Archives of biochemistry and biophysics最新文献

{"title":"Irisin Mitigates Diabetic Cardiac Damage and Is Associated with Improved Redox Status and Reduced p53/VCAM-1 mRNA Expression in STZ-Treated Rats.","authors":"Rawan AbuDalo, Esam Qnais, Yousra Bsieso, Foad Alzoughool, Muna Oqal, Abdelrahim Alqudah, Sireen Abdul Rahim Shilbayeh","doi":"10.1016/j.abb.2026.110849","DOIUrl":"https://doi.org/10.1016/j.abb.2026.110849","url":null,"abstract":"<p><strong>Background: </strong>Diabetic cardiomyopathy is driven by oxidative stress, impaired myocardial enzyme function, and inflammatory/apoptotic signaling. Irisin has emerged as a cardiometabolic regulator, but its integrated effects on cardiac redox status, enzyme activities, and injury biomarkers in diabetes remain incompletely understood.</p><p><strong>Methods: </strong>Diabetes-like cardiometabolic injury was induced in male Wistar rats by fructose pre-treatment followed by low-dose streptozotocin (40 mg/kg, i.p.). Diabetic rats were treated with irisin (100 or 500 μg/kg/day, i.p.) or metformin (200 mg/kg/day, i.p.) for 21 days. Cardiac oxidative stress markers (MDA and GSH), antioxidant enzyme activities (SOD, CAT, GPx, and GST), ATPase activities (Na⁺/K⁺-ATPase, Ca²⁺/Mg²⁺-ATPase, and Mg²⁺-ATPase), phosphatase activities (ALP and ACP), and cardiac p53 and VCAM-1 mRNA expression were assessed. Serum injury biomarkers (CK-MB, cTnI, cTnT, and NT-proBNP) and histopathological changes were also evaluated.</p><p><strong>Results: </strong>Cardiac MDA was higher, and GSH was lower in diabetic rats (both p < 0.001) with marked reductions in SOD, CAT, GPx, and GST activities (p < 0.001). Diabetes also inhibited the activities of Na + /K + -ATPase, Ca 2+ /Mg 2+ -ATPase, and Mg 2+ -ATPase (p <0.001) and reduced ALP and ACP (p <0.001). The mRNA levels of cardiac p53 and VCAM-1 were significantly elevated (p < 0.001), along with serum CK-MB, cTnI, cTnT, and NT-proBNP (p < 0.001). At 100 and 500 μg/kg, irisin significantly decreased MDA content and restored antioxidant enzymes, ATPases, phosphatases (all p < 0.001 vs diabetic control), and was associated with reduced p53 and VCAM-1 expression (p < 0.001); it also reduced CK-MB, troponins, and NT-proBNP levels (p < 0.001) more effectively at a higher tested dose (500 μg/kg). The histology results showed better myocardial architecture with irisin, similar to metformin.</p><p><strong>Conclusion: </strong>Irisin produced marked improvement in biochemical and histological indices of diabetes-induced myocardial injury and was associated with improved redox balance, reduced p53 and VCAM-1 mRNA expression, and lower circulating cardiac injury biomarkers. These findings support a descriptive association between irisin treatment and attenuation of diabetes-related myocardial injury, while further protein-level and pathway-focused studies are needed to confirm the underlying mechanisms.</p>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110849"},"PeriodicalIF":3.0,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855794","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}

