Archives of biochemistry and biophysics最新文献

{"title":"BHMT Prevents renal ischemia/reperfusion injury via suppressing ROS-induced apoptosis by targeting NOX4","authors":"Chong Sun ,&nbsp;Hao Hu ,&nbsp;Xinwei Yuan ,&nbsp;Xingyu Chen ,&nbsp;Fang Fang ,&nbsp;Yunlong Liu ,&nbsp;Zhijun Chen ,&nbsp;Han Guan","doi":"10.1016/j.abb.2026.110745","DOIUrl":"10.1016/j.abb.2026.110745","url":null,"abstract":"<div><h3>Background</h3><div>Ischemia/reperfusion injury (IRI) is a major cause of acute kidney injury (AKI), primarily driven by the increased production of reactive oxygen species (ROS). Elevated ROS levels can lead to cell apoptosis. However, effective therapeutic targets for IRI remain limited.</div></div><div><h3>Purpose</h3><div>This study aims to investigate the potential mechanisms by which BHMT modulates IRI.</div></div><div><h3>Methods</h3><div>RT-qPCR and Western blot were used to assess RNA and protein expression levels. MTT assay, flow cytometry, and ROS-related assays were employed to evaluate renal cell injury <em>in vitro</em>. Mechanistic studies were conducted to explore molecular interactions, while <em>in vivo</em> assays were used to assess IRI.</div></div><div><h3>Results</h3><div>Betaine-homocysteine S-methyltransferase (BHMT) was found to be downregulated in both ischemia/reperfusion (I/R) and hypoxia/reoxygenation (H/R) models. BHMT overexpression mitigated the effects of H/R or I/R on ROS production and cell apoptosis. Mechanistically, BHMT enhanced the synthesis of S-adenosylmethionine (SAM), which in turn increased DNA-methyltransferase (DNMT) activity. This facilitated methylation of the NADPH Oxidase 4 (NOX4) promoter, suppressing NOX4 transcription and expression. Rescue assays confirmed that BHMT reduced ROS production and cell apoptosis in H/R-treated renal cells by downregulating NOX4. Furthermore, elevated expression of Samd4a in I/R accelerated renal fibrosis progression through activation of the Wnt/β-catenin signaling pathway.</div></div><div><h3>Conclusion</h3><div>BHMT reduces ROS-induced apoptosis by downregulating NOX4, offering protection against renal IRI. Additionally, targeting Samd4a expression may provide a therapeutic approach for preventing chronic kidney disease in kidney injury models.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"778 ","pages":"Article 110745"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123378","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":"Exosomes derived from HISLA overexpressed-adipose stem cells accelerate wound healing in diabetic foot ulcers by regulating HIF-1α signal transduction","authors":"Wei Zhao ,&nbsp;Haili Zhang ,&nbsp;Shujun Liu ,&nbsp;Yahui Cao ,&nbsp;Caisheng Wang ,&nbsp;Yanfei Wang","doi":"10.1016/j.abb.2026.110747","DOIUrl":"10.1016/j.abb.2026.110747","url":null,"abstract":"<div><div>Diabetic foot ulcers (DFUs), characterized by impaired angiogenesis and a chronic inflammatory milieu, represent a severe complication of diabetes. This study investigates the therapeutic potential of exosomes derived from HISLA-overexpressing adipose-derived stem cells (HISLA-ex) in enhancing DFU healing. <em>In vitro</em>, under high glucose conditions, HISLA-ex significantly elevated HISLA expression by approximately 3-fold in endothelial cells, markedly improving cell viability at 24–72 h in HMEC-1 cells, reducing pro-inflammatory cytokines IL-1 and IL-6, and enhancing tube formation capacity as evidenced by increased branching points and total tube length. Subsequently, a DFU rat model was established by inducing diabetes with streptozotocin followed by creation of a full-thickness cutaneous wound on the foot dorsum. HISLA-ex application substantially accelerated wound closure and modulated key angiogenic factors: upregulating VEGFA and Ang-1 while suppressing TSP-1. Furthermore, HISLA-ex shifted the helper T (Th)1/Th2 balance by inhibiting T-bet and pro-inflammatory cytokines (IFN-γ and TNF-α) and promoting GATA3 and anti-inflammatory cytokines (IL-4 and IL-13) <em>in vivo</em> and <em>in vitro</em>. Mechanistically, these effects were mediated through activation of the HIF-1α pathway, confirmed by both gain- and loss-of-function experiments, and abolished upon HIF-1α inhibition. Collectively, our results demonstrate that HISLA-ex synchronously promotes angiogenesis and corrects Th immune dysfunction, offering a novel RNA-based exosomal therapeutic strategy for the treatment of DFUs.