Biochemical and biophysical research communications最新文献

{"title":"Corrigendum to \"CLDND1 as a prognostic ferroptosis-associated biomarker in oral squamous cell carcinoma\" [Biochem. Biophys. Res. Commun. 787 (2025) 152788].","authors":"Xiaolong Zang, Di Yan, Yuxing Liu, Xiaojiao Sun, Shouyi Zhang, Xiaoxia Li, Xing Wang","doi":"10.1016/j.bbrc.2026.154843","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.154843","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"154843"},"PeriodicalIF":2.5,"publicationDate":"2026-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149369924","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":"Expression of concern for \"Influence of maternal lipid profile on placental protein expression of LDLr and SR-BI\" [Biochem. Biophys. Res. Commun. 359 (2007), 8-14, 10.1016/j.bbrc.2007.05.002].","authors":"","doi":"10.1016/j.bbrc.2026.154708","DOIUrl":"10.1016/j.bbrc.2026.154708","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"154708"},"PeriodicalIF":2.5,"publicationDate":"2026-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135026","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":"Expression of concern for \"Two membrane juxtaposed signaling modules in ANF-RGC are interlocked\" [Biochem. Biophys. Res. Commun. 332, (2005), 149-156, 10.1016/j.bbrc.2005.04.102].","authors":"","doi":"10.1016/j.bbrc.2026.154707","DOIUrl":"10.1016/j.bbrc.2026.154707","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"154707"},"PeriodicalIF":2.5,"publicationDate":"2026-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126562","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":"Restoration of BDNF/TrkB signaling rescues presynaptic dysfunction in GM1 gangliosidosis iPSC-derived neurons","authors":"Tadahiro Numakawa,&nbsp;Ryutaro Kajihara,&nbsp;Chisato Horita,&nbsp;Takumi Era","doi":"10.1016/j.bbrc.2026.154842","DOIUrl":"10.1016/j.bbrc.2026.154842","url":null,"abstract":"<div><div>GM1 gangliosidosis is a lysosomal storage disease characterized by progressive neurodegeneration and severe central nervous system (CNS) dysfunction. Although the abnormal intracellular accumulation of GM1 ganglioside is recognized as a major pathological feature, the molecular mechanisms underlying neuronal dysfunction remain unclear. Brain-derived neurotrophic factor (BDNF) plays essential roles in CNS development and the maintenance of synaptic function and plasticity; however, its contribution to the pathology of lysosomal storage diseases remains unclear. We previously identified a marked impairment of neurotransmitter release in GM1 gangliosidosis neurons, accompanied by reduced expression of synapse-related molecules. In this study, we investigated the potential involvement of endogenous BDNF signaling in synaptic dysfunction using human iPSC-derived neurons. We found that endogenous BDNF expression was significantly reduced in GM1 gangliosidosis neurons, accompanied by a marked decrease in full-length tropomyosin receptor kinase B (TrkB), a key mediator of BDNF signaling. Further, the gene expression of synapse-related molecules involved in neurotransmitter release, including SNAP25 and VAMP2, was reduced. Importantly, exogenous BDNF supplementation ameliorated presynaptic dysfunction and substantially restored the expression of synapse-related molecules, which were reduced in disease neurons. Furthermore, 7,8-dihydroxyflavone (7,8-DHF), a selective TrkB agonist, markedly reversed presynaptic dysfunction. These findings suggest that impaired BDNF/TrkB signaling contributes to presynaptic dysfunction in GM1 gangliosidosis and identify the enhancement of this pathway as a potential therapeutic strategy.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"842 ","pages":"Article 154842"},"PeriodicalIF":2.5,"publicationDate":"2026-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149353460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of Concern to \"Mesenchymal stem cell-derived extracellular vesicles alone or in conjunction with a SDKP-conjugated self-assembling peptide improve a rat model of myocardial infarction\" [Biochem. Biophys. Res. Commun. 524, (2020), 903-909].","authors":"","doi":"10.1016/j.bbrc.2026.154652","DOIUrl":"10.1016/j.bbrc.2026.154652","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"154652"},"PeriodicalIF":2.5,"publicationDate":"2026-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079517","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":"Expression of Concern to \"MicroRNA let-7i induced autophagy to protect T cell from apoptosis by targeting IGF1R\" [Biochem. Biophys. Res. Commun. 453 (2014) 728].","authors":"","doi":"10.1016/j.bbrc.2026.154651","DOIUrl":"10.1016/j.bbrc.2026.154651","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"154651"},"PeriodicalIF":2.5,"publicationDate":"2026-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079508","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 \"Low-nanomolar chetomin in human skin cells: Preserved viability and wound closure, reduced basal IL-6 and IL-1β release, and preliminary tolerability in Galleria mellonella\" [Biochem. Biophys. Res. Commun. 838, (2026), 154637].","authors":"Dominika Kunachowicz, Wojciech Szlasa, Urszula Szwedowicz, Jarosław Kalinin, Magdalena Kloc, Natalia Zaręba-Wdowiak, Dorota Bęben, Malwina Brożyna, Anna Szewczyk, Anna Choromańska","doi":"10.1016/j.bbrc.2026.154781","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.154781","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"154781"},"PeriodicalIF":2.5,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149261717","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":"Cytoophidia: Implications and opportunities for cancer treatment","authors":"Zelin Pan ,&nbsp;Kaili Deng ,&nbsp;Zhe Sun","doi":"10.1016/j.bbrc.2026.153504","DOIUrl":"10.1016/j.bbrc.2026.153504","url":null,"abstract":"<div><div>Cytidine triphosphate synthase (CTPS), the rate-limiting enzyme in de novo CTP synthesis, forms filamentous structures known as cytoophidia, which are evolutionarily conserved