Archives of biochemistry and biophysics最新文献_第7页

The role of miR-491-3p in early diagnosis and prognosis evaluation of acute myocardial infarction miR-491-3p在急性心肌梗死早期诊断及预后评价中的作用

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-02-01 Epub Date: 2025-12-03 DOI: 10.1016/j.abb.2025.110691

Tai Dou , Lijie Qin , Peirong Zhang, Lijun Xu, Yanwei Cheng, Peng Wang

Aims

To investigate the expression characteristics, clinical implications, and underlying mechanisms of miR-491-3p in patients with acute myocardial infarction (AMI).

Methods

Serum samples were collected from patients with AMI and healthy controls. miR-491-3p expression was measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Receiver operating characteristic (ROC) curves evaluated its diagnostic accuracy for AMI. Correlations between miR-491-3p levels and myocardial injury markers or inflammatory factors were analyzed. A one-year follow-up assessed its predictive value for major adverse cardiovascular events (MACE). A hypoxia/reoxygenation (H/R) model of human AC16 cardiomyocytes was established to explore the mechanism of miR-491-3p in H/R-induced injury via targeting aquaporin 9 (AQP9).

Results

Serum miR-491-3p was significantly downregulated in AMI patients, with an AUC of 0.893 for AMI diagnosis (sensitivity 83 %, specificity 79.5 %). Levels were negatively correlated with myocardial injury markers and inflammatory factors. AMI patients with low miR-491-3p expression had a higher incidence of MACE, and low expression was identified as a risk factor. In the H/R model, miR-491-3p was downregulated. Overexpression of miR-491-3p improved cell proliferation, reduced apoptosis, and decreased inflammatory factors by targeting and inhibiting AQP9.

Conclusions

miR-491-3p may be involved in the pathological process of AMI by targeting and regulating AQP9. This makes it a promising candidate as both a diagnostic and prognostic marker for AMI, as well as a potential therapeutic target.

目的：探讨miR-491-3p在急性心肌梗死（AMI）患者中的表达特征、临床意义及其机制。方法：分别采集AMI患者和健康对照者的血清样本。采用逆转录定量聚合酶链反应（RT-qPCR）检测miR-491-3p的表达。受试者工作特征（ROC）曲线评价其诊断AMI的准确性。分析miR-491-3p水平与心肌损伤标志物或炎症因子的相关性。1年随访评估其对主要不良心血管事件（MACE）的预测价值。建立人AC16心肌细胞缺氧/再氧化（H/R）模型，通过靶向水通道蛋白9 （AQP9）探讨miR-491-3p在H/R诱导损伤中的作用机制。结果：AMI患者血清miR-491-3p明显下调，AMI诊断AUC为0.893（敏感性83%，特异性79.5%）。其水平与心肌损伤标志物和炎症因子呈负相关。miR-491-3p低表达的AMI患者MACE发生率较高，低表达被认为是一个危险因素。在H/R模型中，miR-491-3p下调。过表达miR-491-3p通过靶向和抑制AQP9促进细胞增殖，减少细胞凋亡，降低炎症因子。结论：miR-491-3p可能通过靶向调控AQP9参与AMI的病理过程。这使其成为AMI的诊断和预后标志物，以及潜在的治疗靶点。

{"title":"The role of miR-491-3p in early diagnosis and prognosis evaluation of acute myocardial infarction","authors":"Tai Dou , Lijie Qin , Peirong Zhang, Lijun Xu, Yanwei Cheng, Peng Wang","doi":"10.1016/j.abb.2025.110691","DOIUrl":"10.1016/j.abb.2025.110691","url":null,"abstract":"<div><h3>Aims</h3><div>To investigate the expression characteristics, clinical implications, and underlying mechanisms of miR-491-3p in patients with acute myocardial infarction (AMI).</div></div><div><h3>Methods</h3><div>Serum samples were collected from patients with AMI and healthy controls. miR-491-3p expression was measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Receiver operating characteristic (ROC) curves evaluated its diagnostic accuracy for AMI. Correlations between miR-491-3p levels and myocardial injury markers or inflammatory factors were analyzed. A one-year follow-up assessed its predictive value for major adverse cardiovascular events (MACE). A hypoxia/reoxygenation (H/R) model of human AC16 cardiomyocytes was established to explore the mechanism of miR-491-3p in H/R-induced injury via targeting aquaporin 9 (AQP9).</div></div><div><h3>Results</h3><div>Serum miR-491-3p was significantly downregulated in AMI patients, with an AUC of 0.893 for AMI diagnosis (sensitivity 83 %, specificity 79.5 %). Levels were negatively correlated with myocardial injury markers and inflammatory factors. AMI patients with low miR-491-3p expression had a higher incidence of MACE, and low expression was identified as a risk factor. In the H/R model, miR-491-3p was downregulated. Overexpression of miR-491-3p improved cell proliferation, reduced apoptosis, and decreased inflammatory factors by targeting and inhibiting AQP9.</div></div><div><h3>Conclusions</h3><div>miR-491-3p may be involved in the pathological process of AMI by targeting and regulating AQP9. This makes it a promising candidate as both a diagnostic and prognostic marker for AMI, as well as a potential therapeutic target.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110691"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145686944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Predictive value of LncRNA LINC00667 in the development and prognosis of papillary thyroid carcinoma and its possible regulation of cellular processes via miR-34c-5p LncRNA LINC00667在甲状腺乳头状癌发生和预后中的预测价值及其可能通过miR-34c-5p调控细胞过程。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-02-01 Epub Date: 2025-12-01 DOI: 10.1016/j.abb.2025.110683

Qinghua Zhang , Zhao Liu , Zhiyong Li , Xiancun Hou , Changli Ouyang

Background

As a major type of endocrine malignancy, thyroid cancer (THCA) has a relatively high occurrence rate around the world. However, the underlying mechanism through which LINC00667 acts in papillary thyroid carcinoma (PTC) remains unelucidated.