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"778 ","pages":"Article 110747"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146045943","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":"New insight into the self-association of human apolipoprotein A-I","authors":"Bryan Y. Kang ,&nbsp;Juliette M. Warner ,&nbsp;Paul M.M. Weers","doi":"10.1016/j.abb.2026.110731","DOIUrl":"10.1016/j.abb.2026.110731","url":null,"abstract":"<div><div>Apolipoprotein A-I (apoA-I) is a critical plasma protein responsible for high-density lipoprotein formation, playing a vital role in reverse-cholesterol transport. Lipid-free apoA-I has two domains, an N-terminal helix bundle and a structurally less organized C-terminal (CT) region. In solution, apoA-I self-associates, which is mediated by the CT domain. To gain insight into the self-associated state, cysteine was introduced in each of the three putative α-helices of the CT domain: S201C for helix-8, Q216C for helix-9, and S231C for helix-10, and a S25C mutation served as a control. The single cysteine mutants were covalently labeled with pyrene, a spatially sensitive probe producing fluorescence excimers when in close proximity. At a protein concentration of 0.2 mg/mL, strong excimers were observed for S201C-pyrene-labeled apoA-I, while excimer intensity was weaker for Q216C- and S231C-pyrene-labeled apoA-I. When the protein was diluted 10-fold, pyrene excimer fluorescence was reduced, but excimer fluorescence remained strong for S201C-apoA-I, implying the protein remained in a self-associated state. Cysteine-specific crosslinking was more efficient for S201C compared to Q216C and S231C apoA-I mutants, in agreement with the pyrene excimer analysis. Size-exclusion chromatography demonstrated that at 0.02 mg/mL, apoA-I is present as a mixture of monomers and dimers, and therefore the observed pyrene excimers at 0.02 mg/mL are caused by dimerization of apoA-I. In the apoA-I dimer, helix-8 is more buried and positioned near a neighboring helix-8, while helices-9 and -10 are further apart and more exposed. This structural arrangement potentially results in an optimal position for helix-10 to engage in lipid binding.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"778 ","pages":"Article 110731"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145931877","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":"Influence of HIF1A-AS2 and miR-590-3p on trophoblast function and inflammation control in HTR-8/SVneo trophoblast cells","authors":"Peiqu Zhong ,&nbsp;Xiaoping Jia ,&nbsp;Qiongfang Chen ,&nbsp;Fengmei Tang ,&nbsp;Wanying Liang ,&nbsp;Youcai Liang ,&nbsp;Jiayuan Zhang ,&nbsp;Lijian Zhao","doi":"10.1016/j.abb.2026.110738","DOIUrl":"10.1016/j.abb.2026.110738","url":null,"abstract":"<div><div>Hypoxia-inducible factor 1 alpha antisense RNA 2 (HIF1A-AS2) and microRNA-590-3p (miR-590-3p) have been linked to inflammation and preeclampsia. In HTR-8/SVneo cells, HIF1A-AS2 was overexpressed and miR-590-3p mimic was introduced, and proliferation, migration/invasion and apoptosis were assessed by proliferation assays, wound-healing and Matrigel invasion assays, and flow cytometry, while molecular alterations were analyzed by quantitative reverse transcription polymerase chain reaction, western blotting, and immunofluorescence. HIF1A-AS2 overexpression enhanced proliferation and motility and reduced apoptosis, increased insulin-like growth factor 2 messenger RNA-binding protein 1 (IGF2BP1), and decreased NLR family pyrin domain containing 3 (NLRP3), gasdermin D (GSDMD) and cleaved caspase-1. Conversely, miR-590-3p suppressed IGF2BP1 and partially reversed HIF1A-AS2-associated phenotypes. Together, these data defined a HIF1A-AS2–miR-590-3p–IGF2BP1 axis linking trophoblast behaviour to inflammatory effector signalling.