Biochemical and biophysical research communications最新文献

{"title":"Structure-based identification of dual targeting lead inhibitor to Marburg virus glycoprotein and Chandipura virus nucleoprotein: Insights from molecular docking, dynamics and binding free energy analyses","authors":"Sinosh Skariyachan ,&nbsp;Swathi Vijayan ,&nbsp;Denoj Sebastian ,&nbsp;Vinod Naracham Veettil ,&nbsp;Narayanappa Rajeswari ,&nbsp;Rachana Kaitheri Edathil","doi":"10.1016/j.bbrc.2025.152239","DOIUrl":"10.1016/j.bbrc.2025.152239","url":null,"abstract":"<div><div>Marburg virus (MARV) and Chandipura virus (CHPV), belonging to the families filoviridae and rhabdoviridae, respectively, are RNA viruses producing a hemorrhagic fever and severe encephalitis with a high mortality rate. The present study computationally explores the antiviral potential of bioactive molecules from <em>Glycyrrhiza glabra</em> (Licorice root) against the glycoprotein (GP) of MARV and nucleoprotein (NP) of CHPV. The 3D structures of GP and NP are not available in their native forms, and these structures were computationally modelled and validated for their structural and stereochemical properties. Licorice compounds with satisfactory pharmacokinetics such as drug likeness and ADMET, were docked against these targets, and comparison was made with the docking results of the reference antiviral drug, favipiravir and the target VP35 by using their binding affinities. Apigenin possessed the highest binding affinity with GP and NP at −6.3 and −7.1 kcal/mol, respectively, with greater binding affinities compared to favipiravir and VP35 at −4.2 kcal/mol. Additional stability of apigenin-protein complexes was investigated by MD simulations, including RMSD, RMSF, H-bonds, PCA, FEL, and DCCM analyses. These revealed a stable conformational stability and interaction formation in apigenin-protein complexes, however, apigenin-GP complex was found more stable than apigenin-NP. Binding free energy calculations, conducted using MM/GBSA and MM/PBSA, also estimated ΔG values of −679.65 kcal/mol and −92.30 kcal/mol for apigenin-GP and apigenin-NP complexes. This <em>in silico</em> model highlights apigenin from <em>Glycyrrhiza glabra</em> as a potential dual targeting antiviral therapeutic against both CHPV and MARV, and finds significant applications in further <em>in vitro</em> and <em>in vivo</em> validation.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152239"},"PeriodicalIF":2.5,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144338397","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":"Methuselah proteins in Drosophila: Structural and evolutionary insights from mathematical genomics","authors":"Sk Sarif Hassan ,&nbsp;Debaleena Nawn ,&nbsp;Ankita Ghosh ,&nbsp;Moumita Sil ,&nbsp;Arunava Goswami ,&nbsp;Pallab Basu ,&nbsp;Kenneth Lundstrom ,&nbsp;Vladimir N. Uversky","doi":"10.1016/j.bbrc.2025.152240","DOIUrl":"10.1016/j.bbrc.2025.152240","url":null,"abstract":"<div><div>This study provides a quantitative and comprehensive analysis of 18 Methuselah (mth) protein variants from fruit flies, which are part of the G-protein-coupled receptor (GPCR) family and are implicated in aging and longevity. Phylogenetic analysis identified two major clades of mth proteins, with the first clade indicating conserved functions across Drosophila species and the second clade reflecting gene duplication and diversification. The study found five distinct functional subclasses of mth proteins through amino acid frequency and poly-string analyses, linked to their structural diversity and role in longevity. Structural topology and post-translational modifications reveal similarities with G-protein-coupled receptors (GPCRs), suggesting that mth proteins are crucial for signal transduction and cellular health. Variability in propeptide cleavage sites and intrinsic protein disorder further highlight adaptive roles in signaling. The findings underscore the importance of a quantitative approach to studying Methuselah genes, offering insights into their functional versatility and evolutionary dynamics. This enhanced quantitative understanding contributes to advancing research on aging and longevity.