Acta biochimica et biophysica Sinica最新文献

{"title":"Lonidamine ameliorates MASH by reducing SREBP1 and inhibiting the MAPK pathway.","authors":"Yuhan Chen, Feiyan Pan, Lusheng Tang, Yi Lu, Sainan Li, Yunyi Wu, Chen Yang, Xueying Ren, Yi Zhou, Hangqi Huang, Huanjuan Li, Tiexin Li, Jing Du, Xiangmin Tong, Haoran Li","doi":"10.3724/abbs.2026033","DOIUrl":"https://doi.org/10.3724/abbs.2026033","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatohepatitis (MASH) has become a global epidemic, and effective therapeutic strategies are urgently needed. Lonidamine (LND) has been reported to possess anti-inflammatory effects; however, few studies have investigated whether LND exerts a therapeutic effect on MASH. Therefore, in this study, we aim to explore the effects of LND on inflammatory responses and abnormal lipid metabolism in MASH mice. A mouse MASH model is established by feeding C57BL/6 mice a high-fat, high-cholesterol (CL) diet. The results show that LND attenuates CL-induced increases in body weight, serum glucose and lipid levels, inflammatory responses, and hepatocellular steatosis. In addition, the mitogen-activated protein kinase (MAPK) signaling pathway is inhibited, and the expression level of sterol regulatory element-binding protein 1 (SREBP1) protein is significantly reduced. Meanwhile, <i>in vitro</i> models of cellular inflammation and lipid metabolism are simulated, and molecular docking and biolayer interferometry (BLI) analysis are used to verify that LND and SREBP1 have a direct interaction and that LND promotes the degradation of SREBP1. Furthermore, specific knockdown of <i>Srebp1</i> in AML12 cells is performed to further verify the effect of LND on MASH. The results confirm that LND exerts anti-inflammatory effects in MASH by inhibiting the activity of the MAPK signaling pathway and improves abnormal lipid metabolism through its interaction with SREBP1. Overall, LND holds promise as a potential therapeutic agent for the treatment of MASH.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147363798","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}

{"title":"Super-resolution imaging reveals higher-order structures within common fragile sites in human mitotic chromosomes.","authors":"Jiabin Wang, Daniel M Czajkowsky, Zhifeng Shao","doi":"10.3724/abbs.2026014","DOIUrl":"https://doi.org/10.3724/abbs.2026014","url":null,"abstract":"<p><p>Common fragile sites (CFSs) are large genomic loci that are frequently deleted under replication stress and are thought to play a role in carcinogenesis as well as developmental disorders during early embryogenesis. They often appear as gaps or breaks in mitotic chromosomes by conventional optical microscopy and are also loci that are replicated in mitosis in a process called mitotic DNA synthesis (MiDAS). However, we still have a very poor understanding of the potential mechanisms underlying their genomic instability. We recently found that in normal mitotic chromosomes, there is a two-level hierarchy in the higher-order chromatin structure, with mechanically resistant ~90 nm Mitotic NanoDomains (MNDs) assembling into ~125 nm compact granules (CGs). In this work, we combine multiple super-resolution imaging techniques, including binding-activated localization microscopy (BALM), atomic force microscopy (AFM), and stochastic optical reconstruction microscopy (STORM), to characterize CFSs. Our super-resolution data indicate that sites that appear as gaps by conventional microscopy can be filled with chromatin of the size and shape of MNDs but not CGs. Moreover, we find that MiDAS loci only form an array of MNDs with no CGs. Taken together, our work suggests that under replication stress, CFS loci can not only be replicated but also assembled into higher-order chromatin. However, this organization is limited to the level of MNDs, which suggests that a failure to progress beyond MNDs to form CGs constitutes a key structural deficiency at these loci.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147353348","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}

