Acta biochimica et biophysica Sinica最新文献_第4页

Predictive value of LCP1 and ADPGK for immune-related adverse events across multiple cancer types in patients receiving immunotherapy-based regimens. LCP1和ADPGK对接受免疫治疗方案的多种癌症类型患者免疫相关不良事件的预测价值。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2026016

Xi Zhang, Yaqian Li, Li Zhang, Hongyu Liu, Wei Sun, Junhua Li, Dan Xue, Fan Zhang, Yuting Bai, Jing Zhang, Xing Gou, Dongzi Pang, Xueqin Zeng, Shuqing Wei

引用次数: 0

RNA cytidine acetylation in archaea. 古细菌中RNA胞苷乙酰化。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2026135

Jin-Tao Wang, Xiao-Long Zhou

引用次数: 0

Sti1 participates in the dynamics of protein aggregation triggered by glucose signaling in Saccharomyces cerevisiae. 在酿酒酵母中，Sti1参与葡萄糖信号触发的蛋白质聚集动力学。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2026071

Jiawei Chen, Jiayu Zhou, Keren Sun, Hanlin Zhang, Yanqiu Ji, Letong Li, Wanjie Li, Fei Dou

引用次数: 0

S-palmitoylation stabilizes OGT and the OGT-PPP1CC complex. s -棕榈酰化稳定OGT和OGT- ppp1cc复合物。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-24 DOI: 10.3724/abbs.2026173

Xiaoxuan Lu, Ting Xu, Jie Li, Yihan Liu, Wen Zhou, Kai Wang, Chang Niu, Ni Tang, Leiliang Zhang, Jing Li

{"title":"S-palmitoylation stabilizes OGT and the OGT-PPP1CC complex.","authors":"Xiaoxuan Lu, Ting Xu, Jie Li, Yihan Liu, Wen Zhou, Kai Wang, Chang Niu, Ni Tang, Leiliang Zhang, Jing Li","doi":"10.3724/abbs.2026173","DOIUrl":"https://doi.org/10.3724/abbs.2026173","url":null,"abstract":"O-linked β- N-acetylglucosamine ( O-GlcNAc) transferase (OGT) is the sole writer for intracellular O-GlcNAcyl7ation. It catalyzes the O-GlcNAcylation of thousands of protein substrates, but relatively little is known about the post-translational modifications that occur on OGT itself. Herein, we demonstrate that OGT is S-palmitoylated at Cys-472 and Cys-477, which is mediated by the S-acyltransferase zinc finger DHHC-type palmitoyl transferase 14 (zDHHC14) and removed by acyl protein thioesterase 2 (APT2). S-palmitoylation stabilizes OGT by shunting it away from the lysosomal chaperone-mediated autophagy (CMA) pathway, as S-palmitoylation decreases the interaction between OGT and heat shock cognate 70 kDa protein (HSC70), the CMA chaperone. Using label-free quantitative mass spectrometry, we find that S-palmitoylation increases the affinity between OGT and protein phosphatase 1 catalytic subunit gamma (PPP1CC) but not protein phosphatase 1 catalytic subunit beta (PPP1CB). We further demonstrate that S-palmitoylation of OGT augments binding to Yes-associated protein-1 (YAP), a protein that associates with PPP1CC, and subsequently enhances YAP O-GlcNAcylation. Our work uncovers S-palmitoylation of OGT and CMA-mediated degradation of lysosomal OGT, which together fine-tune the activity of key OGT complexes, such as OGT-PPP1CC, and contribute to OGT substrate selectivity.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149035819","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

Midazolam suppresses glioma progression by attenuating neuronal activity and downregulating IGF1 signaling. 咪达唑仑通过减弱神经元活性和下调IGF1信号传导抑制胶质瘤进展。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-22 DOI: 10.3724/abbs.2026109

Zhihui Qi, Zhiming Ye, Kahei Chan, Yumin Wu, Yu Yu, Yang Hu, Yi Lu, Jiaoyan Ren, Maojin Yao, Zhongxing Wang

{"title":"Midazolam suppresses glioma progression by attenuating neuronal activity and downregulating IGF1 signaling.","authors":"Zhihui Qi, Zhiming Ye, Kahei Chan, Yumin Wu, Yu Yu, Yang Hu, Yi Lu, Jiaoyan Ren, Maojin Yao, Zhongxing Wang","doi":"10.3724/abbs.2026109","DOIUrl":"https://doi.org/10.3724/abbs.2026109","url":null,"abstract":"Glioma is the most common primary malignant tumor of the brain, and accumulating evidence indicates that neuronal activity plays a pivotal role in tumor progression. In this study, neuronal activity was modulated in vitro through potassium chloride (KCl)-induced depolarization and midazolam (MDZ)-mediated suppression. MDZ is a neuronal activity modulation medication that is commonly used for sedation, anxiolysis, and amnesia in the clinic. After treatment, conditioned media derived from these neuronal cultures are subsequently co-cultured with glioma cells. EdU incorporation assays demonstrate that MDZ significantly inhibits glioma cell proliferation in vitro. Furthermore, an orthotopic xenograft glioma model is established to assess the anti-tumor efficacy of MDZ in vivo, as evaluated by tumor volume and Ki-67 immunostaining. Mechanistically, insulin-like growth factor 1 (IGF1) is identified as the neuronal-activity-regulated factor that promotes glioma growth through activation of the PI3K/AKT signaling pathway. Moreover, transcriptomic profiling of brain tissues reveals that MDZ attenuates neuronal activity and downregulates neuron-derived growth factors in both glioma and non-tumor regions, thereby exerting anti-tumor effects in vivo. Collectively, these findings demonstrate that MDZ suppresses glioma progression by suppressing neuronal activity and inhibiting neuron-derived trophic factors, providing new insights into the development of therapeutic strategies for glioma.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029391","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