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152240"},"PeriodicalIF":2.5,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144471726","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":"Multi-omics investigation of the mechanism underlying castration-induced subcutaneous fat deposition in male mice","authors":"Huan Yao ,&nbsp;Dong Li ,&nbsp;Shihui Ye ,&nbsp;Tianzeng Song ,&nbsp;Xianyin Zeng","doi":"10.1016/j.bbrc.2025.152233","DOIUrl":"10.1016/j.bbrc.2025.152233","url":null,"abstract":"<div><div>Obesity is a global epidemic that threatens public health. Castration promotes the deposition of subcutaneous fat. However, the underlying mechanism remains unclear. The gut microbiota and their associated metabolites may regulate castration-induced subcutaneous fat deposition. In this study, we found surgical castration significantly increased subcutaneous fat deposition, adipocyte size, and fatty acid abundance in mice. Castration affected the β diversity of cecal bacteria and changed the interaction between bacteria and fungi. Castration enhanced cecal glycerolipid metabolism, which was significantly positively correlated with <em>clavispora</em>, <em>Galactomyces</em>, <em>Ligilactobacillus</em>, <em>Adlercreutzia</em>, <em>Anaerovorax</em>, <em>Christensenella</em>, and the <em>Prevotellaceae NK3B3l group</em>. Castration enhanced the abundance of glycerol, sn-glycerol 3-phosphate, dihydroxyacetone phosphate, and lipoteichoic acid in the serum, which influenced the expression of <em>Gpat4</em>, <em>Lpin1</em>, <em>Gpat3</em>, <em>Gpam</em>, <em>Akr1b10</em>, <em>Agpat1</em>, and <em>Akr1a1</em> in the subcutaneous fat. These genes were involved in glycerolipid metabolism and the regulation of lipid droplet formation. Furthermore, they showed a significant positive correlation with subcutaneous fat weight. Gene set enrichment analysis confirmed that castration enhanced lipid droplet storage and fatty acid synthesis in the subcutaneous fat. These results confirm that glycerolipid metabolism regulates subcutaneous fat deposition in mice after castration from the gut-serum-subcutaneous fat axis.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152233"},"PeriodicalIF":2.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480264","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":"Rehmannioside A alleviates renal inflammation and fibrosis in hypertensive nephropathy via AT1R/MAPK14/IL-17 signaling pathway","authors":"Furong Liu ,&nbsp;Junqiang Wang ,&nbsp;Zhenhua Sun ,&nbsp;Xiaoying Yu","doi":"10.1016/j.bbrc.2025.152237","DOIUrl":"10.1016/j.bbrc.2025.152237","url":null,"abstract":"<div><h3>Background</h3><div>This study aimed to observe the influences and potential mechanism of rehmannioside A (ReA) in hypertensive nephropathy (HN).</div></div><div><h3>Methods</h3><div>HN model in mice and rat tubular epithelial cells were constructed by angiotensin II (Ang II). The biomarkers of renal function, including uric acid (UA), creatinine (Cre), blood urea nitrogen (BUN), and urine albumin, were assessed.</div></div><div><h3>Results</h3><div>Ang II induced severe kidney injury, while the injury was ameliorated by ReA. In Ang II-induced hypertensive mice model, ReA decreased the levels of UA, Cre, BUN, urine albumin, transforming growth factor (TGF)-β, Fibronectin, Collagen I, interleukin (IL)-6, IL-1β, and tumour necrosis factor (TNF)-α. In Ang II-treated cells, ReA reduced the levels of TGF-β, Fibronectin, Col1agen I, IL-6, IL-1β, and TNF-α. In vivo and in vitro, ReA promoted angiotensin converting enzyme 2 (ACE2) expression and inhibited the expression of angiotensin II type 1 receptor (AT1R), ACE, IL-17, mitogen activated protein kinase 14 (MAPK14), phosphorylated (p)-MAPK14, p–NF–κB P65, and matrix metallopeptidase 9 (MMP-9) in HN model. Moreover, there was a docking for ReA and MAPK14 protein, and ReA inhibited MAPK14 protein expression by promoting MAPK14 ubiquitination. Under Ang II treatment, MAPK14 overexpression reversed the promotive effect of ReA on cell viability and the inhibitory effects of ReA on fibrosis and inflammation in NRK-52E cells.