surgery and in vitro via oxygen-glucose deprivation (OGD) treatment. 2,3,5-Triphenyl tetrazolium chloride staining is conducted to determine the infarct size. RT-qPCR is used to determine mRNA expression. Immunofluorescence assay is used to detect the expressions of KDM4A and biomarkers of microglia. Western blot analysis is used to determine the expressions of KDM4A and serine peptidase inhibitor Kazal type 5 (SPINK5). The enrichment of H3K9me3 on the promoter of SPINK5 is determined via chromatin immunoprecipitation assay. Neuronal apoptosis is detected via TUNEL assay. We find that KDM4A is upregulated in IS models. Downregulation of KDM4A mitigates neurological dysfunction, enhances motor capacity, and reduces inflammatory infiltration in vivo while suppressing microglial activation and promoting M2 polarization. Mechanistically, KDM4A reduces the enrichment of H3K9me3 on the SPINK5 promoter, thereby increasing SPINK5 expression. Moreover, overexpression of SPINK5 inhibits M2 microglial polarization and neuronal apoptosis. Overall, KDM4A exacerbates ischemic stroke-induced brain injury by promoting proinflammatory microglial polarization via SPINK5 signaling.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147359","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

MSCs attenuate airway remodeling in HDM-induced asthma by inhibiting the Timp1-Wnt2b axis. MSCs通过抑制Timp1-Wnt2b轴减弱hdm诱导哮喘的气道重塑。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-09-26 DOI: 10.3724/abbs.2025159

Kai Yu, Xinyu Feng, Rong Zhang, Jian Fan, Jiaying Yuan, Yan Shang, Jiayi Zhao

{"title":"MSCs attenuate airway remodeling in HDM-induced asthma by inhibiting the Timp1-Wnt2b axis.","authors":"Kai Yu, Xinyu Feng, Rong Zhang, Jian Fan, Jiaying Yuan, Yan Shang, Jiayi Zhao","doi":"10.3724/abbs.2025159","DOIUrl":"https://doi.org/10.3724/abbs.2025159","url":null,"abstract":"MSCs have demonstrated their unique therapeutic potential in early clinical trials for a variety of respiratory diseases in recent years, but their use in the treatment of asthma has rarely been reported. In this study, a chronic murine asthma model that is more similar to clinical asthma is constructed via sustained HDM induction for 70 days, followed by treatment via tail vein injection of MSCs after modeling. The mechanism by which MSCs alleviate airway remodeling is investigated via RNA-seq. The airways on the day following treatment are used to screen for transcriptomic changes resulting from the MSC treatment under study, filtering for differentially expressed genes (DEGs), identifying their enrichment pathways, and finally confirming the DEGs gained via western blot analysis. After HDM treatment, airway remodeling is reversed, asthma and the HIF-1 signaling pathway are inhibited, and the expression levels of Timp1 and Wnt2b in the fibrosis pathway are also significantly decreased. STRING analysis reveals a reciprocal interaction in their expression, which is also confirmed by western blot analysis. To verify whether MSCs alleviate airway remodeling by inhibiting Timp1, we construct MSCs overexpressing Timp1 and evaluate their effects in vitro and in vivo. The ability of MSCs to alleviate airway remodeling is reversed after Timp1 is overexpressed. These findings demonstrate that MSCs alleviate asthma-induced airway remodeling by inhibiting the Timp1-Wnt2b axis.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147354","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

Rapid detection of Escherichia coli in bloodstream infection via CRISPR-Cas9 engineered reporter phage T7:: Nluc and microfluidic chip platform. 利用CRISPR-Cas9工程报告噬菌体T7:: Nluc和微流控芯片平台快速检测血流感染中的大肠杆菌。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-09-26 DOI: 10.3724/abbs.2025150

Minwei Li, Zhiyun Hao, Jing Yan, Ximeng Chen, Hangyi Li, Chengbin Wang, Chi Wang

{"title":"Rapid detection of Escherichia coli in bloodstream infection via CRISPR-Cas9 engineered reporter phage T7:: Nluc and microfluidic chip platform.","authors":"Minwei Li, Zhiyun Hao, Jing Yan, Ximeng Chen, Hangyi Li, Chengbin Wang, Chi Wang","doi":"10.3724/abbs.2025150","DOIUrl":"https://doi.org/10.3724/abbs.2025150","url":null,"abstract":"Rapid identification of pathogens responsible for bloodstream infection is critical for early intervention and effective treatment. Reporter phages, which are known for their exceptional sensitivity and specificity in pathogen detection, have garnered significant interest. In this study, we systematically evaluate phage genome editing strategies that combine homologous recombination with the CRISPR-Cas9 system. We investigate the impacts of homologous arm length, sgRNA activity, target site, and plasmid interactions on editing efficiency. Our results demonstrate that successful genome editing depends on both sufficient cleavage pressure and optimal homologous arm length, particularly when using low-activity sgRNAs. On the basis of these findings, we develop a highly efficient gene editing strategy TPMSR (triple-plasmid-mediated synchronous recombination) that overcomes the limitations of conventional methods that rely on high-activity sgRNA and restricted editing sites. Using the TPMSR strategy, we integrate the Nluc gene into phage T7, generating the reporter phage T7:: Nluc, which is then incorporated into a microfluidic chip. Validation with 51 clinical isolates demonstrates outstanding sensitivity, specificity, and accuracy in detecting E. coli in blood within 1.5 h at concentrations less than 30 CFU/mL. This study presents a robust strategy for phage genome engineering and develops a promising method for the rapid diagnosis of bloodstream infections caused by Escherichia coli.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147375","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