{"title":"Interplay Between NRF2 Post-Translational Modifications and Protein-Protein Interactions: Perspectives from Emerging Structural and Functional Evidence.","authors":"Adem Ozleyen, Seda Savranoglu Kulabas, Miroslav Novak, Milena Cichoń, Cristina Matas De Las Heras, Tadashi Honda, Richard G Doveston, Albena T Dinkova-Kostova, Anna Grochot-Przeczek, Tugba Boyunegmez Tumer","doi":"10.1016/j.abb.2026.110847","DOIUrl":"https://doi.org/10.1016/j.abb.2026.110847","url":null,"abstract":"<p><p>Nuclear factor erythroid 2-related factor 2 (NRF2), a redox-sensitive transcription factor, is a master regulator of cellular adaptation to diverse types of stressors. Under basal conditions, the regulation of NRF2 is governed by Kelch-like ECH-associated protein 1 (KEAP1), an adaptor subunit of the CUL3-based E3 ubiquitin ligase, which promotes the ubiquitination and subsequent degradation of NRF2. However, when electrophilic or oxidative stressors alter the conformation of the KEAP1-NRF2 complex, KEAP1 loses its regulatory control over newly synthesized NRF2, leading to its accumulation and nuclear translocation, where it exerts transcriptional activity. NRF2 stability and activity are also shaped by a broader spectrum of protein-protein interactions (PPIs), including recently emerging regulators such as peptidyl prolyl isomerase (PIN1). Significantly, many of these dynamic PPI networks are regulated by post-translational modifications (PTMs), which, in turn, can be governed by these PPIs. While major PTMs such as phosphorylation and ubiquitination constitute the central regulatory processes, atypical or less-characterized modifications, including SUMOylation and O-GlcNAcylation, are gaining increasing attention for their tissue and condition-specific roles. This review compiles the latest structural and functional evidence on well-known as well as understudied PTMs and PPIs of NRF2, emphasizing the dynamic interplay between these regulatory mechanisms in shaping NRF2 signaling under physiological and stress conditions.</p>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110847"},"PeriodicalIF":3.0,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832935","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}

{"title":"miR-33a promotes peri-implantitis by facilitating M1-type polarization of macrophages and inhibiting osteogenesis.","authors":"Jianan Kang, Yi Yang, Zhen Yan","doi":"10.1016/j.abb.2026.110844","DOIUrl":"https://doi.org/10.1016/j.abb.2026.110844","url":null,"abstract":"<p><strong>Objective: </strong>miR-33a exhibits abnormal expression in patients with periodontitis. However, the underlying mechanism of miR-33a in peri-implantitis remains elusive. This study centered on investigating the mechanism of the miR-33a/SIRT6 axis in peri-implantitis.</p><p><strong>Methods: </strong>First, compare the expression levels of miR-33a in peri-implantitis tissues and healthy tissues. Second, examine the impacts of miR-33a on ALP, osteogenic markers (RUNX2, BMP-2, OCN, COL1A1), and M1-type markers (CD86, INOS, TNF-α, IL-6) in periodontal ligament stem cells (PDLSCs) or M1-type macrophages. Moreover, the effect of polarization on osteogenesis was explored by culturing PDLSCs in a medium obtained from M1-type macrophages. Finally, the regulatory effect of miR-33a on SIRT6 was validated via a dual luciferase reporter assay, and the influence of the miR-33a/SIRT6 axis on osteogenesis and macrophage polarization was investigated.</p><p><strong>Results: </strong>In clinical investigations, the expression level of miR-33a was elevated in the peri-implantitis tissues. In PDLSCs, the overexpression of miR-33a led to a reduction in the activity of ALP and the expression of osteogenic factors at both the mRNA and protein levels. Nevertheless, as the downstream target of miR-33a, SIRT6 exerted a potent promotional effect on osteogenesis. The M1-type polarization of macrophages impeded osteogenic differentiation. Furthermore, the miR-33a/SIRT6 axis also played a regulatory role in the polarization. Inhibiting miR-33a significantly downregulated the expression of M1 markers in macrophages by upregulating SIRT6.</p><p><strong>Conclusion: </strong>Peri-implantitis may be associated with miR-33a. The miR-33a/SIRT6 axis might participate in the development of peri-implantitis through the regulation of periodontal bone formation and the bone immune microenvironment.</p>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110844"},"PeriodicalIF":3.0,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832943","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}

