Acta biochimica et biophysica Sinica最新文献_第9页

Glycosylation in aging and neurodegenerative diseases. 衰老和神经退行性疾病中的糖基化。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-08-15 DOI: 10.3724/abbs.2024136

Weilong Zhang, Tian Chen, Huijuan Zhao, Shifang Ren

{"title":"Glycosylation in aging and neurodegenerative diseases.","authors":"Weilong Zhang, Tian Chen, Huijuan Zhao, Shifang Ren","doi":"10.3724/abbs.2024136","DOIUrl":"10.3724/abbs.2024136","url":null,"abstract":"Aging, a complex biological process, involves the progressive decline of physiological functions across various systems, leading to increased susceptibility to neurodegenerative diseases. In society, demographic aging imposes significant economic and social burdens due to these conditions. This review specifically examines the association of protein glycosylation with aging and neurodegenerative diseases. Glycosylation, a critical post-translational modification, influences numerous aspects of protein function that are pivotal in aging and the pathophysiology of diseases such as Alzheimer's disease, Parkinson's disease, and other neurodegenerative conditions. We highlight the alterations in glycosylation patterns observed during aging, their implications in the onset and progression of neurodegenerative diseases, and the potential of glycosylation profiles as biomarkers for early detection, prognosis, and monitoring of these age-associated conditions, and delve into the mechanisms of glycosylation. Furthermore, this review explores their role in regulating protein function and mediating critical biological interactions in these diseases. By examining the changes in glycosylation profiles associated with each part, this review underscores the potential of glycosylation research as a tool to enhance our understanding of aging and its related diseases.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":"56 8","pages":"1208-1220"},"PeriodicalIF":3.3,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11466714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118673","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

Immunoglobulin G glycosylation and its alterations in aging-related diseases. 免疫球蛋白 G 糖基化及其在衰老相关疾病中的改变

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-08-08 DOI: 10.3724/abbs.2024137

Yongqi Wu, Zhida Zhang, Lin Chen, Shisheng Sun

{"title":"Immunoglobulin G glycosylation and its alterations in aging-related diseases.","authors":"Yongqi Wu, Zhida Zhang, Lin Chen, Shisheng Sun","doi":"10.3724/abbs.2024137","DOIUrl":"10.3724/abbs.2024137","url":null,"abstract":"Immunoglobulin G (IgG) is an important serum glycoprotein and a major component of antibodies. Glycans on IgG affect the binding of IgG to the Fc receptor or complement C1q, which in turn affects the biological activity and biological function of IgG. Altered glycosylation patterns on IgG emerge as important biomarkers in the aging process and age-related diseases. Key aging-related alterations observed in IgG glycosylation include reductions in galactosylation and sialylation, alongside increases in agalactosylation, and bisecting GlcNAc. Understanding the role of IgG glycosylation in aging-related diseases offers insights into disease mechanisms and provides opportunities for the development of diagnostic and therapeutic strategies. This review summarizes five aspects of IgG: an overview of IgG, IgG glycosylation, IgG glycosylation with inflammation mediation, IgG glycan changes with normal aging, as well as the relevance of IgG glycan changes to aging-related diseases. This review provides a reference for further investigation of the regulatory mechanisms of IgG glycosylation in aging-related diseases, as well as for evaluating the potential of IgG glycosylation changes as markers of aging and aging-related diseases.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"1221-1233"},"PeriodicalIF":3.3,"publicationDate":"2024-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11399422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141911326","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

Evolutionary analysis of paired box gene family and biological function exploration of Lr. Pax7 in lamprey ( Lethenteron reissneri). 配对盒基因家族的进化分析及Lr.Pax7的生物学功能探索灯鱼（Lethenteron reissneri）中的 Pax7。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-08-05 DOI: 10.3724/abbs.2024121