Integrative analysis of the CLE gene family identifies GhTDIF and GhCLE14 as key regulators of cotton fiber secondary cell wall thickening. CLE基因家族的整合分析发现GhTDIF和GhCLE14是棉纤维次级细胞壁增厚的关键调控因子。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-18 DOI: 10.3724/abbs.2026143

Yanan Gao, Jinglong Cai, Xiangyang Sun, Youzhong Li, Wenliang Xu

{"title":"Integrative analysis of the CLE gene family identifies GhTDIF and GhCLE14 as key regulators of cotton fiber secondary cell wall thickening.","authors":"Yanan Gao, Jinglong Cai, Xiangyang Sun, Youzhong Li, Wenliang Xu","doi":"10.3724/abbs.2026143","DOIUrl":"https://doi.org/10.3724/abbs.2026143","url":null,"abstract":"Clavata3/embryo surrounding region-related (CLE) signaling peptides constitute a family of small peptides that play pivotal roles in plant growth and development as well as in responses to environmental cues, serving as key regulators of cell proliferation and differentiation across diverse plants. In this study, we conduct a genome-wide characterization of CLE genes in Gossypium hirsutum and identify two CLE genes highly expressed during the cotton fiber secondary wall thickening stage: GhTDIF and GhCLE14. Silencing of the GhCLE genes results in abnormal leaf morphology. Histological sectioning reveals a significant reduction in xylem cell number within leaf veins. Furthermore, mature fibers from silenced lines exhibit shortened length, reduced fiber twists, thinner cell walls, and decreased crystalline cellulose content. The expression of secondary cell wall (SCW) cellulose synthase genes ( GhCesAs) and the SCW biosynthesis-associated transcription factor GhMYB46_D13 is significantly downregulated in the silenced lines. Collectively, our findings demonstrate that GhCLE peptides play critical regulatory roles during cotton fiber development. This work not only expands the transcriptional regulatory network underlying CLE-mediated control of cotton fiber SCW biosynthesis but also provides a theoretical basis for the potential application of exogenous CLE peptides to improve fiber quality.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001076","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

Celastrol alleviates SGLT2 inhibitor-induced diabetic hyperketonemia by inhibiting hepatic ketogenesis. Celastrol通过抑制肝脏生酮来减轻SGLT2抑制剂诱导的糖尿病高酮血症。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-15 DOI: 10.3724/abbs.2026117

Yinghan Zhu, Yiting Wang, Minglong Zhang, Lingxu Liu, Yang Tian, Zeyu Guo, Ran Zhang, Jinrui Zhang, Zhenyu Ma, Fude Fang, Li Yan, Xiaojun Liu

{"title":"Celastrol alleviates SGLT2 inhibitor-induced diabetic hyperketonemia by inhibiting hepatic ketogenesis.","authors":"Yinghan Zhu, Yiting Wang, Minglong Zhang, Lingxu Liu, Yang Tian, Zeyu Guo, Ran Zhang, Jinrui Zhang, Zhenyu Ma, Fude Fang, Li Yan, Xiaojun Liu","doi":"10.3724/abbs.2026117","DOIUrl":"https://doi.org/10.3724/abbs.2026117","url":null,"abstract":"SGLT2 inhibitor (SGLT2i)-induced diabetic hyperketonemia is a life-threatening acute complication of diabetes. While celastrol has been reported to have beneficial effects on obesity, its potential role in ketogenesis remains unclear. In this study, celastrol administration significantly attenuates the fasting-induced increase in blood β-hydroxybutyrate levels. Moreover, a 7-day course of celastrol (1 mg/kg/day) leads to reductions in body weight and fat mass. Mechanistically, celastrol specifically downregulates HMGCS2 expression and suppresses hepatic ketogenesis through the inhibition of PPARα expression in the short term (≤ 2 days). However, after prolonged treatment for 7 days, celastrol modulates both PPARα and serum free fatty acid (FFA) levels. Furthermore, the anti-ketogenic effect of celastrol is abolished in Pparα -/- mice. Importantly, celastrol effectively ameliorates SGLT2i-induced hyperketonemia. In summary, celastrol curbs hepatic ketone overproduction in a PPARα-dependent manner, indicating its protective potential against SGLT2i-induced hyperketonemia.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975196","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