{"title":"EZH2 inhibition overcomes immune evasion in lung adenocarcinoma by restoring CCL5-mediated T-cell recruitment and MHC class I antigen presentation.","authors":"Qinuo Lin, Fangtian Wu, Lanlin Zhang, Yao Zhang, Si Sun, Xianghua Wu, Hui Yu","doi":"10.3724/abbs.2026013","DOIUrl":"https://doi.org/10.3724/abbs.2026013","url":null,"abstract":"<p><p>Immunotherapy represents a pivotal advancement in lung cancer treatment. However, its efficacy remains limited, necessitating a deeper understanding of intrinsic tumor cell mechanisms that modulate the immune microenvironment. Here, we investigate how EZH2 inhibition alters chemokine secretion and antigen presentation in lung adenocarcinoma (LUAD). TCGA and GEO analyses show significant overexpression of <i>EZH2</i> in LUAD, which correlates with poorer survival. Immune cell infiltration using MCP-Counter demonstrates that EZH2 expression inversely correlates with CD8 ⁺ T cell and dendritic cell (DC) infiltration. Spatial analysis of early lung cancer samples reveals an inverse EZH2-CCL5 correlation, suggesting that EZH2 promotes progression via CCL5 suppression. <i>In vitro</i> assays included CCK-8 proliferation assays following EZH2 inhibition, qRT-PCR and ELISA to quantify CCL5 expression and secretion, transwell migration assays to assess CD8 ⁺ T-cell chemotaxis, and co-culture cytotoxicity assays to evaluate MHC class I-dependent T-cell killing. Inhibition of EZH2 markedly reduces tumor cell proliferation, increases CCL5 expression and secretion, enhances CD8 ⁺ T-cell migration, and promotes MHC class I expression and T-cell-mediated cytotoxicity without altering PD-L1 levels. In conclusion, <i>EZH2</i> overexpression promotes immune evasion in LUAD by suppressing CCL5-mediated T-cell recruitment and MHC class I antigen presentation. Targeting EZH2 augments antitumor immunity, supporting its therapeutic potential in combination immunotherapy strategies.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343234","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}

{"title":"Transcriptional regulation of GPSM2 by ZNF263 in colorectal cancer: implications for tumor aggressiveness.","authors":"Youquan Shi, Shantanu Baral, Youlei Zhang, Yongjun Jiang, Ruiqi Li, Yue Zhang, Wei Wang, Daorong Wang","doi":"10.3724/abbs.2025181","DOIUrl":"https://doi.org/10.3724/abbs.2025181","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most prevalent and lethal cancers worldwide and is characterized by uncontrolled cell invasion, migration, and proliferation. The progression of CRC is driven by genetic mutations and alterations in key signaling pathways. This study investigates the role of <i>GPSM2</i> and <i>ZNF263</i> implicated in CRC progression. The <i>GPSM2</i> gene, which regulates G protein signaling pathways, plays a vital role in cell movement and growth, contributing to the metastatic potential of cancer cells. The <i>ZNF263</i> gene, a zinc finger protein involved in gene expression regulation, is also linked to CRC progression, with its dysregulation affecting the cell cycle, apoptosis, and migration. In particular, this study explores how ZNF263 acts as a transcription factor, modulating the expression of GPSM2 to increase CRC cell invasion, migration, and proliferation. This study confirms that ZNF263 activates the cell cycle pathway in a GPSM2-dependent manner, driving the aggressive behavior of CRC cells. Bioinformatics analysis using the GEO database further supports these findings, identifying key genetic alterations in CRC. These insights provide a deeper understanding of the molecular mechanisms underlying CRC progression and highlight the potential of ZNF263 and GPSM2 as therapeutic targets for intervention. This study underscores the importance of early detection and exploration of targeted therapies to improve CRC patient outcomes.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343185","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}

{"title":"A flavonoid-rich medicinal herb extract ameliorates high-fat diet-induced obesity and insulin resistance in mice.","authors":"Mengyu Li, Haiying Zong, Xiaoqin Yang, Qingqing Liu, Junjie Wang, Menglei Wang, Dengfang Wu, Shujie Zheng, Han Wang, Qiaoming Long","doi":"10.3724/abbs.2026007","DOIUrl":"https://doi.org/10.3724/abbs.2026007","url":null,"abstract":"<p><p>Obesity has emerged as a critical global health challenge, contributing to severe metabolic and neoplastic complications. However, most existing anti-obesity drugs exhibit significant adverse effects, necessitating the development of safer therapeutic alternatives. In this study, we evaluate the efficacy and safety of a flavonoid-rich medicinal herb extract (MHE) in a high-fat diet (HFD)-induced murine obesity model. Daily oral administration of MHE does not alter food intake or induce hepatic injury but significantly attenuates HFD-induced weight gain ( <i>P</i> < 0.05) and adiposity accumulation. Furthermore, MHE treatment improves systemic insulin sensitivity and glycemic control. Notably, MHE enhances whole-body energy expenditure, as evidenced by elevated oxygen consumption (VO ₂), carbon dioxide production (VCO ₂), and heat generation ( <i>P</i> < 0.01). Mechanistically, MHE selectively promotes the proliferation of beneficial gut microbiota, including <i>Lactobacillus</i>, <i>Akkermansia</i>, and <i>Bifidobacterium</i> species, resulting in increased production of the short-chain fatty acid propionate (PA). Elevated circulating PA levels subsequently stimulate the browning/beiging of inguinal white adipose tissue (iWAT) and upregulate thermogenic pathways. Collectively, our findings demonstrate that MHE exerts anti-obesity effects through gut microbiota modulation and adipose tissue remodeling, offering a promising natural alternative for obesity management.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343211","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}