</div></div><div><h3>Conclusions</h3><div>ReA alleviated renal dysfunction and reduced fibrosis and inflammation, which was related to the inhibition of AT1R/MAPK14/IL-17 pathway. For HN treatment, ReA may be a promising pharmacological strategy.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152237"},"PeriodicalIF":2.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144335992","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 basis of the therapeutic effect of butyrate in glioblastoma revealed by in vitro and in silico approach","authors":"K. Ashwini ,&nbsp;Ranjitha Acharya ,&nbsp;P.G. Roopashree ,&nbsp;Ananthan Raghotham ,&nbsp;Stéphanie Baud ,&nbsp;Rajas M. Rao ,&nbsp;N. Suchetha Kumari","doi":"10.1016/j.bbrc.2025.152216","DOIUrl":"10.1016/j.bbrc.2025.152216","url":null,"abstract":"<div><div>Glioblastoma (GBM) remains among the most difficult to treat cancers globally. Complexity of this disease and the existing inadequacies of modern therapy put forward the need for ongoing research into new therapies. Short Chain Fatty Acids (SCFAs) are among the major metabolites secreted by the gut microbiome, and are thought to play an important role in gut microbiome-brain interactions. While earlier experimental studies have hinted towards a therapeutic potential of butyrate in glioblastoma, we demonstrate here the molecular mechanism behind this effect through a combination of <em>in vitro</em> and <em>in silico</em> approaches. LN229 and U87 GBM cells were treated with butyrate, and anti-proliferative potential was evaluated through colony formation assay, flow cytometry and qRT-PCR experiments. Molecular mechanism was mapped through butyrate target prediction, molecular docking, molecular dynamics simulations and analyses of binding free energy calculations. Butyrate inhibited the proliferation, and colony formation in U87 and LN229 GBM cell lines. We also found that it arrested the cell cycle progression at the G0/G1 phase in U87 cells and the G2/M Phase in LN229 cell lines, along with initiation of apoptosis in both the cells. Similarly, butyrate treatment also reduced the expression of Epidermal Growth Factor Receptor (EGFR) in a dose-dependent manner. The molecular mechanism behind the anti-cancer effect of butyrate was demonstrated through molecular docking and simulation studies. Butyrate bound to Histone Deacetylase-3 (HDAC3)-Nuclear CoRepressor2 complex, and induced allosteric dynamics that further blocked HDAC3 activation. The observations in this study demonstrate the potential of butyrate as a viable therapeutic agent for glioblastoma.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152216"},"PeriodicalIF":2.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480266","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":"Corrigendum to \"Evidence for cooperative binding of chlorpromazine with hemoglobin: equilibrium dialysis, fluorescence quenching and oxygen release study\" [Biochem. Biophys. Res. Commun. (1990) 167(3):1146-53].","authors":"Maitree Bhattacharyya, U Chaudhuri, R K Poddar","doi":"10.1016/j.bbrc.2025.152138","DOIUrl":"10.1016/j.bbrc.2025.152138","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"152138"},"PeriodicalIF":2.