Methods

A total of 120 PTC patients were enrolled. The expression of LINC00667 was analyzed using reverse transcription-quantitative polymerase chain reaction. To evaluate the clinical significance of LINC00667, chi-square analysis was performed, a Kaplan-Meier survival curve was generated, and multivariate Cox analysis was conducted to determine its association with the clinical-pathological characteristics and prognostic outcomes of PTC. Cell Counting Kit-8 and Transwell assays evaluated changes in cellular processes. A dual luciferase reporter assay and RNA Immunoprecipitation were employed to analyze the binding relationship between LINC00667 and miR-34c-5p.

Results

LINC00667 exhibited significant up-regulation in PTC tissues, with elevated expression levels associated with tumor malignancy. Increased LINC00667 expression was a marker of unfavorable prognostic outcomes and functioned as an independent risk indicator for PTC. Knockdown of LINC00667 expression inhibited the proliferation, migration capability, and invasive properties of PTC cells. Furthermore, LINC00667 was identified to exert a negative regulatory effect on miR-34c-5p, and the silencing of miR-34c-5p weakened the inhibitory impacts induced by LINC00667 depletion on the malignant behaviors of PTC cells.

Conclusions

Up-regulated LINC00667 may serve as a biomarker for PTC. Knockdown of LINC00667 may inhibit the progression of PTC by regulating miR-34c-5p.

背景：甲状腺癌（THCA）是一种主要的内分泌恶性肿瘤，在世界范围内发病率较高。然而，LINC00667在甲状腺乳头状癌（PTC）中的作用机制尚不清楚。方法：共纳入120例PTC患者。采用逆转录-定量聚合酶链反应分析LINC00667的表达。为了评价LINC00667的临床意义，我们进行卡方分析，生成Kaplan-Meier生存曲线，并进行多因素Cox分析，以确定其与PTC临床病理特征及预后结局的相关性。细胞计数试剂盒-8和Transwell检测评估细胞过程的变化。采用双荧光素酶报告基因法和RNA免疫沉淀法分析LINC00667与miR-34c-5p的结合关系。结果：LINC00667在PTC组织中表达显著上调，表达水平升高与肿瘤恶性相关。升高的LINC00667表达是不良预后的标志，是PTC的独立风险指标。抑制LINC00667表达抑制PTC细胞的增殖、迁移能力和侵袭特性。此外，我们发现LINC00667对miR-34c-5p具有负调控作用，miR-34c-5p的沉默减弱了LINC00667缺失对PTC细胞恶性行为的抑制作用。结论：上调的LINC00667可能作为PTC的生物标志物。敲低LINC00667可能通过调节miR-34c-5p抑制PTC的进展。

{"title":"Predictive value of LncRNA LINC00667 in the development and prognosis of papillary thyroid carcinoma and its possible regulation of cellular processes via miR-34c-5p","authors":"Qinghua Zhang , Zhao Liu , Zhiyong Li , Xiancun Hou , Changli Ouyang","doi":"10.1016/j.abb.2025.110683","DOIUrl":"10.1016/j.abb.2025.110683","url":null,"abstract":"<div><h3>Background</h3><div>As a major type of endocrine malignancy, thyroid cancer (THCA) has a relatively high occurrence rate around the world. However, the underlying mechanism through which LINC00667 acts in papillary thyroid carcinoma (PTC) remains unelucidated.</div></div><div><h3>Methods</h3><div>A total of 120 PTC patients were enrolled. The expression of LINC00667 was analyzed using reverse transcription-quantitative polymerase chain reaction. To evaluate the clinical significance of LINC00667, chi-square analysis was performed, a Kaplan-Meier survival curve was generated, and multivariate Cox analysis was conducted to determine its association with the clinical-pathological characteristics and prognostic outcomes of PTC. Cell Counting Kit-8 and Transwell assays evaluated changes in cellular processes. A dual luciferase reporter assay and RNA Immunoprecipitation were employed to analyze the binding relationship between LINC00667 and miR-34c-5p.</div></div><div><h3>Results</h3><div>LINC00667 exhibited significant up-regulation in PTC tissues, with elevated expression levels associated with tumor malignancy. Increased LINC00667 expression was a marker of unfavorable prognostic outcomes and functioned as an independent risk indicator for PTC. Knockdown of LINC00667 expression inhibited the proliferation, migration capability, and invasive properties of PTC cells. Furthermore, LINC00667 was identified to exert a negative regulatory effect on miR-34c-5p, and the silencing of miR-34c-5p weakened the inhibitory impacts induced by LINC00667 depletion on the malignant behaviors of PTC cells.</div></div><div><h3>Conclusions</h3><div>Up-regulated LINC00667 may serve as a biomarker for PTC. Knockdown of LINC00667 may inhibit the progression of PTC by regulating miR-34c-5p.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110683"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145666861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Kinetic investigation on d-amino acid containing peptides and carboxypeptidase Y 含d -氨基酸肽与羧肽酶Y的动力学研究。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-02-01 Epub Date: 2025-12-09 DOI: 10.1016/j.abb.2025.110699