Retraction to: Single-cell dissection of avian (chicken) H1N1 influenza virus coinfection dynamics in mammalian (mouse) and avian (chicken) hosts. 撤回到：禽（鸡）H1N1流感病毒在哺乳动物（小鼠）和禽（鸡）宿主中共感染动力学的单细胞解剖。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-15 DOI: 10.3724/abbs.2026153

Yuelong Zhou, Xueyu Zhang, Fei Chen, Weidong Deng, Pu Wang

引用次数: 0

piR-45962 exacerbates autophagic apoptosis in aged myocardial ischemia-reperfusion injury through modulation of the HNRNPH1/GATA5 signaling axis. piR-45962通过调节HNRNPH1/GATA5信号轴加重老年心肌缺血再灌注损伤的自噬凋亡。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-14 DOI: 10.3724/abbs.2026160

Qianqian Wu, Xinru Li, Yuwei An, Chen Wang, Ben Ma, Min Su, Xin Yu, Xiangyu Zhao, Jingwei Ma, Yideng Jiang, Yajuan Fu, Yuee Chai, Yuankui Chu, Shengchao Ma

{"title":"piR-45962 exacerbates autophagic apoptosis in aged myocardial ischemia-reperfusion injury through modulation of the HNRNPH1/GATA5 signaling axis.","authors":"Qianqian Wu, Xinru Li, Yuwei An, Chen Wang, Ben Ma, Min Su, Xin Yu, Xiangyu Zhao, Jingwei Ma, Yideng Jiang, Yajuan Fu, Yuee Chai, Yuankui Chu, Shengchao Ma","doi":"10.3724/abbs.2026160","DOIUrl":"https://doi.org/10.3724/abbs.2026160","url":null,"abstract":"Myocardial ischemia-reperfusion (I/R) injury is a significant contributor to poor prognosis after myocardial infarction, and the degree of irreversible myocardial damage is closely related to age. In I/R injury, ischemic and hypoxic stress triggers the coordinated activation of apoptosis and autophagy in cardiomyocytes. Although Piwi-interacting RNAs (piRNAs) have been implicated in the regulation of both apoptosis and autophagy, their specific roles and particularly their functional integration in governing this dual cell death response during I/R injury remain poorly understood. Using left anterior descending coronary artery ligation in an aging rat model and a D-galactose-induced rat cardiomyocyte line to construct an aging cardiomyocyte model, we investigate the cell apoptosis and autophagy following reperfusion injury both in vitro and in vivo. The present study focuses on the upregulation of piR-45962 in reperfusion injury in vitro and in vivo, and the indicators of apoptosis and autophagy are significantly different. Mechanistic research of piR-45962 shows that heterogeneous nuclear ribonucleoprotein 1 (HNRNPH1) is a target protein for piR-45962, and as an RNA-binding protein implicated in apoptotic regulation, HNRNPH1 could interact with GATA binding protein 5 (GATA5) to exacerbate autophagic apoptosis. Together, our results reveal the mechanism by which piR-45962 downregulates GATA5 expression through upregulation of HNRNPH1, thereby establishing a novel piR-45962-HNRNPH1-GATA5 regulatory axis that contributes to aged myocardial injury during I/R.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966034","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

Exosomal miR-484 impairs CD8 ⁺ T cell homeostasis in sepsis through the YPEL1/Cyclin E axis. 外泌体miR-484通过YPEL1/Cyclin E轴损害脓毒症中的CD8 + T细胞稳态。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-11 DOI: 10.3724/abbs.2026107

Jiaqian Ling, Zhouyi Chen, Yile Zhou, Guangshan Jin, Yuanyang Chen, Jianxin Dong, Xia Sun, Yi Shi, Hao Fang

{"title":"Exosomal miR-484 impairs CD8 + T cell homeostasis in sepsis through the YPEL1/Cyclin E axis.","authors":"Jiaqian Ling, Zhouyi Chen, Yile Zhou, Guangshan Jin, Yuanyang Chen, Jianxin Dong, Xia Sun, Yi Shi, Hao Fang","doi":"10.3724/abbs.2026107","DOIUrl":"https://doi.org/10.3724/abbs.2026107","url":null,"abstract":"Sepsis induces profound CD8 + T cell dysfunction, contributing to immunosuppression and poor outcomes. Exosomes mediate intercellular communication during sepsis, but the role of exosomal microRNAs in regulating CD8 + T cell homeostasis remains unclear. Sepsis patients and healthy controls are prospectively enrolled to investigate plasma exosomes and CD8 + T cell responses. Exosomes from sepsis patients (SE) promote CD8 + effector differentiation and dysregulate cell cycle progression compared to those from healthy donors (HE). miRNA sequencing identifies miR-484 as the most upregulated miRNA in SE. Functionally, SE-derived miR-484 suppresses YPEL1 expression in CD8 + T cells, leading to increased Cyclin E levels and aberrant cell cycle distribution. Inhibition of miR-484 restores YPEL1 and normalizes Cyclin E expression, which is associated with a reversal of the sepsis exosome-induced bias toward CD8 + effector differentiation. Our findings reveal that exosomal miR-484 impairs CD8 + T cell homeostasis in sepsis by targeting the YPEL1/Cyclin E pathway, highlighting a potential mechanism for immune dysregulation and a target for intervention.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148943919","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