across species and cell types. These dynamic structures are regulated by cellular metabolic states, stress, and post-translational modifications. Cytoophidia are believed to play a vital role in regulating nucleotide biosynthesis, ensuring cellular homeostasis, and responding to metabolic stress through the modulation of CTPS activity. In cancer cells, where the demand for nucleotides is heightened, cytoophidia may be essential for supporting proliferation and survival. This review delves into the growing understanding of cytoophidia, highlighting their significance in cancer biology and potential as therapeutic targets. Understanding how cytoophidia regulate the balance between CTPS stabilization and degradation could provide valuable insights into cancer metabolism, offering novel therapeutic opportunities. Targeting the mechanisms that govern cytoophidia formation presents a potential strategy for cancer therapy.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"810 ","pages":"Article 153504"},"PeriodicalIF":2.2,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147316184","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":"Hyperparathyroidism drives periodontitis progression via parathyroid hormone-induced endoplasmic reticulum stress","authors":"Huiyi Wang ,&nbsp;Jing Wu ,&nbsp;Zhendong Huang ,&nbsp;Zhengkun Yang ,&nbsp;Jiayi Ding ,&nbsp;Xiaoxuan Wang ,&nbsp;Zhengguo Cao","doi":"10.1016/j.bbrc.2026.153512","DOIUrl":"10.1016/j.bbrc.2026.153512","url":null,"abstract":"<div><h3>Aims</h3><div>Given the high prevalence of periodontitis and potential for undetected primary hyperparathyroidism (pHPT) to exacerbate periodontal damage, managing pHPT in advanced periodontitis (stages III/IV) is critical. The causal link between pHPT and periodontitis remains unclear. This study aims to investigate the causal effect and mechanisms between hyperparathyroidism and periodontitis.</div></div><div><h3>Methods</h3><div>A two-sample Mendelian randomization study used genome-wide association studies (GWAS) summary data to explore the causal link between hyperparathyroidism and periodontitis, employing single nucleotide polymorphisms (SNPs) as instrumental variables and methods like MR-Egger regression and Weighted median for robust results. PTH levels were detected on samples from both healthy and periodontitis-affected gingival tissues and gingival crevicular fluids. We assessed the impact of PTH on periodontal inflammation through treating gingival fibroblasts with PTH and detecting endoplasmic reticulum stress-related markers. Transcriptomics and metabolomics analyses were integrated to explore genetic pathways related to PTH.</div></div><div><h3>Results</h3><div>Hyperparathyroidism increased the risk of periodontitis, but analyses of periodontitis on hyperparathyroidism showed no reverse causality. PTH levels increased in gingival tissues and gingival crevicular fluid. Multi-omics analysis revealed significant gene and metabolite enrichment in calcium signaling and parathyroid hormone pathways. Since calcium ions are mainly from the endoplasmic reticulum, we focused on endoplasmic reticulum stress and found its effect on lessening PTH-induced periodontal inflammation.</div></div><div><h3>Conclusions</h3><div>This study suggests that periodontitis may serve as a warning sign for pHPT, highlighting the importance of screening for hyperparathyroidism in periodontitis patients. The principal molecules involved in the endoplasmic reticulum stress pathway present promising therapeutic targets for improving periodontal health in patients with hyperparathyroidism.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"810 ","pages":"Article 153512"},"PeriodicalIF":2.2,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343500","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":"RECK attenuates CAF-mediated promotion of epithelial-mesenchymal transition in breast cancer","authors":"Nada H. Hussein ,&nbsp;Mahadi Hasan ,&nbsp;Renata Akhmetzianova ,&nbsp;Hai Yu ,&nbsp;Susumu Kohno ,&nbsp;Takiko Daikoku ,&nbsp;Akira Orimo ,&nbsp;Chiaki Takahashi","doi":"10.1016/j.bbrc.2026.153498","DOIUrl":"10.1016/j.bbrc.2026.153498","url":null,"abstract":"<div><div>Cancer associated fibroblasts (CAFs) play pivotal roles in modulating behaviors of tumor cells through various mechanisms. Here we analyzed a pair of fibroblastic cells derived from stromal tissue of breast cancer (BC-CAFs) or corresponding normal mammary microenvironment (NMFs). We found that the reversion-inducing cysteine-rich protein with Kazal motif (RECK) was highly expressed only in NMFs. Conditioned media derived from BC-CAFs enhanced epithelial-mesenchymal transition (EMT) in breast cancer cells significantly stronger than NMFs. Similarly, BC-CAFs induced EMT in co-injected breast cancer cells when xenografted into immune-compromised mice. These activities of BC-CAFs were significantly suppressed by RECK overexpression. BC-CAFs exhibited higher rate of active/latent TGF-β1 and active/pro-MMP-2. Induction of RECK in BC-CAFs significantly antagonized EMT induction with diminished activation of TGF-β1 and pro-MMP-2. Inversely, depletion of RECK in NMFs promoted EMT with enhancement of TGF-β1 and pro-MMP2 activation. BC-CAFs express higher level of histone deacetylase 1/2 (HDAC-1/2). Multiple HDAC inhibitors induced RECK in BC-CAFs with concomitant decrease in TGF-β 1and pro-MMP2 activation and ability to induce EMT. BC-CAFs exhibited higher histone acetylation in the promoter of RECK. These findings suggest that RECK ectopic expression in BC-CAFs suppresses TGF-β1 maturation by inhibiting pro-MMP-2 activation thereby attenuates EMT and that RECK promoter deacetylation occurs in fibroblasts associated with developing breast cancer. HDAC inhibitors may exhibit therapeutic efficacy in breast cancer by inducing RECK in BC-CAFs.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"810 ","pages":"Article 153498"},"PeriodicalIF":2.2,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147347132","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}