Joshua I. Putman, Arzoo Patel, Maria Olds, Alaa Aziz, Haritha Asokan-Sheeja, He Dong, Kayunta L. Johnson-Winters, Daniel W. Armstrong

Carboxypeptidases catalyze the hydrolysis of the peptide bond of C terminal amino acid residues. Carboxypeptidase Y can hydrolyze all 20 naturally-occurring amino acids at varying rates under optimal conditions. Previous data suggests that carboxypeptidase Y has more difficulty hydrolyzing d-amino acids from the C terminus of peptides than l-amino acids. This enzyme was used for amino acid sequence determination prior to modern proteomics. However, most modern proteomic methods assume that all peptides are comprised of l-amino acids and do not distinguish L-from d-amino acids within the peptide sequence. Most existing methods that allow for chiral differentiation require synthetic standards or incur racemization. Steady-state kinetic analysis was performed to elucidate differences in hydrolytic rates between peptides composed solely of l-amino acids at the carboxy-terminal and those incorporating d-amino acids. Our data suggests that the l-amino acid exclusive peptides are hydrolyzed at a rate two-to-five orders of magnitude higher than d-amino acid containing peptides. Such differences are necessary to completely digest and eliminate l-amino acid exclusive peptides while leaving the carboxy-terminal d-amino acid peptides intact. The d-amino acid containing peptides can then be preconcentrated to enhance detection limits to facilitate scouting for the desired d-amino acid containing peptides. Interestingly, the peptide epimers bind equally well to carboxypeptidase Y on a low μM level, indicating high substrate affinity.

羧基肽酶催化C端氨基酸残基肽键的水解。羧基肽酶Y能在最佳条件下以不同速率水解所有20种天然氨基酸。先前的数据表明，羧基肽酶Y水解肽C端的d -氨基酸比水解l -氨基酸更困难。在现代蛋白质组学出现之前，这种酶被用于氨基酸序列测定。然而，大多数现代蛋白质组学方法假设所有肽都由L-氨基酸组成，并且在肽序列中不能区分L-氨基酸和d -氨基酸。大多数允许手性分化的现有方法需要合成标准或引起外消旋。稳态动力学分析阐明了在羧基端仅由l -氨基酸组成的肽和含有d -氨基酸的肽之间水解速率的差异。我们的数据表明，不含l-氨基酸的肽的水解速率比含d -氨基酸的肽高2到5个数量级。这种差异对于完全消化和消除l-氨基酸专有肽而保持羧基末端d-氨基酸肽完整是必要的。然后将含d-氨基酸的多肽预浓缩以提高检测限，以便于寻找所需的含d-氨基酸的多肽。有趣的是，肽外显子在低μM水平上与羧基肽酶Y结合良好，表明具有高底物亲和力。

{"title":"Kinetic investigation on d-amino acid containing peptides and carboxypeptidase Y","authors":"Joshua I. Putman, Arzoo Patel, Maria Olds, Alaa Aziz, Haritha Asokan-Sheeja, He Dong, Kayunta L. Johnson-Winters, Daniel W. Armstrong","doi":"10.1016/j.abb.2025.110699","DOIUrl":"10.1016/j.abb.2025.110699","url":null,"abstract":"<div><div>Carboxypeptidases catalyze the hydrolysis of the peptide bond of C terminal amino acid residues. Carboxypeptidase Y can hydrolyze all 20 naturally-occurring amino acids at varying rates under optimal conditions. Previous data suggests that carboxypeptidase Y has more difficulty hydrolyzing <span>d</span>-amino acids from the C terminus of peptides than <span>l</span>-amino acids. This enzyme was used for amino acid sequence determination prior to modern proteomics. However, most modern proteomic methods assume that all peptides are comprised of <span>l<em>-</em></span>amino acids and do not distinguish L<span>-</span>from <span>d<em>-</em></span>amino acids within the peptide sequence. Most existing methods that allow for chiral differentiation require synthetic standards or incur racemization. Steady-state kinetic analysis was performed to elucidate differences in hydrolytic rates between peptides composed solely of <span>l</span>-amino acids at the carboxy-terminal and those incorporating <span>d</span>-amino acids. Our data suggests that the <span>l<em>-</em></span>amino acid exclusive peptides are hydrolyzed at a rate two-to-five orders of magnitude higher than <span>d</span>-amino acid containing peptides. Such differences are necessary to completely digest and eliminate <span>l<em>-</em></span>amino acid exclusive peptides while leaving the carboxy-terminal <span>d<em>-</em></span>amino acid peptides intact. The <span>d<em>-</em></span>amino acid containing peptides can then be preconcentrated to enhance detection limits to facilitate scouting for the desired <span>d<em>-</em></span>amino acid containing peptides. Interestingly, the peptide epimers bind equally well to carboxypeptidase Y on a low μM level, indicating high substrate affinity.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110699"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145740718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

mmu_circ_0000684/hsa_circ_0067098 mediates renal tubular epithelial cells apoptosis to ischemia-reperfusion-induced acute kidney injury by targeting the mmu_miR_671-5p/ARID3B axis mmu_circ_0000684/hsa_circ_0067098通过靶向mmu_miR_671-5p/ARID3B轴介导肾小管上皮细胞凋亡至缺血再灌注诱导的急性肾损伤

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-02-01 Epub Date: 2025-11-29 DOI: 10.1016/j.abb.2025.110679

Ben Yang , Qiang Zheng , Yan Pu , Yingying Hu , Dongshan Zhang

Objective

This investigation sought to explore the possible role of mmu_circ_0000684 and its homolog hsa_circ_0067098 in the evolution of ischemia-reperfusion-induced acute kidney injury (AKI), with an emphasis on their viability as therapeutic targets.