Ayqeqan Nurmamat, Zihao Yan, Yao Jiang, Haoran Guan, Ruyu Zhuang, Shuyuan Zhang, Yuesi Zhou, Min Xiu, Ya Pang, Ding Li, Liang Zhao, Xin Liu, Yinglun Han

引用次数: 0

lncRNA CYTOR promotes lung adenocarcinoma gemcitabine resistance and epithelial-mesenchymal transition by sponging miR-125a-5p and upregulating ANLN and RRM2. lncRNA CYTOR通过疏导miR-125a-5p并上调ANLN和RRM2，促进肺腺癌吉西他滨耐药和上皮-间质转化。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-08-05 DOI: 10.3724/abbs.2024113

Qijun Cao, Haixia Wang, Jialong Zhu, Chen Qi, Hairong Huang, Xiaoyuan Chu

引用次数: 0

Structural basis for the inhibition of coronaviral main proteases by PF-00835231. PF-00835231 抑制冠状病毒主要蛋白酶的结构基础

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-07-29 DOI: 10.3724/abbs.2024122

Xuelan Zhou, Xiaolu Lu, Cheng Lin, Xiaofang Zou, Wenwen Li, Xiangyi Zeng, Jie Wang, Pei Zeng, Weiwei Wang, Jin Zhang, Haihai Jiang, Jian Li

{"title":"Structural basis for the inhibition of coronaviral main proteases by PF-00835231.","authors":"Xuelan Zhou, Xiaolu Lu, Cheng Lin, Xiaofang Zou, Wenwen Li, Xiangyi Zeng, Jie Wang, Pei Zeng, Weiwei Wang, Jin Zhang, Haihai Jiang, Jian Li","doi":"10.3724/abbs.2024122","DOIUrl":"10.3724/abbs.2024122","url":null,"abstract":"The main protease (M pro) of coronaviruses plays a key role in viral replication, thus serving as a hot target for drug design. PF-00835231 is a promising inhibitor of SARS-CoV-2 M pro. Here, we report the inhibitory potency of PF-00835231 against SARS-CoV-2 M pro and seven M pro mutants (G15S, M49I, Y54C, K90R, P132H, S46F, and V186F) from SARS-CoV-2 variants. The results confirm that PF-00835231 has broad-spectrum inhibition against various coronaviral M pros. In addition, the crystal structures of SARS-CoV-2 M pro, SARS-CoV M pro, MERS-CoV M pro, and seven SARS-CoV-2 M pro mutants (G15S, M49I, Y54C, K90R, P132H, S46F, and V186F) in complex with PF-00835231 are solved. A detailed analysis of these structures reveals key determinants essential for inhibition and elucidates the binding modes of different coronaviral M pros. Given the importance of the main protease for the treatment of coronaviral infection, structural insights into M pro inhibition by PF-00835231 can accelerate the design of novel antivirals with broad-spectrum efficacy against different human coronaviruses.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"1813-1822"},"PeriodicalIF":3.3,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11693862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141791631","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

O-glycosylation of SARS-CoV-2 spike protein by host O-glycosyltransferase strengthens its trimeric structure. 宿主O-糖基转移酶对SARS-CoV-2尖峰蛋白的O-糖基化加强了其三聚体结构。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-07-26 DOI: 10.3724/abbs.2024127

Zhijue Xu, Han Zhang, Jiaqi Tian, Xin Ku, Rumeng Wei, Jingli Hou, Can Zhang, Fang Yang, Xia Zou, Yang Li, Hiroyuki Kaji, Sheng-Ce Tao, Atsushi Kuno, Wei Yan, Lin-Tai Da, Yan Zhang

