Acta biochimica et biophysica Sinica最新文献_第7页

SIRPα modulates the podocyte cytoskeleton through influencing the phosphorylation of FAK at tyrosine residue 597. SIRPα 通过影响酪氨酸残基 597 处的 FAK 磷酸化来调节荚膜细胞的细胞骨架。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-11-18 DOI: 10.3724/abbs.2024198

Yuanyuan Xia, Yue Zhao, Jing Tian, Xue Yang, Yun Fan, Shihui Dong, Fan Yang, Mingchao Zhang, Caihong Zeng

{"title":"SIRPα modulates the podocyte cytoskeleton through influencing the phosphorylation of FAK at tyrosine residue 597.","authors":"Yuanyuan Xia, Yue Zhao, Jing Tian, Xue Yang, Yun Fan, Shihui Dong, Fan Yang, Mingchao Zhang, Caihong Zeng","doi":"10.3724/abbs.2024198","DOIUrl":"https://doi.org/10.3724/abbs.2024198","url":null,"abstract":"Signal regulatory protein α (SIRPα) is recognized as a significant transmembrane protein within the glomeruli that is specifically localized in podocytes, where it plays a role in modulating downstream signaling pathways through phosphorylation. Upon tyrosine phosphorylation of the immunoreceptor tyrosine-based inhibitory motif (ITIM) within SIRPα, protein tyrosine phosphatases are recruited to facilitate the dephosphorylation of downstream signals. Nevertheless, the specific downstream signaling pathways affected by this mechanism have yet to be elucidated. In this study, phosphoproteomic analysis is conducted on podocytes with SIRPα deficiency to identify proteins whose phosphorylation is regulated by SIRPα and the associated signaling pathways in human podocytes. The results reveal significant alterations in biological processes related to cytoskeleton arrangement and cytoskeleton protein binding. Specifically, an increase in FAK tyrosine phosphorylation at Y576 is identified as a potentially crucial signal of the influence of SIRPα on the podocyte cytoskeleton. Our study suggests that SIRPα may facilitate podocyte cytoskeleton rearrangement and migration through the Src/FAK/p38 MAPK signaling pathway. For the first time, we discover increased level of SIRPα, which is strongly linked to urinary protein, in the urine of patients with nephrotic syndrome (NS). Additionally, an increase in urinary FAK level is observed in NS patients, which is positively correlated with both urinary protein level and urinary SIRPα level. These findings suggest that SIRPα and FAK may serve as promising biomarkers for podocytopathies.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646746","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

Functions and applications of RNA interference and small regulatory RNAs. RNA 干扰和小调控 RNA 的功能与应用。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-11-18 DOI: 10.3724/abbs.2024196

Xuezhu Feng, Shouhong Guang

引用次数: 0

Mechanism of RSL3-induced ferroptotic cell death in HT22 cells: crucial role of protein disulfide isomerase. RSL3诱导HT22细胞铁凋亡的机制：蛋白二硫异构酶的关键作用

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-11-15 DOI: 10.3724/abbs.2024165

Ming-Jie Hou, Xuanqi Huang, Bao Ting Zhu

{"title":"Mechanism of RSL3-induced ferroptotic cell death in HT22 cells: crucial role of protein disulfide isomerase.","authors":"Ming-Jie Hou, Xuanqi Huang, Bao Ting Zhu","doi":"10.3724/abbs.2024165","DOIUrl":"10.3724/abbs.2024165","url":null,"abstract":"Protein disulfide isomerase (PDI) was recently shown to be an upstream mediator of erastin-induced, glutathione depletion-associated ferroptosis through its catalysis of nitric oxide synthase (NOS) dimerization and nitric oxide (NO) accumulation. A recent study reported that RSL3, a known ferroptosis inducer and glutathione peroxidase 4 (GPX4) inhibitor, can inhibit thioredoxin reductase 1 (TrxR1). The present study seeks to test the hypothesis that RSL3 may, through its inhibition of TrxR1, facilitate PDI activation ( i. e., in a catalytically active, oxidized state), thereby enhancing RSL3-induced ferroptosis through NOS dimerization and NO accumulation. Using HT22 mouse neuronal cells as an in vitro model, we show that treatment of these cells with RSL3 strongly increases NOS protein levels and that PDI-mediated NOS dimerization is activated by RSL3, resulting in NO accumulation. Mechanistically, we find that PDI is activated in cells treated with RSL3 because of its inhibition of TrxR1, and the activated PDI then catalyzes NOS dimerization, which is followed by the accumulation of cellular NO, ROS and lipid-ROS and ultimately ferroptotic cell death. Genetic or pharmacological inhibition of PDI or TrxR1 partially abrogates RSL3-induced NOS activation and the subsequent accumulation of cellular NO, ROS/lipid-ROS, and ultimately ferroptosis in HT22 cells. The results of this study clearly show that PDI activation resulted from RSL3 inhibition of TrxR1 activity contributes crucially to RSL3-induced ferroptosis in a cell culture model through the PDI→NOS→NO→ROS/lipid-ROS pathway, in addition to its known inhibition of GPX4 activity.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611931","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