Method

A model was constructed employing Boston University mouse proximal tubule (BUMPT) cells, human renal tubular epithelial (HK-2) cells, and murine kidney tissue. The mmu_circ_0000684, miR-671-5p, and ARID3B mRNA levels, along with their corresponding protein expression, underwent quantification via real-time quantitative polymerase chain reaction and Western blot. A comprehensive examination of the biological roles and signaling cascade of mmu_circ_0000684 and hsa_circ_0067098 was executed utilizing bioinformatics prediction, luciferase reporter assays, fluorescence in situ hybridization, flow cytometry, hematoxylin and eosin staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining.

Results

Ischemic stress was observed to induce mmu_circ_0000684 expression. Functionally, mmu_circ_0000684 was implicated in promoting BUMPT cell apoptosis as a consequence of ischemia-reperfusion injury. Mechanistically, mmu_circ_0000684 acted as a molecular sponge for miR-671-5p, thereby facilitating the upregulation of ARID3B, which in turn contributed to apoptosis induction. Moreover, silencing mmu_circ_0000684 markedly mitigated ischemia-triggered AKI via modulation of the miR-671-5p/ARID3B axis. Notably, hsa_circ_0067098, the homolog of mmu_circ_0000684, exhibited an analogous regulatory role in HK-2 cells.

Conclusion

The mmu_circ_0000684, hsa_circ_0067098/miR-671-5p/ARID3B signaling cascade emerges as an essential mechanism during ischemic AKI progression. Consequently, hsa_circ_0067098 represents a promising therapeutic candidate for addressing ischemic AKI.

目的：本研究旨在探讨mmu_circ_00684及其同源基因hsa_circ_0067098在缺血-再灌注诱导的急性肾损伤（AKI）进化中的可能作用，并重点研究它们作为治疗靶点的可行性。方法：采用波士顿大学小鼠近端小管细胞（BUMPT）、人肾小管上皮细胞（HK-2）和小鼠肾组织构建模型。mmu_circ_0000684、miR-671-5p和ARID3B mRNA水平及其相应的蛋白表达通过实时定量聚合酶链反应和Western blot进行定量。利用生物信息学预测、荧光素酶报告基因测定、荧光原位杂交、流式细胞术、苏木精和伊红染色、末端脱氧核苷酸转移酶dUTP标记染色，对mmu_circ_0000684和hsa_circ_0067098的生物学作用和信号级联进行了全面的研究。结果：缺血应激诱导mmu_circ_0000684表达。功能上，mmu_circ_0000684参与促进BUMPT细胞因缺血再灌注损伤而凋亡。在机制上，mmu_circ_0000684作为miR-671-5p的分子海绵，从而促进ARID3B的上调，进而促进细胞凋亡的诱导。此外，沉默mmu_circ_0000684可通过调节miR-671-5p/ARID3B轴显著减轻缺血触发的AKI。值得注意的是，hsa_circ_0067098， mmu_circ_0000684的同源物，在HK-2细胞中表现出类似的调节作用。结论：mmu_circ_0000684， hsa_circ_0067098/miR-671-5p/ARID3B信号级联是缺血性AKI进展的重要机制。因此，hsa_circ_0067098代表了解决缺血性AKI的有希望的治疗候选者。

{"title":"mmu_circ_0000684/hsa_circ_0067098 mediates renal tubular epithelial cells apoptosis to ischemia-reperfusion-induced acute kidney injury by targeting the mmu_miR_671-5p/ARID3B axis","authors":"Ben Yang , Qiang Zheng , Yan Pu , Yingying Hu , Dongshan Zhang","doi":"10.1016/j.abb.2025.110679","DOIUrl":"10.1016/j.abb.2025.110679","url":null,"abstract":"<div><h3>Objective</h3><div>This investigation sought to explore the possible role of mmu_circ_0000684 and its homolog hsa_circ_0067098 in the evolution of ischemia-reperfusion-induced acute kidney injury (AKI), with an emphasis on their viability as therapeutic targets.</div></div><div><h3>Method</h3><div>A model was constructed employing Boston University mouse proximal tubule (BUMPT) cells, human renal tubular epithelial (HK-2) cells, and murine kidney tissue. The mmu_circ_0000684, miR-671-5p, and ARID3B mRNA levels, along with their corresponding protein expression, underwent quantification via real-time quantitative polymerase chain reaction and Western blot. A comprehensive examination of the biological roles and signaling cascade of mmu_circ_0000684 and hsa_circ_0067098 was executed utilizing bioinformatics prediction, luciferase reporter assays, fluorescence in situ hybridization, flow cytometry, hematoxylin and eosin staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining.</div></div><div><h3>Results</h3><div>Ischemic stress was observed to induce mmu_circ_0000684 expression. Functionally, mmu_circ_0000684 was implicated in promoting BUMPT cell apoptosis as a consequence of ischemia-reperfusion injury. Mechanistically, mmu_circ_0000684 acted as a molecular sponge for miR-671-5p, thereby facilitating the upregulation of ARID3B, which in turn contributed to apoptosis induction. Moreover, silencing mmu_circ_0000684 markedly mitigated ischemia-triggered AKI via modulation of the miR-671-5p/ARID3B axis. Notably, hsa_circ_0067098, the homolog of mmu_circ_0000684, exhibited an analogous regulatory role in HK-2 cells.</div></div><div><h3>Conclusion</h3><div>The mmu_circ_0000684, hsa_circ_0067098/miR-671-5p/ARID3B signaling cascade emerges as an essential mechanism during ischemic AKI progression. Consequently, hsa_circ_0067098 represents a promising therapeutic candidate for addressing ischemic AKI.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110679"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145647308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Apelin-13 ameliorates myocardial ischemia/reperfusion injury by modulating macrophage polarization Apelin-13通过调节巨噬细胞极化改善心肌缺血/再灌注损伤。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-02-01 Epub Date: 2025-12-20 DOI: 10.1016/j.abb.2025.110710