{"title":"O-glycosylation of SARS-CoV-2 spike protein by host O-glycosyltransferase strengthens its trimeric structure.","authors":"Zhijue Xu, Han Zhang, Jiaqi Tian, Xin Ku, Rumeng Wei, Jingli Hou, Can Zhang, Fang Yang, Xia Zou, Yang Li, Hiroyuki Kaji, Sheng-Ce Tao, Atsushi Kuno, Wei Yan, Lin-Tai Da, Yan Zhang","doi":"10.3724/abbs.2024127","DOIUrl":"10.3724/abbs.2024127","url":null,"abstract":"Protein O-glycosylation, also known as mucin-type O-glycosylation, is one of the most abundant glycosylation in mammalian cells. It is initially catalyzed by a family of polypeptide GalNAc transferases (ppGalNAc-Ts). The trimeric spike protein (S) of SARS-CoV-2 is highly glycosylated and facilitates the virus's entry into host cells and membrane fusion of the virus. However, the functions and relationship between host ppGalNAc-Ts and O-glycosylation on the S protein remain unclear. Herein, we identify 15 O-glycosites and 10 distinct O-glycan structures on the S protein using an HCD-product-dependent triggered ETD mass spectrometric analysis. We observe that the isoenzyme T6 of ppGalNAc-Ts (ppGalNAc-T6) exhibits high O-glycosylation activity for the S protein, as demonstrated by an on-chip catalytic assay. Overexpression of ppGalNAc-T6 in HEK293 cells significantly enhances the O-glycosylation level of the S protein, not only by adding new O-glycosites but also by increasing O-glycan heterogeneity. Molecular dynamics simulations reveal that O-glycosylation on the protomer-interface regions, modified by ppGalNAc-T6, potentially stabilizes the trimeric S protein structure by establishing hydrogen bonds and non-polar interactions between adjacent protomers. Furthermore, mutation frequency analysis indicates that most O-glycosites of the S protein are conserved during the evolution of SARS-CoV-2 variants. Taken together, our finding demonstrate that host O-glycosyltransferases dynamically regulate the O-glycosylation of the S protein, which may influence the trimeric structural stability of the protein. This work provides structural insights into the functional role of specific host O-glycosyltransferases in regulating the O-glycosylation of viral envelope proteins.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"1118-1129"},"PeriodicalIF":3.3,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11399440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141764810","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

Hedy: a groundbreaking revelation of cartilage oxygen homeostasis. Hedy：软骨氧平衡的突破性发现。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-07-22 DOI: 10.3724/abbs.2024116

Haoliang Hu, Labapuchi Labapuchi, Kerui Huang, Yanling Long, Linxi Chen

引用次数: 0

ZIPK collaborates with STAT5A in p53-mediated ROS accumulation in hyperglycemia-induced vascular injury. ZIPK 与 STAT5A 合作，在高血糖诱导的血管损伤中参与 p53 介导的 ROS 积累。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-07-19 DOI: 10.3724/abbs.2024120

Qichao Wu, Tingting Xie, Chang Fu, Chenyu Sun, Yan Ma, Zhengzhe Huang, Jiao Yang, Xiaoxiao Li, Wenqian Li, Changhong Miao