{"title":"KLF5-mediated transcriptional activation of miR-203a inhibits EMT and increases cisplatin sensitivity by targeting SNAI2 in Tongue cancer.","authors":"Subham Kumar Behera, Anthony Lalruatfela, Sruti Biswal, Priyajit Biswal, Jiban Jyoti Dash, Deepak Kumar Behera, Bibekanand Mallick","doi":"10.1016/j.abb.2026.110845","DOIUrl":"https://doi.org/10.1016/j.abb.2026.110845","url":null,"abstract":"<p><p>Distant metastasis, cancer recurrence, and resistance to chemotherapy together are responsible for poor prognosis and create challenges for effective treatment of tongue squamous cell carcinoma (TSCC) or tongue cancer. Consequently, identifying key molecular regulators that simultaneously modulate tumor progression and drug resistance is crucial to improving therapeutic outcomes. In this study, we investigated hub transcription factors (TFs) that regulate multiple tumorigenic and drug-resistance-associated processes and elucidated their downstream regulatory molecular mechanisms by integrating gene and miRNA expression analyses, pathway enrichment, miRNA target prediction, and several experimental molecular assays in TSCC cell lines, including cisplatin-resistant cells. We identified that KLF5 is significantly downregulated in TSCC, where it functions as a key suppressor of cell migration and epithelial-mesenchymal transition (EMT). Mechanistically, KLF5 transcriptionally activates miR-203a, which suppresses EMT and restores cisplatin sensitivity in resistant TSCC cells by directly targeting SNAI2. Furthermore, the drug efflux transporter ABCC1 is co-expressed with SNAI2, and miR-203a-mediated inhibition of SNAI2 reduced ABCC1 expression, leading to increased cisplatin accumulation, DNA damage, and cell death. Collectively, our findings reveal a KLF5-miR-203a-SNAI2 regulatory axis that modulates EMT and chemoresistance in TSCC, highlighting a potential therapeutic approach to overcome cisplatin resistance.</p>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110845"},"PeriodicalIF":3.0,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832863","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}

{"title":"Inhibitory Effects of Polyphyllin VII on Cytochrome P450 2C19, 2D6, 2E1, and 3A4 in Human Liver Microsomes.","authors":"Zhongxia Guo, Xiaolin An, Hui Liu","doi":"10.1016/j.abb.2026.110842","DOIUrl":"https://doi.org/10.1016/j.abb.2026.110842","url":null,"abstract":"<p><strong>Background: </strong>Polyphyllin VII is a major active component extracted from the traditional Chinese medicinal plant Paris polyphylla. It exhibits antitumor and anti-inflammatory activities, positioning it as a promising drug candidate. Nevertheless, its potential to induce drug-drug interactions remains unknown.</p><p><strong>Objective: </strong>The effects of polyphyllin VII on eight key cytochrome P450 (CYP450) isoenzymes were assessed using human liver microsomes, providing insights to inform its drug development and clinical use.</p><p><strong>Methods: </strong>Using specific probe substrates, the effects of polyphyllin VII on CYP1A2, 2A6, 2C9, 2D6, 2C19, 2C8, 2E1, and 3A4 were evaluated in human liver microsomes. The inhibition patterns were characterized through Lineweaver-Burk plots to determine the corresponding kinetic parameters.</p><p><strong>Results: </strong>Polyphyllin VII suppressed the activity of CYP2C19, 2D6, 2E1, and 3A4. The inhibition of CYP2C19, 2D6, 2E1, and 3A4 by polyphyllin VII was concentration-dependent, with IC₅₀ values of 21.41 ± 2.59, 18.88 ± 2.20, 9.83 ± 1.85, and 12.54 ± 1.93 μM, respectively. Polyphyllin VII was a competitive inhibitor of CYP2C19, 2D6, and 2E1, and a noncompetitive inhibitor of CYP3A4, with K_i values of 10.70, 9.52, 5.28, and 6.39 μM, respectively. Additionally, the inhibitory effect of polyphyllin VII on CYP3A4 was time-dependent, with K_I and K_inact values of 5.60 μM and 0.038 min^-1.</p><p><strong>Conclusions: </strong>This study highlights the inhibitory characteristics of polyphyllin VII on the activity of CYP2C19, 2D6, 2E1, and 3A4. Although these findings require further in vivo studies and clinical validation, polyphyllin VII has the potential to interact with other drugs metabolized by CYP2C19, 2D6, 2E1, and 3A4.</p>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110842"},"PeriodicalIF":3.0,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832906","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}