Hui Jia , Qiyue Zhao , Jing Yuan , Xin Wang , Hua Chen , Jinghui Dong , Chunhua Zhu , Leonid N. Maslov , Natalia V. Naryzhnaya , Yue Guan , Huijie Ma , Zan Guo

Macrophage polarization plays a crucial role in myocardial ischemia/reperfusion (I/R) injury. Although Apelin-13 is known for its anti-inflammatory effects, its impact on macrophage polarization during myocardial I/R injury remains unclear. This study aimed to investigate the effects of Apelin-13 on macrophage polarization and cardiac function in a rat I/R model and H9c2 cells in vitro. I/R injury was induced by ligating the left anterior descending coronary artery with reperfusion times of 2 h and 7 days. H9c2 cells and peritoneal macrophages were cultured in vitro. We show that Apelin-13 significantly improves cardiac function and reduces infarct size in a rat I/R model, as evidenced by improved hemodynamic and echocardiographic parameters. Apelin-13 treatment decreased myocardial apoptosis by modulating the Bcl-2/Bax ratio and shifted macrophage polarization from the pro-inflammatory M1 phenotype to the reparative M2 phenotype in vivo. In vitro, Apelin-13 suppressed LPS-induced pro-inflammatory cytokine production and promoted M2 markers in rat peritoneal macrophages. Furthermore, conditioned medium from Apelin-13-treated macrophages enhanced H9c2 cell survival following oxygen-glucose deprivation/reoxygenation. These findings suggest Apelin-13 as a promising therapeutic strategy for myocardial I/R injury by modulating macrophage polarization and reducing cardiomyocyte apoptosis.

巨噬细胞极化在心肌缺血/再灌注（I/R）损伤中起重要作用。尽管Apelin-13以其抗炎作用而闻名，但其对心肌I/R损伤时巨噬细胞极化的影响尚不清楚。本研究旨在探讨Apelin-13对大鼠I/R模型和体外H9c2细胞巨噬细胞极化和心功能的影响。结扎左冠状动脉前降支诱导I/R损伤，再灌注时间分别为2小时和7天。体外培养H9c2细胞和腹腔巨噬细胞。通过改善血流动力学和超声心动图参数，我们发现Apelin-13可以显著改善大鼠I/R模型的心功能，减少梗死面积。Apelin-13处理通过调节Bcl-2/Bax比值减少心肌凋亡，并将巨噬细胞极化从促炎M1表型转移到修复M2表型。在体外，Apelin-13抑制lps诱导的大鼠腹膜巨噬细胞中促炎细胞因子的产生，并促进M2标记物的产生。此外，apelin -13处理巨噬细胞的条件培养基提高了氧-葡萄糖剥夺/再氧化后H9c2细胞的存活率。这些发现表明Apelin-13通过调节巨噬细胞极化和减少心肌细胞凋亡，作为一种有希望的治疗心肌I/R损伤的策略。

{"title":"Apelin-13 ameliorates myocardial ischemia/reperfusion injury by modulating macrophage polarization","authors":"Hui Jia , Qiyue Zhao , Jing Yuan , Xin Wang , Hua Chen , Jinghui Dong , Chunhua Zhu , Leonid N. Maslov , Natalia V. Naryzhnaya , Yue Guan , Huijie Ma , Zan Guo","doi":"10.1016/j.abb.2025.110710","DOIUrl":"10.1016/j.abb.2025.110710","url":null,"abstract":"<div><div>Macrophage polarization plays a crucial role in myocardial ischemia/reperfusion (I/R) injury. Although Apelin-13 is known for its anti-inflammatory effects, its impact on macrophage polarization during myocardial I/R injury remains unclear. This study aimed to investigate the effects of Apelin-13 on macrophage polarization and cardiac function in a rat I/R model and H9c2 cells in vitro. I/R injury was induced by ligating the left anterior descending coronary artery with reperfusion times of 2 h and 7 days. H9c2 cells and peritoneal macrophages were cultured in vitro. We show that Apelin-13 significantly improves cardiac function and reduces infarct size in a rat I/R model, as evidenced by improved hemodynamic and echocardiographic parameters. Apelin-13 treatment decreased myocardial apoptosis by modulating the Bcl-2/Bax ratio and shifted macrophage polarization from the pro-inflammatory M1 phenotype to the reparative M2 phenotype in vivo. In vitro, Apelin-13 suppressed LPS-induced pro-inflammatory cytokine production and promoted M2 markers in rat peritoneal macrophages. Furthermore, conditioned medium from Apelin-13-treated macrophages enhanced H9c2 cell survival following oxygen-glucose deprivation/reoxygenation. These findings suggest Apelin-13 as a promising therapeutic strategy for myocardial I/R injury by modulating macrophage polarization and reducing cardiomyocyte apoptosis.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110710"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145809257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