{"title":"The EBV-MS paradigm: beyond molecular mimicry toward new therapeutic strategies.","authors":"Huating Xie, Weidong Huang, Weikun Li, Shiying Lai, Zhiqun Lin, Rongqing Zhong, Wen Wang, Xu Lin, Zhaowei Xu","doi":"10.3724/abbs.2026026","DOIUrl":"https://doi.org/10.3724/abbs.2026026","url":null,"abstract":"<p><p>Epstein-Barr virus (EBV) is now recognized as the definitive environmental driver of multiple sclerosis (MS), shifting the conceptual landscape of this autoimmune disorder to an infection-triggered model. In this review, we systematically evaluate the multidimensional evidence linking EBV to MS. This evidence ranges from epidemiological associations and the identification of mimotopes to emerging therapeutic strategies. We also discuss the broader implications of infection-driven immune dysregulation for autoimmune research. This pathogenic link is underpinned by molecular mimicry, where immune responses against the viral protein EBNA1 cross-react with the central nervous system (CNS) protein GlialCAM. Beyond this initial insult, EBV reprograms B cells to survive and proliferate abnormally, creating a compartmentalized viral reservoir within the CNS that sustains chronic neuroinflammation. These mechanistic insights catalyze a transition from broad immunosuppression to precision therapies targeting the EBV-MS axis, including CNS-penetrant kinase inhibitors and EBV-specific CAR-T cells. By integrating etiological discovery with mechanism-based intervention, the EBV-MS paradigm serves as a blueprint for transforming idiopathic autoimmune diseases into mechanistically tractable conditions with actionable therapeutic targets.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343200","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}

{"title":"Luteolin reprograms macrophage polarization via the STING-TBK1 pathway to accelerate bone repair.","authors":"Dinglei Zhang, Yilun Wang, Lili Luo, Huihui Bian, Zhimin Gao, Yinghua Li, Tianlong Zhang, Li Su, Hongli Liao, Ying Liu, Yi Liang","doi":"10.3724/abbs.2026021","DOIUrl":"https://doi.org/10.3724/abbs.2026021","url":null,"abstract":"<p><p>Macrophages play a pivotal role in bone regeneration, making their polarization a key target for immune regulation and therapeutic intervention. Modulating macrophage polarization represents a promising strategy for enhancing bone repair. Luteolin, a plant-derived flavonoid with well-documented anti-inflammatory properties, has been explored for its role in bone repair. However, its specific effects on macrophage polarization in bone repair remain unclear. This study investigates the role of luteolin in macrophage polarization and its underlying mechanisms. Our findings demonstrate that luteolin promotes M2 polarization while suppressing M1 polarization, as indicated by a reduction in the expression of pro-inflammatory markers, including IL-6 and iNOS, and an increase in the expression of anti-inflammatory factors, such as CD206, IL-10, and TGF-β. Mechanistically, luteolin inhibits STING oligomerization, thereby suppressing the STING-TBK1 pathway and mitigating downstream inflammatory responses. <i>In vivo</i>, in a mouse tibial bone defect model, luteolin effectively alleviates inflammation, facilitates angiogenesis, enhances collagen deposition, and improves bone density. Collectively, these findings highlight the potential of luteolin as a therapeutic agent for bone repair by modulating macrophage polarization and inhibiting STING-TBK1 signaling.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147353339","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}

{"title":"Sanguinarine exerts anti-hepatocellular carcinoma activity by targeting FDX1 to induce FDX1/LIAS/DLAT/HSP70 axis-dependent cuproptosis.","authors":"Xiaoyan Hao, Yiqiao Qiu, Ling Li, Siqi Chen, Yuxuan Gao, Ketao Ma, Lili Wei, Qiang Zhang, Liang Zhang","doi":"10.3724/abbs.2026025","DOIUrl":"https://doi.org/10.3724/abbs.2026025","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC), the predominant type of primary liver cancer, represents an extremely aggressive malignancy. The induction of cuproptosis has developed into a favorable therapeutic direction for HCC, considering its strong association with HCC. Sanguinarine (San), a benzophenanthridine alkaloid derived from traditional herbs such as <i>Chelidonium majus</i> L., demonstrates broad-spectrum anticancer activities against various cancer cell types. However, the precise molecular mechanisms underlying its effects in the treatment of HCC remain largely undefined. This investigation seeks to examine the anti-HCC effects of San and to explore the mechanisms underlying these effects through the induction of cuproptosis. <i>In vitro</i> experiments demonstrate that San markedly inhibits the proliferation, movement, and epithelial-mesenchymal transition of HCC cells while enhancing their apoptosis. <i>In vivo</i>, San notably impedes tumor growth and upregulates the cuproptosis signature markers ferredoxin 1 (FDX1), oligomeric dihydrolipoamide S-acetyltransferase (DLAT), and heat shock protein 70 (HSP70) in HCC xenograft tumor models. Mechanistically, San induces proteotoxic stress and cuproptosis in HCC cells by increasing copper concentration, upregulating the expression of FDX1, lipoic acid synthetase (LIAS), HSP70, and lipoylated DLAT aggregation, and simultaneously reducing mitochondrial membrane potential and intracellular glutathione and pyruvate levels. Moreover, the combination of San with copper ionophores (Elesclomol-CuCl ₂) exhibits synergistic effects in promoting cuproptosis. <i>FDX1</i> silencing markedly diminishes San-induced suppression of cell proliferation and FDX1 and HSP70 levels in HCC cells. Additionally, molecular docking analysis predicts that San exhibits the highest potential for binding with FDX1. Surface plasmon resonance experiments and cellular thermal shift assay confirm that San strongly interacts with FDX1 and markedly enhances the thermostability of FDX1. In conclusion, our findings indicate that San substantially inhibits the progression of HCC by targeting FDX1/LIAS/DLAT/HSP70 axis-dependent cuproptosis.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321160","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}