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"778 ","pages":"Article 110738"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028318","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":"LncRNA KCNQ1OT1 modulates M2 macrophage polarization and angiogenic signaling via the miR-142-3p/TRIM24 axis in retinal neovascularization","authors":"Chunhong Yu ,&nbsp;Weiwei Xiong ,&nbsp;Yuezhi Zhang ,&nbsp;Hongwei Lu ,&nbsp;Liwen Xu ,&nbsp;Zijing Ouyang","doi":"10.1016/j.abb.2026.110750","DOIUrl":"10.1016/j.abb.2026.110750","url":null,"abstract":"<div><h3>Background</h3><div>Retinopathy of prematurity (ROP) is a major cause of childhood blindness, driven by hypoxia-induced VEGF overproduction. Anti-VEGF therapy has limitations including recurrence and potential side effects, highlighting the need for upstream interventions. M2 macrophages contribute to ROP pathogenesis, but the regulatory mechanisms controlling their polarization remain unclear.</div></div><div><h3>Methods</h3><div>We explored the regulatory interplay among lncRNA KCNQ1OT1, miR-142-3p, and TRIM24 in RAW264.7 and THP-1 macrophages, human retinal microvascular endothelial cells (HRMECs), and an oxygen-induced retinopathy (OIR) mouse model. Interactions were validated via dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. Effects on macrophage polarization and endothelial function were assessed using flow cytometry, immunofluorescence, and proliferation, migration, and tube formation assays. OIR mice received AAV-mediated KCNQ1OT1 delivery, followed by retinal histology, immunostaining, cytokine measurements, TUNEL assays, RT-qPCR, and Western blot analyses.</div></div><div><h3>Results</h3><div>KCNQ1OT1 acted as a competitive endogenous RNA to sequester miR-142-3p, partially relieving suppression of TRIM24 and attenuating STAT6-mediated M2 polarization. In macrophages, KCNQ1OT1 overexpression reduced M2 markers and VEGFA expression, diminishing pro-angiogenic effects on HRMECs. In OIR mice, AAV-KCNQ1OT1 delivery was associated with reduced retinal neovascularization, decreased M2 macrophage infiltration, and lower VEGFA and inflammatory cytokine levels.</div></div><div><h3>Conclusions</h3><div>The KCNQ1OT1/miR-142-3p/TRIM24 axis influences macrophage polarization and angiogenic signaling in ROP. While preliminary, these findings suggest that targeting this upstream regulatory network may complement existing VEGF-targeted therapies.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"778 ","pages":"Article 110750"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137063","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":"The regulation of CP-31398 on liquid-liquid phase separation of p53","authors":"Yang Liu ,&nbsp;Chang Xu ,&nbsp;Fangming Jiang ,&nbsp;Xiaorong Yang","doi":"10.1016/j.abb.2026.110735","DOIUrl":"10.1016/j.abb.2026.110735","url":null,"abstract":"<div><div>The tumor suppressor p53 could regulate the cell cycle arrest, DNA repair and apoptosis. It underwent liquid-liquid phase separation (LLPS) to form droplets. CP-31398 was thought as the activator of p53. In this work, the regulation of CP-31398 on the LLPS of p53 was investigated. The results revealed that CP-31398 promoted the LLPS of p53, delayed the solidification of p53 droplets and increased the mobility of p53 droplets. It also enhanced the tolerance of p53 droplets to the negative charges, and improved the phase behavior of heterotypic p53-pol II CTD droplets. The p53-CP-31398 droplets were driven by hydrogen bonds, hydrophobic and electrostatic interactions. These findings clarified that CP-31398 could elevate the transcriptional function of p53 probably by modulating the phase behavior. The study provided new insights into the regulation mechanism of p53 and potential therapeutic avenues for cancer.