{"title":"A ninhydrin-based colorimetric assay for monitoring (S)-Norcoclaurine synthase activity through dopamine quantification.","authors":"Brunno A Salvatti, Yan F X Ladeira, Diego M Martins, Amanda S de Miranda, Adolfo H Moraes","doi":"10.1016/j.abb.2026.110828","DOIUrl":"10.1016/j.abb.2026.110828","url":null,"abstract":"<p><p>(S)-Norcoclaurine synthase ((S)-NCS) catalyzes the stereoselective Pictet-Spengler condensation between dopamine and 4-hydroxyphenylacetaldehyde, forming (S)-norcoclaurine, a central precursor in benzylisoquinoline alkaloid biosynthesis. Beyond its biological role, (S)-NCS is a promising biocatalyst for the sustainable synthesis of chiral tetrahydroisoquinolines, which are valuable scaffolds in medicinal chemistry. However, broader application of this enzyme in biocatalysis remains limited by the lack of simple, selective, non-expensive, and high-throughput methods to quantify its activity. Herein, we describe a straightforward colorimetric method to monitor (S)-NCS activity by selectively detecting dopamine using ninhydrin. Our protocol combines ethanol-induced enzyme precipitation with mild incubation conditions, ensuring reliable, interference-free quantification by standard UV-Vis spectrophotometry. This low-cost, straightforward assay provides a robust alternative to conventional analytical methods. It has the potential to be adapted for high-throughput screening and may serve as a starting point for developing methods to monitor other enzymatic reactions that consume primary amines, facilitating studies in enzyme engineering and sustainable biocatalysis.</p>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110828"},"PeriodicalIF":3.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809999","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}

{"title":"Unlocking ferroptosis: A novel link between triple-negative breast cancer and immune regulation","authors":"Laura Montero-León ,&nbsp;Alfredo Cruz-Gregorio ,&nbsp;Estefani Yaquelin Hernández-Cruz ,&nbsp;Edda Sciutto ,&nbsp;Gladis Fragoso ,&nbsp;José Pedraza-Chaverri","doi":"10.1016/j.abb.2026.110760","DOIUrl":"10.1016/j.abb.2026.110760","url":null,"abstract":"<div><div>Breast cancer is the most diagnosed malignant tumor worldwide and remains the leading cause of cancer-related death among women. Among its subtypes, triple-negative breast cancer (TNBC) is the most aggressive form, resulting in limited treatment options and a poorer prognosis. The development of novel therapeutic strategies is both urgent and challenging. Ferroptosis is a recently identified form of regulated cell death that is iron-dependent and characterized by the abnormal accumulation of lipid peroxides and iron ions. Ferroptosis is critical for tumorigenesis, progression, metastasis, and therapeutic resistance in breast cancer, positioning its modulation as a promising complementary strategy. Furthermore, the tumor microenvironment is affected by either inhibiting or inducing ferroptosis in immune cells—promoting tumor proliferation, therapeutic resistance, or, in combination with radiotherapy, antioxidants, or ferritinophagy activators, facilitating tumor eradication. Despite the expanding literature on ferroptosis and cancer, a critical gap remains in understanding how ferroptosis operate in tumor cells versus immune cells within the TNBC microenvironment. This lack of integration hampers the rational design of therapeutic strategies that induce ferroptosis in cancer cells while preserving- or enhancing-antitumor immunity. This review addresses this gap by providing a unified framework linking ferroptosis, immune regulation, and emerging therapeutic strategies in TNBC.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"779 ","pages":"Article 110760"},"PeriodicalIF":3.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146148959","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}