{"title":"ZIPK collaborates with STAT5A in p53-mediated ROS accumulation in hyperglycemia-induced vascular injury.","authors":"Qichao Wu, Tingting Xie, Chang Fu, Chenyu Sun, Yan Ma, Zhengzhe Huang, Jiao Yang, Xiaoxiao Li, Wenqian Li, Changhong Miao","doi":"10.3724/abbs.2024120","DOIUrl":"https://doi.org/10.3724/abbs.2024120","url":null,"abstract":"In this study we investigate the role of Zipper-interacting protein kinase (ZIPK) in high glucose-induced vascular injury, focusing on its interaction with STAT5A and its effects on p53 and inducible nitric oxide synthase (NOS2) expression. Human umbilical vein endothelial cells (HUVECs) are cultured under normal (5 mM) and high (25 mM) glucose conditions. Protein and gene expression levels are assessed by western blot analysis and qPCR respectively, while ROS levels are measured via flow cytometry. ZIPK expression is manipulated using overexpression plasmids, siRNAs, and shRNAs. The effects of the ZIPK inhibitor TC-DAPK6 are evaluated in a diabetic rat model. Our results show that high glucose significantly upregulates ZIPK, STAT5A, p53, and NOS2 expressions in HUVECs, thus increasing oxidative stress. Silencing of STAT5A reduces p53 and NOS2 expressions and reactive oxygen species (ROS) accumulation. ZIPK is essential for high glucose-induced p53 expression and ROS accumulation, while silencing of ZIPK reverses these effects. Overexpression of ZIPK combined with STAT5A silencing attenuates glucose-induced alterations in p53 and NOS2 expression, thereby preventing cell damage. Coimmunoprecipitation reveals a direct interaction between ZIPK and STAT5A in the nucleus under high-glucose condition. In diabetic rats, TC-DAPK6 treatment significantly decreases ZIPK, p53, and NOS2 expressions. Our findings suggest that ZIPK plays a critical role in high glucose-induced vascular injury via STAT5A-mediated pathways, proposing that ZIPK is a potential therapeutic target for diabetic vascular complications.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141726711","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

Lung metastases formed by disseminated tumor cells exhibit different proliferation states. 由扩散的肿瘤细胞形成的肺转移瘤表现出不同的增殖状态。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-07-08 DOI: 10.3724/abbs.2024118

Jiajun Liu, Shihui Liu, Jianhui Tian, Jiaxuan Li, Minghua Li, Zujun Que

引用次数: 0

Role of Emerin in regulating fibroblast differentiation and migration at the substrate of stiffness coupled topology. Emerin在调节成纤维细胞分化和迁移过程中的作用--刚性耦合拓扑基质

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-07-08 DOI: 10.3724/abbs.2024094

Tiantian Yang, Li Wang, Haiyang Ma, Kailun Li, Yajing Wang, Wenjie Tang, Zichen Wang, Meiwen An, Xiang Gao, Ludan Xu, Yunyun Guo, Jiqiang Guo, Yong Liu, Hugen Wang, Yang Liu, Quanyou Zhang

{"title":"Role of Emerin in regulating fibroblast differentiation and migration at the substrate of stiffness coupled topology.","authors":"Tiantian Yang, Li Wang, Haiyang Ma, Kailun Li, Yajing Wang, Wenjie Tang, Zichen Wang, Meiwen An, Xiang Gao, Ludan Xu, Yunyun Guo, Jiqiang Guo, Yong Liu, Hugen Wang, Yang Liu, Quanyou Zhang","doi":"10.3724/abbs.2024094","DOIUrl":"10.3724/abbs.2024094","url":null,"abstract":"In hypertrophic scars, the differentiation and migration of fibroblasts are influenced by the extracellular matrix microenvironment, which includes factors such as stiffness, restraint, and tensile force. These mechanical stresses incite alterations in cell behavior, accompanied by cytoskeletal protein reorganization. However, the role of nucleo-skeletal proteins in this context remains underexplored. In this study, we use a polyacrylamide hydrogel (PAA) to simulate the mechanical stress experienced by cells in scar tissue and investigate the impact of Emerin on cell behavior. We utilize atomic force microscopy (AFM) and RNA interference technology to analyze cell differentiation, migration, and stiffness. Our findings reveal that rigid substrates and cellular restriction elevate Emerin expression and diminish differentiation. Conversely, reducing Emerin expression leads to attenuated cell differentiation, where stiffness and constraining factors exert no notable influence. Furthermore, a softening of cells and an enhanced migration rate are also markedly observed. These observations indicate that variations in nuclear skeletal proteins, prompted by diverse matrix microenvironments, play a pivotal role in the pathogenesis of hypertrophic scars (HSs). This research offers novel insights and a reference point for understanding scar fibrosis formation mechanisms and preventing fibrosis.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"1387-1400"},"PeriodicalIF":3.3,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11532208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141557726","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