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336297","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":"Cyclin-dependent kinase 12 influences protein kinase D1 kinase activity","authors":"Sanjeev Shukla ,&nbsp;Jean-Pierre (Trey) Kanumuambidi ,&nbsp;Reynier Rodriguez Rosales ,&nbsp;Arjun Venkatesh ,&nbsp;Mohammed Al-Toubat ,&nbsp;Mario Mietzsch ,&nbsp;Robert McKenna ,&nbsp;K.C. Balaji","doi":"10.1016/j.bbrc.2025.152221","DOIUrl":"10.1016/j.bbrc.2025.152221","url":null,"abstract":"<div><div>A unique and aggressive molecular subtype of prostate cancer is driven by recurrent mutations in the cyclin-dependent kinase 12 (CDK12) gene, which occur exclusive of other common genetic alterations. Protein Kinase D1 (PrKD1) is a well-established tumor suppressor in prostate cancer. Phosphoproteomics studies have identified serines 681 and 685 as putative PrKD1 phosphorylation sites in CDK12-mutated tumors; however, whether these proteins interact directly or the potential impact on either protein's function remains unknown. In this study, we demonstrate a direct interaction between PrKD1 and CDK12 in a prostate cancer cell line using co-immunoprecipitation and a bimolecular fluorescence complementation (BiFC) assay. Site-directed mutagenesis of serines 681 and 685, the putative PrKD1 phosphorylation sites in CDK12, did not alter the phosphorylation of the well-established CDK12 substrates, serines 2 and 5 on RNA polymerase II. Interestingly, these site-directed mutagenesis experiments resulted in altered PrKD1 kinase activity. Molecular modeling studies suggest that phosphorylation at serine 681, or both serines 681 and 685, releases PrKD1 from an autoinhibitory conformation, promoting its kinase activity. These findings suggest a potential regulatory role of CDK12 in modulating PrKD1 kinase function in prostate cancer.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152221"},"PeriodicalIF":2.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480306","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":"Development of HiBiT-tagged mumps virus-like particles assembled from authentic viral structural proteins for neutralizing testing","authors":"Aika Wakata ,&nbsp;Chaewon Bae ,&nbsp;Yasuyoshi Hatayama ,&nbsp;Takashi Okura ,&nbsp;Noriyuki Otsuki ,&nbsp;Kumiko Takahashi ,&nbsp;Mami Nagashima ,&nbsp;Kenji Sadamasu ,&nbsp;Fumihiro Kato ,&nbsp;Fuminori Mizukoshi ,&nbsp;Akihide Ryo","doi":"10.1016/j.bbrc.2025.152236","DOIUrl":"10.1016/j.bbrc.2025.152236","url":null,"abstract":"<div><div>Despite widespread vaccination programs, mumps outbreaks persist even in highly vaccinated populations, raising concerns about current vaccine effectiveness against circulating strains. Existing serological methods exhibit limitations in practical implementation and antigenic specificity. To address these challenges, we developed a rapid neutralization assay using HiBiT-tagged mumps virus-like particles (hiMuV-VLPs) composed entirely of authentic viral structural proteins. Transmission electron microscopy confirmed these hiMuV-VLPs morphologically resembled native mumps virions. The VLPs demonstrated efficient cellular entry, quantifiable via luminescent signals generated by HiBiT-LgBiT complementation. Validation against conventional plaque reduction neutralization tests (PRNT) using human sera revealed the biological relevance and practicability of our assay. A key innovation was the successful incorporation of hemagglutinin-neuraminidase (HN) proteins from multiple mumps virus genotypes into the hiMuV-VLP platform, enabling assessment of strain-specific neutralizing antibody responses. This system represents a valuable tool for large-scale seroepidemiological surveillance, evaluation of vaccine-induced immunity against heterologous strains, and prediction of population susceptibility to emerging mumps virus variants.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152236"},"PeriodicalIF":2.