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"778 ","pages":"Article 110735"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145996449","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":"The lncRNA SENCR of polymorphism rs12420823 drives breast cancer progression and its overexpression regulates this process via the miR-3648/FOXD3 axis","authors":"Lingjun Kong ,&nbsp;Jiajie Xue ,&nbsp;Jiaqi Yang ,&nbsp;Jianxing Chen ,&nbsp;Caiqin Mo","doi":"10.1016/j.abb.2026.110732","DOIUrl":"10.1016/j.abb.2026.110732","url":null,"abstract":"<div><div>The roles of long noncoding RNA SENCR (lncRNA SENCR) and its variant rs12420823 in triple-negative breast cancer (TNBC) susceptibility, progression, and molecular mechanisms remain unclear. thus, this study investigated the association of lncRNA SENCR and rs12420823 with TNBC risk and prognosis and explored the functional SENCR/miR-3648/FOXD3 axis. This study involving 205 TNBC patients and 203 controls, the rs12420823 polymorphism was genotyped and clinically correlated, revealing that the C allele is associated with reduced TNBC risk, while the TT genotype correlates with larger tumors, lymph node metastasis, advanced stage, and poorer survival. Prognosis was evaluated using Kaplan. The lncRNA SENCR and its variant rs12420823 play significant roles in TNBC Meier survival analysis and multivariate Cox regression. Through qRT-PCR analysis of serum and cell lines, lncRNA SENCR was found downregulated in TNBC, especially in TT genotype carriers. Mechanistic investigations, including luciferase reporter and RNA immunoprecipitation (RIP) assays, demonstrated that lncRNA SENCR directly binds to miR-3648, which targets FOXD3. Functional assays such as MTT and Transwell experiments showed that SENCR overexpression suppresses TNBC cell proliferation, migration, and invasion, effects reversed by a miR-3648 mimic. Furthermore, SENCR upregulates FOXD3 mRNA, an effect also abolished by miR-3648. In conclusion, the rs12420823 C allele confers protection against TNBC, and lncRNA SENCR acts as a tumor suppressor by sponging miR-3648 to regulate FOXD3, underscoring its prognostic and therapeutic relevance.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"778 ","pages":"Article 110732"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145942268","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":"Structural and biochemical characterization of a GH5_22 enzyme from the seaweed-derived thermophile Geobacillus thermodenitrificans OS27","authors":"Wonkyu Lee ,&nbsp;Tomoya Hino ,&nbsp;Kenta Fujii ,&nbsp;Sugue Tanimoto ,&nbsp;Reno Naka ,&nbsp;Koya Hara ,&nbsp;Takaki Okamoto ,&nbsp;Fumiyoshi Okazaki ,&nbsp;Shingo Nagano ,&nbsp;Takashi Ohshiro ,&nbsp;Hirokazu Suzuki","doi":"10.1016/j.abb.2026.110736","DOIUrl":"10.1016/j.abb.2026.110736","url":null,"abstract":"<div><div><em>Geobacillus thermodenitrificans</em> OS27 is a seaweed-derived thermophile that harbors a GH5_22 gene (<em>bxlA</em>) that encodes for a glycoside hydrolase fused with the cyclin box domain. In this study, we characterized the catalytic activity, enzymatic properties, three-dimensional structure, and physiological role of the gene product, GtBxlA. The enzyme was produced as a thermostable dimer, acting on <em>p</em>-nitrophenyl-β-<span>d</span>-xylopyranoside among 23 substrates. β-1,4-Linked xylooligosaccharides were also hydrolyzed from the nonreducing end. The activity indicated that GtBxlA functions as an exo-β-1,4-xylosidase. We determined the crystal structure of the Glu188Ala variant complexed with β-1,4-xylotriose at 1.52 Å resolution. GtBxlA exhibited an atypical (β/α)₈-barrel architecture. The cyclin box constituted a single α-helix within the core barrel and a lid-like domain that contributes to dimer formation. Structural analysis revealed that Glu188 and Glu318 are positioned to serve as the acid/base and nucleophile catalysts, respectively. Alanine mutagenesis confirmed the essential role of Glu188 and Glu318 in catalysis. We also determined the ligand-free structure of the Glu188Ala variant. Both structures were almost identical; however, a loop at the substrate entry site was fixed in the ligand-free structure, suggesting a conformational change upon substrate binding. Although <em>bxlA</em> deletion did not affect β-1,4-xylan utilization, its expression was induced by β-1,4-xylan. These observations suggest that <em>G</em>. <em>thermodenitrificans</em> OS27 employed GtBxlA in utilizing β-1,4-xylan. Notably, GtBxlA could hydrolyze β-1,3-linked xylooligosaccharides. This highlights the possibility that GtBxlA also assists the host in utilizing β-1,3-xylan, which is abundant in certain seaweeds.