RHAU helicase affects testosterone synthesis by regulating the Star 3′ UTR region RHAU解旋酶通过调节Star 3' UTR区影响睾酮合成。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-02-01 Epub Date: 2025-12-05 DOI: 10.1016/j.abb.2025.110690

Zhongyu Qin , Kaixia Li , Yang Song , Yuwen Wu , Haorui Wang , Xuanjie Li , Jiayi Huang , Shuaishuai Shi , Yiqiang Zhang

This study investigates the role and regulatory mechanism of RNA helicase and RNA-binding protein RHAU in testosterone synthesis. Using molecular biology techniques, such as circular dichroism spectroscopy, RNA-protein interaction assays, gene expression analysis, and ELISA functional assays, we explored the interaction between RHAU and the 3′ untranslated region of Star mRNA, and its effect on mRNA stability and translation efficiency. The results show that conditional knockdown of RHAU leads to decreased testosterone levels in mouse blood, reduced translation of steroidogenic acute regulatory protein (STAR), and significantly increased apoptosis of testicular interstitial cells. RHAU specifically binds to the G-quadruplex structure in the 3′ untranslated region of Star mRNA, regulating STAR expression and affecting testosterone synthesis. This study is the first to reveal the critical role of RHAU in testosterone synthesis and post-transcriptional regulation. Moreover, RHAU emerges as a potential therapeutic target for diseases related to testosterone imbalance.

本研究探讨了RNA解旋酶和RNA结合蛋白RHAU在睾酮合成中的作用及其调控机制。利用分子生物学技术，如圆二色光谱、rna -蛋白相互作用分析、基因表达分析和ELISA功能分析，我们探讨了RHAU与Star mRNA 3'非翻译区相互作用及其对mRNA稳定性和翻译效率的影响。结果表明，有条件地敲低RHAU可导致小鼠血液中睾酮水平降低，类固醇急性调节蛋白（STAR）翻译减少，睾丸间质细胞凋亡显著增加。RHAU特异性结合Star mRNA 3'非翻译区g -四重体结构，调节Star表达并影响睾酮合成。这项研究首次揭示了RHAU在睾酮合成和转录后调控中的关键作用。此外，RHAU成为睾酮失衡相关疾病的潜在治疗靶点。

{"title":"RHAU helicase affects testosterone synthesis by regulating the Star 3′ UTR region","authors":"Zhongyu Qin , Kaixia Li , Yang Song , Yuwen Wu , Haorui Wang , Xuanjie Li , Jiayi Huang , Shuaishuai Shi , Yiqiang Zhang","doi":"10.1016/j.abb.2025.110690","DOIUrl":"10.1016/j.abb.2025.110690","url":null,"abstract":"<div><div>This study investigates the role and regulatory mechanism of RNA helicase and RNA-binding protein RHAU in testosterone synthesis. Using molecular biology techniques, such as circular dichroism spectroscopy, RNA-protein interaction assays, gene expression analysis, and ELISA functional assays, we explored the interaction between RHAU and the 3′ untranslated region of <em>Star</em> mRNA, and its effect on mRNA stability and translation efficiency. The results show that conditional knockdown of RHAU leads to decreased testosterone levels in mouse blood, reduced translation of steroidogenic acute regulatory protein (STAR), and significantly increased apoptosis of testicular interstitial cells. RHAU specifically binds to the G-quadruplex structure in the 3′ untranslated region of <em>Star</em> mRNA, regulating STAR expression and affecting testosterone synthesis. This study is the first to reveal the critical role of RHAU in testosterone synthesis and post-transcriptional regulation. Moreover, RHAU emerges as a potential therapeutic target for diseases related to testosterone imbalance.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110690"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145699350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 impact of urinary calcium-binding and oxalate-binding proteins on modulation of calcium oxalate renal calculi 尿钙结合蛋白和草酸结合蛋白对草酸钙肾结石调控的影响。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-02-01 Epub Date: 2025-12-22 DOI: 10.1016/j.abb.2025.110712

Sudarat Hadpech, Paleerath Peerapen, Visith Thongboonkerd

Cumulative data suggest that proteins with modulatory activities on calcium oxalate (CaOx) renal calculi commonly have calcium-binding and/or oxalate-binding domains/motifs. However, the information on calcium-binding proteins (CaBPs) and oxalate-binding proteins (OxBPs) in the urine of healthy individuals and stone formers was not available. Herein, we addressed the impact of urinary CaBPs and OxBPs on CaOx renal calculi. Large proteome datasets from recent/previous quantitative proteomics studies and all known CaOx stone modulatory proteins listed on the StoneMod (www.stonemod.org) database were retrieved and analyzed for calcium-binding and/or oxalate-binding domains/motifs. The data showed that %CaBPs decreased, whereas no. of oxalate-binding sites/protein increased in stone formers' urine. Among differentially excreted proteins, %CaBPs tended to reduce, whereas no. of oxalate-binding sites/protein tended to be greater in those with increased levels in stone formers’ urine. Interestingly, known CaOx stone inhibitory proteins tended to have greater %CaBPs and no. of calcium-binding sites/protein, whereas known CaOx promoters had no CaBPs and tended to have greater %OxBPs. Moreover, CaOx crystallization fold-change induced by the known modulators inversely correlated with no. of calcium-binding sites/protein. These data implicate the impact of CaBPs and OxBPs on CaOx renal calculi, i.e., CaBPs tend to inhibit, whereas OxBPs tend to promote CaOx calculi development.