Advances in PIWI-piRNA function in female reproduction in mammals. 哺乳动物雌性生殖中 PIWI-piRNA 功能的研究进展。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-11-15 DOI: 10.3724/abbs.2024195

Xiaolong Lv, Hongdao Zhang, Ligang Wu

{"title":"Advances in PIWI-piRNA function in female reproduction in mammals.","authors":"Xiaolong Lv, Hongdao Zhang, Ligang Wu","doi":"10.3724/abbs.2024195","DOIUrl":"10.3724/abbs.2024195","url":null,"abstract":"PIWI-interacting RNAs (piRNAs), which associate with PIWI clade Argonaute proteins to form piRNA-induced silencing complexes (piRISCs) in germline cells, are responsible for maintaining genomic integrity and reproductive function through transcriptional or post-transcriptional suppression of transposable elements and regulation of protein-coding genes. Recent discoveries of crucial PIWI-piRNA functions in oogenesis and embryogenesis in golden hamsters suggest an indispensable role in female fertility that has been obscured in the predominant mouse model of PIWI-piRNA pathway regulation. In particular, studies of piRNA expression dynamics, functional redundancies, and compositional variations across mammal species have advanced our understanding of piRNA functions in male and, especially, female reproduction. These findings further support the use of hamsters as a more representative model of piRNA biology in mammals. In addition to discussing these new perspectives, the current review also covers emerging directions for piRNA research, its implications for female fertility, and our fundamental understanding of reproductive mechanisms.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"148-156"},"PeriodicalIF":3.3,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11802344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611926","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

A novel mutation in SMARCB1 associated with adult Coffin-Siris syndrome and meningioma. 与成人科芬-西里斯综合征和脑膜瘤相关的SMARCB1新型突变。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-11-13 DOI: 10.3724/abbs.2024204

Zhenglong Guo, Jie Bai, Yang Liu, Xianwei Zhang, Wenke Yang, Jinming Wang, Yuwei Zhang, Hai Xiao, Bingtao Hao, Shixiu Liao

{"title":"A novel mutation in SMARCB1 associated with adult Coffin-Siris syndrome and meningioma.","authors":"Zhenglong Guo, Jie Bai, Yang Liu, Xianwei Zhang, Wenke Yang, Jinming Wang, Yuwei Zhang, Hai Xiao, Bingtao Hao, Shixiu Liao","doi":"10.3724/abbs.2024204","DOIUrl":"https://doi.org/10.3724/abbs.2024204","url":null,"abstract":"SMARCB1 encodes a core subunit of the SWI/SNF chromatin remodeling complex, which plays a crucial role in the regulation of gene expression. Germline mutations in the SMARCB1 gene have been linked to early childhood Coffin-Siris syndrome type 3 (CSS3), a rare congenital malformation syndrome characterized by severe developmental delay and intellectual disability. In this study, we report a family of two adult CSS3 patients with a novel missense SMARCB1 mutation (c.1091A>C, p.Lys364Thr) identified through whole-exome sequencing (WES). Both patients exhibit selective difficulties in verbal learning and experience language delays. Additionally, the development of meningioma is confirmed in one of the patients. Mechanistic studies suggest that this missense mutation may abnormally activate the MAPK signaling pathway, which is implicated in the pathogenesis of tumor progression and neurodevelopmental disorders. This is the first reported case of a germline mutation in the SMARCB1 gene associated with both CSS3 and meningioma, thereby expanding the phenotypic spectrum of SMARCB1-related disorders.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142674804","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

The peripheral Atf3 ⁺ neuronal population is responsible for nerve regeneration at the early stage of nerve injury revealed by single-cell RNA sequencing. 单细胞 RNA 测序揭示了外周 Atf3 + 神经元群体在神经损伤早期负责神经再生。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-11-13 DOI: 10.3724/abbs.2024169