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"778 ","pages":"Article 110736"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997181","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":"Systems analysis of the kinetics of in vitro transcription from interactions of T7 RNA polymerase and DNA","authors":"Nathan M. Stover ,&nbsp;Marieke De Bock ,&nbsp;Julie Chen,&nbsp;Jacob Rosenfeld,&nbsp;Maria del Carme Pons Royo,&nbsp;Allan S. Myerson,&nbsp;Richard D. Braatz","doi":"10.1016/j.abb.2026.110737","DOIUrl":"10.1016/j.abb.2026.110737","url":null,"abstract":"<div><div>The in vitro transcription reaction (IVT) is of growing importance for the manufacture of RNA vaccines and therapeutics. While the kinetics of the microscopic steps of this reaction (promoter binding, initiation, and elongation) are well studied, the rate law of overall RNA synthesis that emerges from this system is unclear. In this work, we show that a model that incorporates both initiation and elongation steps is essential for describing trends in IVT kinetics in conditions relevant to RNA manufacturing. In contrast to previous reports, we find that the IVT reaction can be either initiation- or elongation-limited depending on solution conditions. This initiation-elongation model is also essential for describing the effect of salts, which disrupt polymerase-promoter binding, on transcription rates. Polymerase-polymerase interactions during elongation are incorporated into our modeling framework and found to have nonzero but unidentifiable effects on macroscopic transcription rates. Finally, we develop an extension of our modeling approach to quantitatively describe and experimentally evaluate RNA- and DNA-templated mechanisms for the formation of double-stranded RNA (dsRNA) impurities.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"778 ","pages":"Article 110737"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997261","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":"RNA binding motif protein 15 promotes intracerebral hemorrhage progression by regulating mitophagy through E2F transcription factor 1","authors":"Jiwei Sun ,&nbsp;Ning Li ,&nbsp;Yesen Zhang,&nbsp;Jian Song,&nbsp;Yi Han","doi":"10.1016/j.abb.2026.110746","DOIUrl":"10.1016/j.abb.2026.110746","url":null,"abstract":"<div><div>RNA binding motif protein 15 (RBM15) has been implicated in the progression of various diseases. However, its role in intracerebral hemorrhage (ICH) remains inadequately understood. To investigate RBM15's involvement in ICH, an ICH model was established using HT-22 cells and C57BL/6 mice. Elevated RBM15 expression levels were observed, suggesting its critical role in ICH pathogenesis. Our study further revealed that RBM15 depletion significantly mitigated ICH-induced brain injury and enhanced neurological function. Furthermore, RBM15 was found to mediate the N6-methyladenosine (m6A) methylation of E2F transcription factor 1 (E2F1) mRNA, thereby enhancing its stability. Further analysis confirmed that RBM15 regulates mitophagy via E2F1, with E2F1 overexpression effectively counteracting mitophagy in the absence of RBM15. Collectively, these findings indicate that targeting RBM15 may offer a promising therapeutic strategy for ICH.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"778 ","pages":"Article 110746"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146025838","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}