Biochemical and biophysical research communications最新文献

{"title":"Corrigendum to \"YEATS2/TAK1 axis mediates TGF-β1 driven adaptive resistance to sorafenib in hepatocellular carcinoma\" [Biochem. Biophys. Res. Commun. 817 (2026) 153693].","authors":"Lizhi Bai, Yu Wang, Guanyi Li, Yi Song, Yongliang Yu, Rongbin Tang","doi":"10.1016/j.bbrc.2026.153863","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153863","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"153863"},"PeriodicalIF":2.2,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855547","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 potential roles of nicotinic acetylcholine receptors in the pathogenesis of multiple sclerosis: A comprehensive review.","authors":"Narges Dastmalchi, Khalil Hajiasgharzadeh","doi":"10.1016/j.bbrc.2026.153906","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153906","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is a chronic immune-mediated disorder of the central nervous system characterized by inflammation, demyelination, and neurodegeneration. Growing evidence suggests that nicotinic acetylcholine receptors (nAChRs), key components of the cholinergic system, play an important role in regulating immune responses and neuroinflammation. In the present review, we summarize and critically evaluate experimental and clinical evidence supporting the involvement of nAChRs in MS pathogenesis. Particular emphasis is placed on receptor subtype-specific effects, including the anti-inflammatory and immunomodulatory properties of α7-containing nAChRs and the emerging roles of α9 and α10 subunits. We also discuss the complex relationship between smoking, nicotine exposure, and MS progression, highlighting the divergent effects of pure nicotine versus other tobacco smoke constituents. Understanding the mechanisms by which nAChRs influence immune cell function, cytokine production, and neurodegeneration may provide novel therapeutic insights and identify new molecular targets for MS treatment.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153906"},"PeriodicalIF":2.2,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833022","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":"BAG3^V468M impairs proteasomal protein clearance and induces dilated cardiomyopathy in vivo.","authors":"Federica Diofano, Ionela Emilia Giorgiana Madac, Dennis Koeble, Wolfgang Rottbauer, Karolina Weinmann-Emhardt, Steffen Just","doi":"10.1016/j.bbrc.2026.153900","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153900","url":null,"abstract":"<p><p>Idiopathic dilated cardiomyopathy (DCM) is one of the major causes of heart failure, characterized by left ventricular dilation and systolic dysfunction in the absence of an identifiable cause, and is associated with reduced life expectancy. Genetic studies, including genome-wide association studies, have identified variants in BAG3, a key regulator of protein quality control (PQC), as contributors to both familial and sporadic forms of DCM. Impaired PQC and the accumulation of misfolded proteins (proteinopathy) have emerged as potential pathogenic mechanisms. Here, we investigated the molecular consequences of a recently identified BAG3 missense variant (V468 M) associated with familial DCM. To assess the in vivo effects of the variant, human BAG3^V468M was ectopically expressed in wild-type zebrafish embryos. Overexpression of BAG3^V468M resulted in a DCM-like phenotype characterized by ventricular dilation, reduced heart rate, and impaired contractility. Transmission electron microscopy revealed marked disruption of myocardial ultrastructure and sarcomeric organization. To explore the impact on proteostasis, markers of autophagy (LC3-I/II and p62) were analyzed and showed no significant differences between BAG3^V468M and control embryos under basal conditions. In contrast, analysis of the ubiquitin-proteasome system demonstrated a significant accumulation of ubiquitinated proteins in BAG3^V468M-expressing embryos, suggesting impaired proteasomal protein clearance or increased proteotoxic stress. Expression of BAG3^V468M induces a DCM-like phenotype in vivo associated with disrupted myocardial architecture and altered proteostasis. While canonical autophagy markers remain unchanged, the accumulation of ubiquitinated proteins points toward a disturbance in ubiquitin-mediated protein turnover. These findings implicate mutation-specific alterations in proteostasis as a potential mechanism contributing to BAG3-associated cardiomyopathy.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153900"},"PeriodicalIF":2.2,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832862","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":"FFA4 inhibits bleomycin-induced pulmonary fibrosis in mice by suppressing IL-33.","authors":"Jingjing Feng, Hao Dong, Songlou Yin","doi":"10.1016/j.bbrc.2026.153883","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153883","url":null,"abstract":"<p><strong>Background: </strong>Interstitial lung disease is one of the most severe pulmonary complications of connective tissue diseases and is associated with high mortality and poor prognosis due to the lack of effective therapies. Free fatty acid receptor 4, a receptor activated by long-chain unsaturated fatty acids, participates in the regulation of inflammatory responses; however, its direct role and underlying mechanisms in ILD-related pulmonary fibrosis have not yet been reported.</p><p><strong>Methods: </strong>In this study, we investigated the effect of FFA4 on pulmonary fibrosis using both in vivo and in vitro models. A bleomycin-induced pulmonary fibrosis model was established in wild-type and FFAR4 knockout mice. In vitro, a Transwell co-culture system consisting of RAW264.7 macrophages and NIH3T3 fibroblasts was constructed. Transfection, transcriptomic analysis, dual-luciferase reporter assays, RT-qPCR, and Western blotting were performed to explore the molecular mechanisms mediated by FFA4. In addition, pharmacological interventions with the FFA4 agonist CpdA and the NF-κB inhibitor BAY11-7082 were used to evaluate the role of the NF-κB-IL-33 signaling axis in inflammation-driven fibrotic responses.