Li Liu, Junhui Chen, Wen Yin, Po Gao, Yinghui Fan, Daxiang Wen, Yingfu Jiao, Weifeng Yu

{"title":"The peripheral Atf3 + neuronal population is responsible for nerve regeneration at the early stage of nerve injury revealed by single-cell RNA sequencing.","authors":"Li Liu, Junhui Chen, Wen Yin, Po Gao, Yinghui Fan, Daxiang Wen, Yingfu Jiao, Weifeng Yu","doi":"10.3724/abbs.2024169","DOIUrl":"https://doi.org/10.3724/abbs.2024169","url":null,"abstract":"Peripheral nerve injury (PNI) can transform primary somatosensory neurons to a regenerative state. However, the details of the transcriptomic changes associated with the nerve regeneration of somatosensory neurons remain unclear. In this study, single-cell RNA sequencing (scRNA-seq) is conducted on mouse dorsal root ganglion (DRG) cells after the early stage of nerve injury on day 3 after chronic constriction injury (CCI). We observe that a novel CCI-induced neuronal population (CIP) emerge and express high levels of activating transcription factor ( Atf3), a neuronal injury marker. CIP neurons highly express regeneration-associated genes (RAGs) and are enriched in regeneration-related gene ontology (GO) terms, suggesting that these neurons can constitute a pro-regenerative population. Moreover, intercellular communication networks show that CIP neurons closely communicate with satellite glial cells (SGCs) and specifically transmit strong Fgf3- Fgfr1 signaling to SGCs, which could initiate regeneration-associated transcriptional changes in SGCs. We also confirm that regenerative progress occurs at the early stage of nerve injury because immunohistochemistry shows that the expression of ATF3 is significantly increased beginning at 3 days post-CCI and decreased at 1 month post-CCI. Our bioinformatics analysis at single-cell resolution advances the knowledge of regenerative dynamic transcriptional changes in DRG cells after injury and the underlying molecular mechanisms involved.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611934","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

Repurposed genipin targeting UCP2 exhibits antitumor activity through inducing ferroptosis in glioblastoma. 靶向 UCP2 的重塑基因素通过诱导胶质母细胞瘤中的铁凋亡而显示出抗肿瘤活性。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-11-11 DOI: 10.3724/abbs.2024168

Hao Dong, Kaixuan Sun, Xuejie Wang, Meimei Cui, Yaping Ma, Kexin Li, Wanli Duan, Hongxing Zhang, Liying Zhang, Zhimei Sheng, Maotao He, Baogang Zhang

{"title":"Repurposed genipin targeting UCP2 exhibits antitumor activity through inducing ferroptosis in glioblastoma.","authors":"Hao Dong, Kaixuan Sun, Xuejie Wang, Meimei Cui, Yaping Ma, Kexin Li, Wanli Duan, Hongxing Zhang, Liying Zhang, Zhimei Sheng, Maotao He, Baogang Zhang","doi":"10.3724/abbs.2024168","DOIUrl":"https://doi.org/10.3724/abbs.2024168","url":null,"abstract":"Uncoupling protein-2 (UCP2) controls the antioxidant response and redox homeostasis in cancer and is considered a potent molecular target for cancer treatment. However, the specific mechanism of UCP2 inhibition and its role in glioblastoma (GBM) have not yet been elucidated. Here, we attempt to identify a UCP2 inhibitor and study the underlying molecular mechanism in GBM. Bioinformatics analysis and immunohistochemistry are used to validate the high expression of UCP2 in GBM and its prognostic significance. Drug intervention and tumor xenograft experiments are conducted to determine the inhibitory effect of genipin, a UCP2 inhibitor, on UCP2. The mitochondrial membrane potential and key ferroptosis genes are examined to determine the occurrence of ferroptosis. High expression of UCP2 in GBM is associated with poor prognosis, and inhibiting UCP2 can alleviate the malignant behavior of GBM tumors. Genipin can downregulate the expression of GPX4 and upregulate the expression of ACSL4 by inhibiting UCP2, leading to ferroptosis and alleviating the malignant behavior of tumors. In summary, UCP2 is a potential therapeutic target for GBM. Genipin, which targets UCP2, effectively inhibits GBM development by inducing ferroptosis in vivo and in vitro. These findings indicate that genipin treatment based on UCP2 targeting has potential therapeutic applications with a clinical perspective for the treatment of GBM patients.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611933","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