{"title":"Discovery and functional validation of a gut microbiota-metabolite-miRNA axis in diabetic encephalopathy","authors":"Haitian Sun ,&nbsp;Jingzhi Liu ,&nbsp;Yanxiao Jing ,&nbsp;Guanghong Li ,&nbsp;Xinhuan Zhang","doi":"10.1016/j.abb.2026.110759","DOIUrl":"10.1016/j.abb.2026.110759","url":null,"abstract":"<div><h3>Background</h3><div>Diabetic encephalopathy (DE), a severe neurological complication of diabetes, is characterized by cognitive decline and neuronal damage. While gut microbiota dysbiosis has been implicated in diabetes pathogenesis, its specific role and molecular mechanisms in DE remain unclear.</div></div><div><h3>Methods</h3><div>A multi-omics approach integrating 16S rRNA sequencing and untargeted metabolomics was performed on fecal samples from 29 DE patients and 31 diabetic controls (DM). An in vitro DE model was established using high glucose (HG)-treated HT22 cells, which were further incubated with sterile fecal microbiota supernatant (FMS) from DE patients. Neuronal viability, apoptosis, oxidative stress markers (SOD, MDA, ROS), and miR-493-3p expression were assessed. The miR-493-3p/RAF1 interaction was validated using dual-luciferase reporter assays and Western blot.</div></div><div><h3>Results</h3><div>No significant differences in overall microbial diversity were identified in DE and DM cohorts. However, DE patients exhibited distinct gut microbiota composition, with elevated Verrucomicrobiotaand Bacteroidota, and reduced Proteobacteriaand Firmicutes. Metabolomic analysis revealed 160 differentially abundant metabolites enriched in amino acid and lipid metabolism pathways. In vitro, DE-derived FMS dose-dependently exacerbated HG-induced neuronal oxidative damage and apoptosis, concomitant with miR-493-3p upregulation. Inhibition of miR-493-3p attenuated these damaging effects and restored RAF1 expression. RAF1 was confirmed as a direct target of miR-493-3p, and its downregulation was critical in mediating FMS-induced neuronal injury.</div></div><div><h3>Conclusion</h3><div>This study identified a novel gut-brain axis pathway in DE, whereby gut microbiota dysbiosis and metabolic alterations promote neuronal damage via the miR-493-3p/RAF1 signaling axis. These findings provide new insights into DE pathogenesis and suggest potential therapeutic targets for this debilitating complication.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"779 ","pages":"Article 110759"},"PeriodicalIF":3.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146130874","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}

{"title":"CHARACTERIZATION OF A NOVEL NON-CANONICAL THIOREDOXIN FROM Entamoeba histolytica SPECIFIC TO CYSTINE REDUCTION.","authors":"Franco Birocco, Lihue N Gonzalez, Sebastián F Villar, Belén Márquez de Los Santos, Sergio A Guerrero, Alberto A Iglesias, Gerardo Ferrer-Sueta, Diego G Arias","doi":"10.1016/j.abb.2026.110841","DOIUrl":"https://doi.org/10.1016/j.abb.2026.110841","url":null,"abstract":"<p><p>Entamoeba histolytica, a unicellular parasite, has negligible glutathione levels and instead relies on cysteine as its primary intracellular thiol. It has a functional thioredoxin (TRX) system, which consists of four canonical TRXs and thioredoxin reductase (TRXR). We identified a coding sequence for a putative non-canonical TRX with a WCKDC redox-active motif (EhTRX212, Uniprot M2QBU7) within the E. histolytica HM-1:IMSS genome. We produced the recombinant protein and conducted its biochemical characterization. Steady-state kinetic assays revealed that EhTRX212 is not reduced by EhTRXR nor directly reduces protein disulfides. Instead, EhTRX212 catalyzes the reduction of cystine, S-nitrosocysteine, and cysteine-derived heterodisulfides through a coupled reaction with EhTRX8 (a canonical TRX) and EhTRXR. Complementary pre-steady-state kinetics, using stopped-flow methodology, showed that the reduction of cystine by EhTRX212 follows a biphasic temporal progression, consistent with a thiol-disulfide exchange mechanism. The first phase (nucleophilic cysteine attack on the cystine disulfide) followed second-order kinetics (k = 2.4 × 10⁶ M^-1 s^-1), while the second phase (mixed disulfide resolution) followed first-order kinetics (k = 11 s^-1). Chemical modifications, on the amino group of the cysteine in disulfide substrates, impaired reduction by EhTRX212. Finally, confocal microscopy and digitonin subcellular fractionation experiments localized EhTRX212 to the trophozoite cytoplasm. This study strongly supports the existence of a novel class of TRXs with high specificity for cystine reduction, expanding our understanding of TRX function in E. histolytica and suggesting important roles for these proteins in the redox metabolism of this parasitic pathogen.</p>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110841"},"PeriodicalIF":3.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809971","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}

{"title":"Retraction notice to \"The angiotensin-converting enzyme 2/angiotensin (1-7)/mas axis protects against pyroptosis in LPS-induced lung injury by inhibiting NLRP3 activation\" [Arch. Biochem. Biophys. 693 (2020) 108562].","authors":"Haihua Huang, Jin Wang, Zhenwei Liu, Fengying Gao","doi":"10.1016/j.abb.2026.110835","DOIUrl":"https://doi.org/10.1016/j.abb.2026.110835","url":null,"abstract":"","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110835"},"PeriodicalIF":3.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809981","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}