</p><p><strong>Results: </strong>FFA4 expression was reduced in the bleomycin-induced fibrosis model. In both the co-culture system and the mouse model, FFA4 deficiency significantly increased IL-33 expression and aggravated pulmonary fibrosis. In contrast, activation of FFA4 with CpdA reduced IL-33 expression and attenuated pulmonary fibrosis. Moreover, BAY11-7082 also suppressed IL-33 expression. Genetic deletion and pharmacological activation experiments further confirmed that the inhibitory effect of CpdA on IL-33 expression was dependent on FFA4.</p><p><strong>Conclusions: </strong>Collectively, these findings demonstrate that FFA4 restrains inflammatory signal amplification and suppresses pulmonary fibrosis progression by regulating the NF-κB-IL-33 signaling axis, suggesting that FFA4 may serve as a potential therapeutic target for pulmonary fibrosis.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153883"},"PeriodicalIF":2.2,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833043","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":"Bz423 promotes procoagulant platelet formation independently of OSCP.","authors":"Joanna-Marie Howes, Ruby M Baxter, Samuel Dickens, Matthew T Harper","doi":"10.1016/j.bbrc.2026.153884","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153884","url":null,"abstract":"<p><p>Platelet activation is a key driver of in arterial thrombosis and myocardial infarction. Despite current anti-platelet therapies, mortality and morbidity from myocardial infarction remain high. Alternative anti-platelet therapies are needed that can reduce the risk of myocardial infarction without further increasing bleeding risk. Activated platelets rapidly diverge into distinct subpopulations. 'Procoagulant' platelets form through a mitochondria-dependent pathway. These procoagulant platelets expose phosphatidylserine (PS), which localises and amplifies the coagulation cascade leading to a large increase in thrombin generation and stable thrombosis. Procoagulant platelet formation may be a new target for anti-platelet therapies. A key regulatory step controlling progression to procoagulant platelets is opening of the mitochondrial permeability transition pore (mPTP). OSCP acts as a regulatory node for mPTP activity. Since mPTP opening regulates procoagulant platelet formation, we hypothesised that OSCP might also be a key regulatory node in platelets. OSCP is a target of the immunomodulatory benzodiazepine, Bz-423. In this study, we show that Bz-423 increased procoagulant platelet formation. This was associated with mitochondrial hyperpolarisation prior to platelet activation, and increased mPTP opening after activation. Cellular thermal shift assays (CETSA) showed that both Bz-423 and a structurally similar benzodiazepine, 4-chloro-dizaepam, bind OSCP in platelets. Despite this, only Bz-423 increased procoagulant platelet formation. Our findings indicate that Bz-423 promotes procoagulant platelet progression through a target distinct from OSCP.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153884"},"PeriodicalIF":2.2,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855608","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":"Doxorubicin induces a reversible senescence-like state in the EPC fish cell line.","authors":"Keonhee Lee, Kunihiko Futami","doi":"10.1016/j.bbrc.2026.153881","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153881","url":null,"abstract":"<p><p>Cellular senescence is generally defined as a stable and typically irreversible cell cycle arrest triggered by diverse stresses, including DNA damage. However, fish-derived cells exhibit intrinsic resistance to stable senescence, and the extent to which this resistance can be overcome remains unclear. Here, we studied the effects of the DNA-damaging chemotherapeutic agent doxorubicin (DOX) in the fish cell line Epithelioma papulosum cyprini (EPC). DOX treatment induced multiple senescence-associated phenotypes in EPC cells, including morphological changes, senescence-associated β-galactosidase (SA-β-gal) activity, and the secretion of senescence-associated secretory phenotype (SASP) factors. Despite these changes, EPC cells did not undergo irreversible proliferative arrest and were able to resume proliferation in a condition-dependent manner, even after prolonged DOX exposure. Furthermore, these responses in EPC cells were not stably maintained but instead exhibited dynamic regulation across phenotypic, proliferative, and transcriptional states. Together, these findings demonstrate that DOX-induced DNA damage results in a transient and reversible senescence-like state in EPC cells, highlighting fundamental differences between teleost and mammalian senescence programs.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153881"},"PeriodicalIF":2.2,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833012","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 functional insights into an anticancer peptide candidate derived from the EP400NL C-terminal domain.","authors":"Yuxin Liang, Yuanyuan Wang, Shuang Sam, Zidong Li, Faez Iqbal Khan, Jeong Hyeon Park","doi":"10.1016/j.bbrc.2026.153880","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153880","url":null,"abstract":"<p><p>EP400 N-terminal Like (EP400NL) is a recently characterized transcriptional coactivator implicated in chromatin remodeling and oncogenic signaling. Although its precise function remains incompletely understood, emerging evidence suggests that EP400NL contributes to transcriptional regulatory networks relevant to tumor progression. In this study, we investigated the structural and functional properties of the C-terminal domain (CTD) of EP400NL using bioinformatic and molecular modeling approaches and evaluated the anticancer potential of a peptide derived from this region. Molecular dynamics simulations indicated that the CTD forms an extended, flexible tail that may serve as a functional motif mediating protein-protein interactions. Cell-based assays demonstrated that delivery of the EP400NL CTD peptide or shRNA-mediated targeting of the corresponding RNA region suppresses cancer cell proliferation and clonogenicity, supporting a potential inhibitory role of this domain in tumor growth and survival. Collectively, these findings identify the EP400NL CTD as a promising structural motif for anticancer peptide development.