SMG-1 serves as a prognostic indicator for the radiotherapy response in head and neck squamous cell carcinoma xenografts and patients. SMG-1 是头颈部鳞状细胞癌异种移植物和患者放疗反应的预后指标。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-11-04 DOI: 10.3724/abbs.2024180

Xiaofeng Wang, Yuxia Zou, Ren-Bo Ding, Xueying Lyu, Yuanfeng Fu, Xuejun Zhou, Zhihua Sun, Jiaolin Bao

引用次数: 0

R-loop formation contributes to mTORC1 activation-dependent DNA replication stress induced by p53 deficiency. R 环的形成有助于 p53 缺乏诱导的 mTORC1 激活依赖性 DNA 复制压力。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-11-04 DOI: 10.3724/abbs.2024188

Xiaolei Li, Cheng Yang, Xiaohui Zhang, Feiyang Wang, Longhua Sun, Wei Zhang, Xinping Xu

{"title":"R-loop formation contributes to mTORC1 activation-dependent DNA replication stress induced by p53 deficiency.","authors":"Xiaolei Li, Cheng Yang, Xiaohui Zhang, Feiyang Wang, Longhua Sun, Wei Zhang, Xinping Xu","doi":"10.3724/abbs.2024188","DOIUrl":"https://doi.org/10.3724/abbs.2024188","url":null,"abstract":"DNA replication stress is a significant contributor to spontaneous DNA damage and genome instability. While the impact of p53 deficiency on increasing DNA replication stress is known, the specific molecular mechanism underlying this phenomenon remains poorly understood. This study explores how p53 deficiency induces DNA replication stress by activating mTORC1 through R-loop formation, which is facilitated by the upregulation of RNR. Research has shown that p53 deficiency results in increased γH2AX expression and a higher mutation rate in the HPRT gene. Interestingly, these effects can be alleviated by rapamycin, an mTORC1 inhibitor. Additionally, rapamycin reduces the abundance of R-loop structures in p53KO cells, which is linked to mTORC1's regulation of ribonucleotide reductase (RNR) level. These findings suggest that p53 deficiency-induced DNA replication stress relies on mTORC1 activation, with the upregulation of RNR expression and R-loop formation. Overall, this study underscores the importance of R-loops in mTORC1 activation-dependent DNA replication stress triggered by p53 deficiency.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142724612","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

R-loop formation contributes to mTORC1 activation-dependent DNA replication stress induced by p53 deficiency. R 环的形成有助于 p53 缺乏诱导的 mTORC1 激活依赖性 DNA 复制压力 p53 缺乏诱导的 DNA 复制压力会增加 R 环的形成。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-11-04 DOI: 10.3724/abbs.2024188

Xiaolei Li, Cheng Yang, Xiaohui Zhang, Feiyang Wang, Longhua Sun, Wei Zhang, Xinping Xu

{"title":"R-loop formation contributes to mTORC1 activation-dependent DNA replication stress induced by p53 deficiency.","authors":"Xiaolei Li, Cheng Yang, Xiaohui Zhang, Feiyang Wang, Longhua Sun, Wei Zhang, Xinping Xu","doi":"10.3724/abbs.2024188","DOIUrl":"10.3724/abbs.2024188","url":null,"abstract":"DNA replication stress is a significant contributor to spontaneous DNA damage and genome instability. While the impact of p53 deficiency on increasing DNA replication stress is known, the specific molecular mechanism underlying this phenomenon remains poorly understood. This study explores how p53 deficiency induces DNA replication stress by activating mTORC1 through R-loop formation, which is facilitated by the upregulation of RNR. Research has shown that p53 deficiency results in increased γH2AX expression and a higher mutation rate in the HPRT gene. Interestingly, these effects can be alleviated by rapamycin, an mTORC1 inhibitor. Additionally, rapamycin reduces the abundance of R-loop structures in p53KO cells, which is linked to mTORC1's regulation of ribonucleotide reductase (RNR) level. These findings suggest that p53 deficiency-induced DNA replication stress relies on mTORC1 activation, with the upregulation of RNR expression and R-loop formation. Overall, this study underscores the importance of R-loops in mTORC1 activation-dependent DNA replication stress triggered by p53 deficiency.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"1875-1885"},"PeriodicalIF":3.3,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11693875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142724608","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