Biochemical and biophysical research communications最新文献

{"title":"Expression of concern to \"A structurally novel hemopexin fold protein of rice plays role in chlorophyll degradation\" [Biochem. Biophys. Res. Commun. (2012) 420 (4) 862-868].","authors":"Tirthartha Chattopadhyay, Sudipta Bhattacharyya, Amit K Das, Mrinal K Maiti","doi":"10.1016/j.bbrc.2026.153385","DOIUrl":"10.1016/j.bbrc.2026.153385","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"153385"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146197295","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":"NMR-driven insights into the evolutionary adaptation and dynamic regulation of Mycobacterium tuberculosis adenylate kinase: The critical role of glycine-mediated flexibility","authors":"Chae Yeong Lee ,&nbsp;Woo Cheol Lee ,&nbsp;Kyusung Chae ,&nbsp;Eunhee Kim ,&nbsp;Eunha Hwang ,&nbsp;Yangmee Kim","doi":"10.1016/j.bbrc.2026.153357","DOIUrl":"10.1016/j.bbrc.2026.153357","url":null,"abstract":"<div><div>Adenylate kinase (Adk) is essential for cellular energy homeostasis as it catalyzes the reversible transfer of γ-phosphate from ATP to AMP. In most long-variants, such as <em>Escherichia coli</em> Adk, large-scale domain motions, concerted movements of the AMP-binding domain (AMPbd) and ATP-lid, are essential for catalytic efficiency. However, the structural diversity observed in Adk variants, especially the short-variant Adk from <em>Mycobacterium tuberculosis</em> (MtAdk) featuring a truncated ATP-lid, raises questions regarding the adaptation of its dynamic regulation and functional mechanisms to support survival in resource-limited and hostile environments. Here, using ¹⁵N-chemical exchange saturation transfer experiments, we identified key glycine residues, G32 and G46 in AMPbd and G128 within the ATP-lid, that undergo slow conformational exchange on the millisecond timescale. Glycine substitutions with proline revealed their critical roles: G32P and G128P mutations significantly impaired catalytic turnover, whereas G46P exerted a moderate effect. Molecular dynamics simulations revealed that these substitutions restrict local flexibility; G32P and G128P lock the enzyme in an open, less active conformation, whereas G46P destabilizes the hinge region, thereby hindering proper domain closure. Our integrated approach reveals that these glycine-mediated flexibilities are essential for substrate recognition and catalysis in MtAdk. These findings highlight the fundamental mechanistic divergence between short- and long-variant Adks, emphasizing glycine-mediated conformational plasticity as key in enzyme regulation, with promising implications in targeted therapies against bacterial survival strategies.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"Article 153357"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077008","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":"Medium-chain fatty acids activate fructose metabolism via up-regulating GLUT5-KHK axis","authors":"Jiru Hou,&nbsp;Jiaxuan Li,&nbsp;Chong Zhao,&nbsp;Shutao Yin,&nbsp;Hongbo Hu","doi":"10.1016/j.bbrc.2026.153358","DOIUrl":"10.1016/j.bbrc.2026.153358","url":null,"abstract":"<div><div>Fructose is an abundant monosaccharide in the human diet and an important source of energy in the human body. GLUT5, a member of facilitative glucose transporter family, is the only membrane transporter that specifically transports fructose in the human body, and plays an important role in dietary fructose uptake and metabolism. Previous studies have shown that medium-chain fatty acids (MCFAs) can regulate glucose metabolism via modulating glucose transporters. However, it has not been addressed if MCFAs can regulate GLUT5-mediated fructose metabolism. In the present study, we demonstrated for the first time that MCFAs but not short chain or long chain fatty acids are able to promote fructose uptake in both IEC-18 rat intestinal epithelial cells and human MDA-MB-231 breast cancer cells (a commonly used cell line for fructose metabolism-related study) measured by 1-NBD-Fructose-based assay, which are well correlated with the activation of GLUT5-KHK axis. Moreover, the activation of GLUT5-ketohexokinase (KHK) axis was also achieved in vivo by the treatment with tricapylin, a precursor of octanoic acid (OA), leading to the improvement in fructose-based energy recovery after fasting. The findings of the present study not only provide novel mechanistic support for MCFAs as regulator of carbohydrate metabolism, but also denote that MCFAs could be useable for managing fructose-associated metabolic diseases or as an enhancer for energy recovery after fasting or exercise.