{"title":"Tolerogenic dendritic cells induced by withdrawal of polyunsaturated fatty acid DHA and mTOR inhibitor PP242 attenuate allograft rejection.","authors":"Ning Wang, Hong Tang, Zhonghan Wu, Haiyang Xie, Hai Zhu, Danjing Guo, Yangwei Xiang, Zhi Liang, Ruiqi Sun, Shusen Zheng, Weili Han, Ke Zhou","doi":"10.3724/abbs.2025214","DOIUrl":"https://doi.org/10.3724/abbs.2025214","url":null,"abstract":"<p><p>Dendritic cells (DCs) exhibit the capacity to elicit either immune activation or tolerance, contingent upon diverse induction conditions. However, the crucial factors governing the induction of tolerogenic dendritic cells (Tol-DCs) remain obscure. Our study demonstrates that the combined use of docosahexaenoic acid (DHA) and the mammalian target of rapamycin inhibitor PP242 (comb-DHA) markedly hinders DC maturation while maintaining DC phagocytic capabilities in an immature state, thereby enabling substantial and sustained DHA accumulation within cells. Upon withdrawal of exogenous drug intervention, we observe that the retained DHA within the DCs facilitates delayed activation of p-AKT ^Ser473 and PTDSS2-related pathways, ultimately leading to the induction of a novel type of Tol-DC, comb-DHA-DC. These Tol-DCs display significantly reduced expression of costimulatory molecules and possess the ability to profoundly inhibit T-cell proliferation. Adoptive transfer of comb-DHA-DCs suppresses allograft rejection reactions. In summary, our findings reveal a novel strategy for inducing Tol-DCs and present a promising therapeutic avenue for enhancing graft tolerance.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147300797","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}

{"title":"Pearl peptides ( <i>Hyriopsis Cumingii</i>) as tyrosinase inhibitors: identification, characterization, inhibitory activity, conformational change and mechanism.","authors":"Jingying Pei, Yufei Wang, Hao Yan, Juan Sun, Peilong Sun, Yan Wang","doi":"10.3724/abbs.2025226","DOIUrl":"https://doi.org/10.3724/abbs.2025226","url":null,"abstract":"<p><p>Pearl protein extracted from freshwater mussels has been shown to inhibit tyrosinase activity. However, the unclear inhibitory mechanism and associated conformational changes limit their practical applications. In this study, peptides from the crude extract of pearl powder are analyzed via liquid chromatography-tandem mass spectrometry (LC-MS/MS). These peptides are subsequently assessed for their tyrosinase inhibitory potential via molecular docking techniques. Notably, experiments reveal that a small-molecule peptide effectively prevents the interaction between 3,4-dihydroxyphenylalanine (L-DOPA) and tyrosinase, impeding the formation of dopaquinone. The peptide GLGGGLAGAGGADGA (95P, 1099.54 Da) shows particular promise, with synthesized 95P inhibiting both the monophenolase and diphenolase activities of tyrosinase, with IC ₅₀ values of 30.97 ± 0.75 μM and 64.62 ± 3.08 μM,respectively. 95P inhibits tyrosinase activity in a mixed competitive and reversible manner. Molecular dynamics simulations suggest that 95P stabilizes 5M8N, impeding structural contraction identified by model number 5M8N. In conclusion, 95P is a powerful and stable tyrosinase inhibitor with the potential to be used as a skin whitening agent in the pharmaceutical field and an anti-browning agent in the food industry.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147300849","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}