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144329713","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":"Polyphyllin I enhances the anti-tumor efficacy of Palbociclib by reversing M2 macrophage polarization in lung cancer","authors":"Yulan Jiang ,&nbsp;Lu Wang ,&nbsp;Yu Chen ,&nbsp;Ying Li ,&nbsp;Guanping Chen ,&nbsp;Yingyan Lu ,&nbsp;Cheng Jiang ,&nbsp;Kequn Chai ,&nbsp;Yifan Wang","doi":"10.1016/j.bbrc.2025.152228","DOIUrl":"10.1016/j.bbrc.2025.152228","url":null,"abstract":"<div><div>Lung cancer is a significant hazard to human health, with limited treatment options. Although CDK4/6 inhibitors like Palbociclib (Palb) have shown clinical promise, their effectiveness is often compromised by resistance. Our findings indicate that the Palb may promote M2-like macrophage polarization, which can facilitate tumor progression through immunosuppression. This study investigates the effect of Polyphyllin I (PPI) in counteracting Palb-induced M2 macrophage polarization and explored its synergistic anti-tumor potential when combined with Palb. In vitro, a macrophage polarization model showed that Palb enhanced the expression of M2 macrophage markers, which could be reversed by PPI. LLC cells were cultured with macrophage-conditioned medium (CM) showed that the PPI and Palb combination-CM group exhibited decreased proliferation, migration, and invasion capabilities in LLC cells and inhibited epithelial-mesenchymal transition (EMT) compared to the Palb-CM group. Moreover, the combination of PPI and Palb also enhanced anti-tumor effect in vivo. Mechanistically, the JAK-STAT pathway was enriched, and key signaling proteins associated with macrophage polarization, including TWEAK, p-JAK1 and p-STAT1, were significantly upregulated in the PPI-treated group. PPI can reverse Palb-induced M2 polarization by activating the TWEAK/JAK1/STAT1 signaling pathway, which can enhance the anti-tumor efficacy of Palb. These findings support PPI as a potential adjunct to CDK4/6 inhibitors for lung cancer therapy.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152228"},"PeriodicalIF":2.5,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144490189","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":"IRAK-M regulates NTHi-induced inflammation via JNK and NF-κB signal pathways","authors":"Huan Hou ,&nbsp;Jieying Li ,&nbsp;Yilin Huang ,&nbsp;Ying Zhao ,&nbsp;Jinming Gao","doi":"10.1016/j.bbrc.2025.152229","DOIUrl":"10.1016/j.bbrc.2025.152229","url":null,"abstract":"<div><h3>Purpose</h3><div>Nontypeable <em>Haemophilus influenzae</em> (NTHi) is a causative agent of acute exacerbations in chronic lung conditions. Despite antibiotic administration, unresolved hyperinflammation underscores the urgent need to identify host-directed immunomodulatory targets. The bronchial mucosa serves as a primary site for infection initiation and propagation. This study aims to investigate the role of airway-expressed interleukin-1 receptor-associated kinase M (IRAK-M) in modulating NTHi-induced lung inflammation and its potential mechanisms.</div></div><div><h3>Methods</h3><div>We examined the expression of IRAK-M and TLR4 in lung epithelial cells and macrophages following NTHi infection. IRAK-M was silenced or overexpressed to assess its impact on cytokine production. In vitro investigations, JNK and NF-κB inhibitors were applied to test whether IRAK-M-mediated inflammation was partly dependent on these pathways. In vivo, the effects of JNK and NF-κB inhibitors were evaluated in NTHi-infected mice.</div></div><div><h3>Results</h3><div>NTHi infection upregulated IRAK-M and TLR4 expression in both lung epithelial cells and macrophages. Upon NTHi stimulation, inflammatory responses were enhanced by IRAK-M overexpression or suppressed by IRAK-M silencing in lung-resident and immune cells. IRAK-M overexpression led to overactivation of JNK and NF-κB pathways. Inhibition of these pathways counteracted IRAK-M-induced inflammatory responses. In vivo, JNK and NF-κB inhibitors alleviated lung inflammation, and JNK inhibitors improved survival in NTHi-infected mice.</div></div><div><h3>Conclusion</h3><div>IRAK-M regulates NTHi-induced inflammation possibly through NF-κB and JNK signaling pathways. Modulation of IRAK-M and its downstream JNK and NF-κB signaling pathways might represent a novel therapeutic strategy for controlling NTHi-induced inflammation.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152229"},"PeriodicalIF":2.5,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336036","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}