累积数据表明，对草酸钙（CaOx）肾结石具有调节活性的蛋白质通常具有钙结合和/或草酸结合结构域/基序。然而，健康个体和结石患者尿液中钙结合蛋白（CaBPs）和草酸结合蛋白（oxbp）的信息尚不清楚。在此，我们研究了尿cabp和oxbp对CaOx肾结石的影响。从最近/以前的定量蛋白质组学研究中获得的大量蛋白质组学数据集和StoneMod （www.stonemod.org）数据库中列出的所有已知的CaOx stone调节蛋白被检索并分析钙结合和/或草酸结合结构域/基序。数据显示，cabp百分比下降，而没有。结石患者尿液中草酸结合位点/蛋白增加。在差异排泄蛋白中，%CaBPs有降低的趋势，而没有。在结石患者尿中草酸结合位点/蛋白水平增高的人群中草酸结合位点/蛋白水平增高。有趣的是，已知的CaOx结石抑制蛋白往往具有更高的cabp %，而没有。而已知的CaOx启动子没有CaBPs，并且往往具有更高的oxbp百分比。此外，已知调制剂诱导的CaOx结晶折叠变化与no呈负相关。钙结合位点/蛋白。这些数据提示CaBPs和oxbp对CaOx肾结石的影响，即CaBPs倾向于抑制CaOx肾结石的发展，而oxbp倾向于促进CaOx肾结石的发展。

{"title":"The impact of urinary calcium-binding and oxalate-binding proteins on modulation of calcium oxalate renal calculi","authors":"Sudarat Hadpech, Paleerath Peerapen, Visith Thongboonkerd","doi":"10.1016/j.abb.2025.110712","DOIUrl":"10.1016/j.abb.2025.110712","url":null,"abstract":"<div><div>Cumulative data suggest that proteins with modulatory activities on calcium oxalate (CaOx) renal calculi commonly have calcium-binding and/or oxalate-binding domains/motifs. However, the information on calcium-binding proteins (CaBPs) and oxalate-binding proteins (OxBPs) in the urine of healthy individuals and stone formers was not available. Herein, we addressed the impact of urinary CaBPs and OxBPs on CaOx renal calculi. Large proteome datasets from recent/previous quantitative proteomics studies and all known CaOx stone modulatory proteins listed on the StoneMod (<span><span>www.stonemod.org</span><svg><path></path></svg></span>) database were retrieved and analyzed for calcium-binding and/or oxalate-binding domains/motifs. The data showed that %CaBPs decreased, whereas no. of oxalate-binding sites/protein increased in stone formers' urine. Among differentially excreted proteins, %CaBPs tended to reduce, whereas no. of oxalate-binding sites/protein tended to be greater in those with increased levels in stone formers’ urine. Interestingly, known CaOx stone inhibitory proteins tended to have greater %CaBPs and no. of calcium-binding sites/protein, whereas known CaOx promoters had no CaBPs and tended to have greater %OxBPs. Moreover, CaOx crystallization fold-change induced by the known modulators inversely correlated with no. of calcium-binding sites/protein. These data implicate the impact of CaBPs and OxBPs on CaOx renal calculi, i.e., CaBPs tend to inhibit, whereas OxBPs tend to promote CaOx calculi development.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110712"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145826585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Nucleotide-dependent structural dynamics and domain motion in Coxiella burnetii EngA GTPases: Insights from molecular dynamics simulation 伯氏杆菌gtp酶的核苷酸依赖结构动力学和结构域运动：来自分子动力学模拟的见解。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-02-01 Epub Date: 2025-12-04 DOI: 10.1016/j.abb.2025.110693

K.M. Kavya , Guruswaroop C , Upendra N , Krishnaveni S

EngA, a ribosome-associated bacterial GTPase essential for 50S subunit maturation and bacterial growth, lacks a human ortholog, making it an attractive antibacterial target. Its activity is governed by a nucleotide-dependent molecular switch: GTP binding promotes EngA association with the immature 50S subunit and facilitates rRNA processing, whereas GTP hydrolysis to GDP triggers dissociation from the ribosome. Structural studies on Bacillus subtilis EngA revealed that GTP-analog-bound EngA disrupts the GD1-KH interface required for 45S subunit association, while GDP-bound EngA retains these interactions. However, the molecular mechanism by which nucleotides regulate these transitions and whether similar mechanisms exist in other pathogenic species remain unclear. To address this, 1000 ns molecular dynamics simulations of Coxiella burnetii EngA was performed in four nucleotide-bound states: [GDP:GDP], [GDP:GTP-Mg²⁺], [GTP-Mg²⁺:GDP], and [GTP-Mg²⁺:GTP-Mg²⁺]. Analyses of principal components, interaction energies, and distance-angle parameters revealed nucleotide-dependent domain dynamics. In the [GTP-Mg²⁺:GTP-Mg²⁺] state, GD1 and KH domains moved apart, forming an open conformation, while in [GDP:GDP] they approached each other, forming a closed conformation consistent with cryo-EM structures. Community network analysis further showed that GDP binding to GD1 extends connectivity from the nucleotide to SwI, stabilizing SwI-KH interactions and restricting GD1 motion. In contrast, GTP-Mg²⁺ binding disrupts this network, enabling SwI-GD2 interactions that weaken the GD1-KH interface and promote an open conformation. Overall, the results highlight how nucleotide charge-dependent interactions regulate EngA allosteric network and drive its conformational switching mechanism.