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153880"},"PeriodicalIF":2.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832970","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":"Environmental control of flowering through alternative splicing of FLC and COOLAIR.","authors":"Tonghui Wu, Ting Jia, Xueyun Hu","doi":"10.1016/j.bbrc.2026.153877","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153877","url":null,"abstract":"<p><p>Precise control of flowering time allows plants to align reproductive development with favorable environmental conditions. In Arabidopsis thaliana, FLOWERING LOCUS C (FLC) serves as a central floral repressor that integrates inputs from multiple signaling pathways. While FLC expression is classically silenced through vernalization-mediated epigenetic mechanisms, emerging evidence highlights alternative splicing (AS) of both FLC and its antisense transcript COOLAIR as a rapid, reversible, and environmentally responsive layer of post-transcriptional regulation. This review synthesizes current knowledge on how temperature and photoperiod modulate the splicing dynamics of FLC and COOLAIR, thereby fine-tuning FLC expression and flowering responses. We further discuss the gene regulatory networks that link environmental cues to the AS of FLC and COOLAIR. Deciphering these mechanisms offers valuable insights for engineering environment-resilient crops with optimized flowering time through molecular breeding.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153877"},"PeriodicalIF":2.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832960","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":"Molecular mechanisms governing antibiotic transport in spider silk-riboflavin hydrogels.","authors":"Aarti Kumari, Moumita Saharay","doi":"10.1016/j.bbrc.2026.153875","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153875","url":null,"abstract":"<p><p>Silk hydrogels are emerging as versatile biomaterials for drug delivery owing to their biocompatibility, biodegradability, and tunable hierarchical structure. Their trans-port properties are governed by the interplay between peptide secondary structure, hydration, and intermolecular interactions within the network. Understanding how small drug molecules, penicillin, diffuse through silk-based matrices at the molecular level is therefore critical for rational material design. Here, we studied the molecular mechanisms governing antibiotic, penicillin, transport in a spider silk-riboflavin hydrogel using all-atom molecular dynamics simulations. A 61-residue fragment de-rived from the repetitive domain of major ampullate spidroin 1 (MaSp1) was modeled to represent the silk matrix, and riboflavin was incorporated to examine its influence on supramolecular organization and drug mobility. The riboflavin molecules exhibit markedly restricted mobility, reflecting its propensity to form clusters and engage in strong interactions with the silk peptide matrix. In contrast, penicillin shows comparatively higher diffusivity. Collectively, the results establish a clear structure-dynamics relationship in which supramolecular clustering and peptide-drug interactions regulate antibiotic transport. These findings provide molecular-level insight into how controlled aggregation within silk hydrogels can be strategically leveraged to tune diffusion behavior while preserving matrix integrity.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153875"},"PeriodicalIF":2.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810272","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":"EXOC6B promotes cilial elongation via autophagy-dependent protein turnover.","authors":"Kailash Chand, Sai Latha Sabbu, Deeksha Agrawal, Tanuja Kosuri, Katta M Girisha, Kishore V L Parsa","doi":"10.1016/j.bbrc.2026.153828","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153828","url":null,"abstract":"<p><p>Exocyst Complex Component 6b (EXOC6B), a constituent of highly conserved octameric exocyst complex, plays a pivotal role in tethering and spatial targeting of post-Golgi vesicles to the plasma membrane, thereby facilitating exocytosis. Mutations in the EXOC6B gene has been associated with severe neurological and skeletal disorders, such as spondyloepimetaphyseal dysplasia with joint laxity type 3 (SEMDJL3) and Laurin-Sandrow Syndrome, highlighting its critical role in the development. SEMDJL3 patient fibroblasts showed impaired ciliogenesis. Thus, in this study, we investigated the functional importance of EXOC6B in cilium formation and the underlying molecular mechanisms. Here, we observed that cilia were shorter in EXOC6B knockout HEK 293T cells. On the other hand, forced expression of EXOC6B in HEK 293T cells augmented cilia length. Mechanistic analysis of EXOC6B-mediated cilia effects revealed that EXOC6B enhanced basal autophagy through the activation of AMPK and inhibition of mTOR signalling pathways. Analysis of clinically reported mutations in EXOC6B gene showed that the region beyond amino acid Tyr³⁰² is critical for interaction with ciliary proteins, induction of basal autophagy and cilia length enhancement. Taken together, we show that EXOC6B promotes cilia length through the activation of basal autophagy.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153828"},"PeriodicalIF":2.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810301","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}