Single-cell transcriptomics reveals apolipoprotein A4-mediated metabolic-immune reprogramming in lymphocytes during early obesity-related chronic kidney disease. 单细胞转录组学揭示了早期肥胖相关慢性肾脏疾病中载脂蛋白a4介导的淋巴细胞代谢免疫重编程。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-09-25 DOI: 10.3724/abbs.2025171

Yang Wei, Ting Zhang, Yingying Jin, Xiaohuan Liu, Jinting Zhou, Na Huang, Yiying Wang

{"title":"Single-cell transcriptomics reveals apolipoprotein A4-mediated metabolic-immune reprogramming in lymphocytes during early obesity-related chronic kidney disease.","authors":"Yang Wei, Ting Zhang, Yingying Jin, Xiaohuan Liu, Jinting Zhou, Na Huang, Yiying Wang","doi":"10.3724/abbs.2025171","DOIUrl":"https://doi.org/10.3724/abbs.2025171","url":null,"abstract":"Obesity-induced metabolic inflammation is a key driver of chronic kidney disease (CKD), with immune dysregulation, particularly among lymphocytes, contributing to early disease pathology. To explore the role of apolipoprotein A4 (Apoa4) in regulating immune cell metabolism and function, we establish high-fat diet-induced obese (DIO) models using wild-type and Apoa4-knockout (KO) mice. KO mice exhibit exacerbated insulin resistance and renal lipid accumulation. Single-cell RNA sequencing reveals that Apoa4 deletion remodeled the renal immune-metabolic landscape. This remodeling broadly compromises the immune functions of T, NK, and B cells, even as it expands the proportions of cytotoxic Gzma + NK cells and Derl3 + plasma cells. Mechanistically, Apoa4 deletion aggravates metabolic dysregulation and oxidative stress and downregulates the expression levels of key effector genes, including Ifng and Il1b. Furthermore, the regulatory network activities of key transcription factors, such as Lef1 and Runx3 in Cd8 + T cells; Irf8, T-bet, and Eomes in NK cells; and Tcf4, Lmo2, and Xbp1 in B cells, are perturbed. CellChat analysis predicts disruptions in pro-inflammatory (IFN-II and IL-1), immunoregulatory (FASLG), and metabolic regulatory (ENHO and ANGPTL) signaling, alongside enhanced IL-2-mediated suppression. These findings are corroborated by flow cytometry, immunofluorescence staining, and qPCR. Our results establish Apoa4 as a crucial regulator of lymphocyte metabolic and immune homeostasis in the early stages of obesity-associated CKD.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147357","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

Corrigendum to: Magnolol promotes the autophagy of esophageal carcinoma cells by upregulating HACE1 gene expression. 厚朴酚通过上调HACE1基因表达促进食管癌细胞自噬。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-09-25 DOI: 10.3724/abbs.2025129

Kenan Huang, Biao Zhang, Yu Feng, Haitao Ma

引用次数: 0

MAN1A1 promotes colorectal cancer liver metastasis by maintaining TGFBR2 protein stability. MAN1A1通过维持TGFBR2蛋白的稳定性促进结直肠癌肝转移。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-09-25 DOI: 10.3724/abbs.2025164

Yingxi Hu, Yinwen Xu, Kai Chen, Shihua Guan, Huiling Zhou, Tao Li, Rongrui Liang, Min Tao, Yiyi Yu, Xinxin Ge, Yuanyuan Ruan

{"title":"MAN1A1 promotes colorectal cancer liver metastasis by maintaining TGFBR2 protein stability.","authors":"Yingxi Hu, Yinwen Xu, Kai Chen, Shihua Guan, Huiling Zhou, Tao Li, Rongrui Liang, Min Tao, Yiyi Yu, Xinxin Ge, Yuanyuan Ruan","doi":"10.3724/abbs.2025164","DOIUrl":"https://doi.org/10.3724/abbs.2025164","url":null,"abstract":"Emerging biochemical and genetic evidence has firmly established aberrant protein glycosylation as a critical regulator of oncogenic transformation, with glycocalyx remodeling profoundly influencing tumor microenvironment dynamics and metastatic progression. Despite the well-documented association between metastatic dissemination and poor clinical outcomes in patients with colorectal cancer, the underlying molecular mechanisms remain incompletely characterized. Through integrative analysis of single-cell RNA sequencing data from a public database, we identify the Golgi-resident α-1,2-mannosidase MAN1A1 as a consistently upregulated enzyme in malignant epithelial cells derived from colorectal cancer liver metastases. Clinically, elevated MAN1A1 expression is correlated with reduced overall survival, suggesting that MAN1A1 is both a prognostic biomarker and therapeutic target for colorectal cancer liver metastases. Genetic manipulation of MAN1A1 in colorectal cancer cells demonstrates that although the proliferation capacity of colorectal cancer cells remains unchanged, MAN1A1 overexpression significantly enhances migratory and invasive capacities in transwell assays, suggesting its specific involvement in metastatic progression. Mechanistic investigations reveal that MAN1A1 exerts its pro-metastatic effects by significantly prolonging the TGFBR2 protein half-life. Together, our work identifies MAN1A1 as both a prognostic biomarker and a promising therapeutic target, highlighting the critical role of glycan remodeling in the metastatic progression of colorectal cancer.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147367","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

Yaf9 conditionally contributes to cell size control in Candida albicans. Yaf9有条件地参与白色念珠菌的细胞大小控制。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-09-24 DOI: 10.3724/abbs.2025180

Wencheng Zhu, Baodi Dai, Yinxing Xu, Jiangye Chen

引用次数: 0

Reductive stress in cancer immunology and targeted therapy. 减轻应激在癌症免疫和靶向治疗中的作用。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-09-19 DOI: 10.3724/abbs.2025173

Xiaotian Ji, Gang Xiao

引用次数: 0