EngA是一种核糖体相关的细菌GTPase，对50S亚基成熟和细菌生长至关重要，缺乏人类同源物，使其成为一个有吸引力的抗菌靶点。其活性受核苷酸依赖的分子开关控制：GTP结合促进EngA与未成熟的50S亚基结合并促进rRNA加工，而GTP水解为GDP则触发核糖体的解离。对枯草芽孢杆菌EngA的结构研究表明，gpp -类似物结合的EngA破坏了45S亚基结合所需的GD1-KH界面，而gdp -结合的EngA保留了这些相互作用。然而，核苷酸调节这些转变的分子机制以及其他致病物种中是否存在类似机制尚不清楚。为了解决这一问题，研究人员在4种核苷酸结合状态（[GDP:GDP]、[GDP:GTP-Mg2+]、[GTP-Mg2+:GDP]和[GTP-Mg2+:GTP-Mg2+]）下进行了1000 ns的伯氏杆菌EngA分子动力学模拟。主成分、相互作用能和距离角参数的分析揭示了核苷酸依赖的结构域动力学。在[GTP-Mg2+:GTP-Mg2+]状态下，GD1和KH结构域分开，形成一个开放的构象，而在[GDP:GDP]状态下，它们彼此靠近，形成一个封闭的构象，与低温电镜结构一致。社区网络分析进一步表明，GDP与GD1的结合扩展了从核苷酸到SwI的连通性，稳定了SwI- kh相互作用并限制了GD1的运动。相比之下，GTP-Mg2+的结合破坏了这个网络，使wi - gd2相互作用削弱了GD1-KH界面并促进了开放构象。总的来说，结果强调了核苷酸电荷依赖的相互作用如何调节EngA变构网络并驱动其构象转换机制。

{"title":"Nucleotide-dependent structural dynamics and domain motion in Coxiella burnetii EngA GTPases: Insights from molecular dynamics simulation","authors":"K.M. Kavya , Guruswaroop C , Upendra N , Krishnaveni S","doi":"10.1016/j.abb.2025.110693","DOIUrl":"10.1016/j.abb.2025.110693","url":null,"abstract":"<div><div>EngA, a ribosome-associated bacterial GTPase essential for 50S subunit maturation and bacterial growth, lacks a human ortholog, making it an attractive antibacterial target. Its activity is governed by a nucleotide-dependent molecular switch: GTP binding promotes EngA association with the immature 50S subunit and facilitates rRNA processing, whereas GTP hydrolysis to GDP triggers dissociation from the ribosome. Structural studies on <em>Bacillus subtilis</em> EngA revealed that GTP-analog-bound EngA disrupts the GD1-KH interface required for 45S subunit association, while GDP-bound EngA retains these interactions. However, the molecular mechanism by which nucleotides regulate these transitions and whether similar mechanisms exist in other pathogenic species remain unclear. To address this, 1000 ns molecular dynamics simulations of <em>Coxiella burnetii</em> EngA was performed in four nucleotide-bound states: [GDP:GDP], [GDP:GTP-Mg<sup>2+</sup>], [GTP-Mg<sup>2+</sup>:GDP], and [GTP-Mg<sup>2+</sup>:GTP-Mg<sup>2+</sup>]. Analyses of principal components, interaction energies, and distance-angle parameters revealed nucleotide-dependent domain dynamics. In the [GTP-Mg<sup>2+</sup>:GTP-Mg<sup>2+</sup>] state, GD1 and KH domains moved apart, forming an open conformation, while in [GDP:GDP] they approached each other, forming a closed conformation consistent with cryo-EM structures. Community network analysis further showed that GDP binding to GD1 extends connectivity from the nucleotide to SwI, stabilizing SwI-KH interactions and restricting GD1 motion. In contrast, GTP-Mg<sup>2+</sup> binding disrupts this network, enabling SwI-GD2 interactions that weaken the GD1-KH interface and promote an open conformation. Overall, the results highlight how nucleotide charge-dependent interactions regulate EngA allosteric network and drive its conformational switching mechanism.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110693"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 “Dihydrocelastrol induces cell death and suppresses angiogenesis through BCR/AP-1/junb signalling in diffuse large B cell lymphoma” [Arch. Biochem. Biophys. 754 (2024) 109929] “在弥漫性大B细胞淋巴瘤中，双氢celastrol通过BCR/AP-1/junb信号诱导细胞死亡并抑制血管生成”的更正[Arch。物化学。生物工程学报，2016,32(2):389 - 389。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-02-01 Epub Date: 2025-10-29 DOI: 10.1016/j.abb.2025.110652

Yue Lai , Shushan Guo , Qiongwei Tang , Gaomei Chang , Hui Zhang , Bo Li , Qilin Feng , Ke Hu , Zhijian Xu , Xuejie Gao , Qikai Zhang , Hongfei Yi , Dongliang Song , Yifei Zhang , Yu Peng , Haiyan Cai , Weiliang Zhu , Jumei Shi

引用次数: 0

Corrigendum to "Folic acid-functionalized and acetyl-terminated dendrimers as nanovectors for co-delivery of sorafenib and 5-fluorouracil" [Arch. Biochem. Biophys. 762C (2024) 110176]. “叶酸功能化和乙酰端端树突状大分子作为索拉非尼和5-氟尿嘧啶共递送的纳米载体”的勘误表[Arch。物化学。[j].生物医学工程学报，2016,32(2):391 - 391。

IF 3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Archives of biochemistry and biophysics

Pub Date : 2026-01-07 DOI: 10.1016/j.abb.2025.110729

Ali Hussein Mezher, Mahboobeh Salehpour, Zohreh Saadati

引用次数: 0