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"Article 153358"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146071117","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":"CD59 promotes pancreatic cancer progression via a tumor cell-intrinsic JAK2-STAT3 signaling axis","authors":"Zihan Li ,&nbsp;Xingyi Chen ,&nbsp;Yanjun Wu ,&nbsp;Yi Xu","doi":"10.1016/j.bbrc.2026.153609","DOIUrl":"10.1016/j.bbrc.2026.153609","url":null,"abstract":"<div><div>Pancreatic cancer is a highly aggressive malignancy with limited therapeutic options. Although the complement system has been implicated in tumor biology, its tumor cell–intrinsic roles in pancreatic cancer remain unclear. Here, we identify the complement regulatory protein CD59 as a critical driver of pancreatic cancer progression through a cell-intrinsic signaling mechanism. CD59 is significantly upregulated in pancreatic tumors and correlates with poor patient survival. Functional assays demonstrate that CD59 promotes tumor cell proliferation and growth in vitro and in vivo, whereas its depletion suppresses these effects. Mechanistically, CD59 interacts with JAK2 to activate the JAK2–STAT3 pathway, and transcriptomic analyses identify CACNA1D as a STAT3-dependent effector mediating CD59-driven proliferation. Notably, KRAS inhibition induces compensatory activation of the CD59–JAK2–STAT3 axis, while combined targeting of CD59 or STAT3 with KRAS more effectively inhibits tumor cell growth. These findings define a tumor cell–intrinsic oncogenic function of CD59 and highlight the CD59–JAK2–STAT3–CACNA1D pathway as a potential therapeutic target in pancreatic cancer.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"812 ","pages":"Article 153609"},"PeriodicalIF":2.2,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147453424","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":"Crohn's disease under single-cell map: from INFLARE metaplastic cells to rare immune cell subpopulations","authors":"Qianwen Zhu ,&nbsp;Wenhao Gu ,&nbsp;Yuyang Lv ,&nbsp;Zizhao Wu ,&nbsp;Yan Li ,&nbsp;Rongxin Zhang ,&nbsp;Xianli Shi","doi":"10.1016/j.bbrc.2026.153347","DOIUrl":"10.1016/j.bbrc.2026.153347","url":null,"abstract":"<div><div>Crohn's disease (CD) is a chronic inflammatory condition of the gastrointestinal tract characterized by symptoms such as abdominal pain, diarrhea, weight loss, fever, and fatigue. Although the exact etiology of CD remains elusive, dysregulation of immune cells is widely recognized as a primary driver in its pathogenesis, particularly involving T helper 1 (Th1), T helper 17 (Th17), and natural killer T (NKT) cells. Recent advancements in single-cell sequencing technology have provided a powerful tool for analyzing gene expression at the individual cell level, enabling researchers to investigate immune cells within the microenvironment of disease samples with unprecedented resolution. Through the application of this technology, several novel and unique immune cell subsets have been identified in Crohn's disease, which are critical to its development and progression. This review summarizes these CD-associated cell types, including INFLAREs, LND cells, Tc1/17 cells, tissue-resident memory (Trm) CD8⁺ T cells, FOXP3⁺ regulatory T cells (Tregs), CD pop cells, α⁴β⁷⁺CLA⁺ T cells, NKp30⁺ γδ T cells, and Crohn's disease-associated invariant T cells (CAITs). We discuss their specific roles in the pathogenesis of CD and explore their potential as targets for the development of future therapeutic interventions. Thereby, this may serve as a conceptual and practical resource​ for researchers and clinicians seeking to understand the immunological intricacies of CD and translate them into improved patient outcomes in the future.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"803 ","pages":"Article 153347"},"PeriodicalIF":2.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146076674","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 “PTX3 activates POSTN and promotes the progression of glioblastoma via the MAPK/ERK signalling axis” [Biochem. Biophys. Res. Commun. 703 (2024) 149665]","authors":"Yuhang Wang ,&nbsp;Binbin Wang ,&nbsp;Wenping Cao,&nbsp;Xiupeng Xu","doi":"10.1016/j.bbrc.2026.153382","DOIUrl":"10.1016/j.bbrc.2026.153382","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"803 ","pages":"Article 153382"},"PeriodicalIF":2.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123469","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 “Carboxyl ester lipase truncation mutant unveils lipotoxicity induced pancreatic β-cell demise” [Biochem. Biophys. Res. Commun. 789 (2025) 152800]","authors":"Jianli Lin ,&nbsp;Yi Lin ,&nbsp;Jinxin Li ,&nbsp;Qinwen Liu ,&nbsp;Xiafang Lin ,&nbsp;Qinyu Liu ,&nbsp;YingHua Luo ,&nbsp;Ying Lin ,&nbsp;Haohua Chen ,&nbsp;Junping Wen","doi":"10.1016/j.bbrc.2026.153368","DOIUrl":"10.1016/j.bbrc.2026.153368","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"803 ","pages":"Article 153368"},"PeriodicalIF":2.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123399","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":"Cancer stemness-modulating circular RNAs in colorectal tumorigenesis: target proteins and regulatory mechanisms","authors":"Chiu-Jung Huang ,&nbsp;Kong Bung Choo","doi":"10.1016/j.bbrc.2026.153343","DOIUrl":"10.1016/j.bbrc.2026.153343","url":null,"abstract":"<div><div>Cancer stem cells (CSCs), a small subpopulation of tumor cells with well-defined traits, play critical roles in tumorigenesis. Circular RNAs (circRNAs) have emerged as important regulators of cancer stemness and tumorigenesis. Applying stringent selection criteria, this review aims to systematically evaluate the literature to functionally define a distinct class of cancer stemness-modulating circRNAs (CSM-circRNAs) in colorectal cancer (CRC). In CRC, fourteen dysregulated CSM-circRNAs are identified all of which were validated in spheroid formation assays and expression of multiple stemness markers. All CSM-circRNAs, except circFNDC3B, are up-regulated in CRC, and many (7/14) are selectively pan-cancer dysregulated. Most (9/14) act through miRNA sponging, while the remainder (5/14) function via interactions with RNA-binding proteins. CSM-circRNA dysregulation affects key CSC traits, confirming their role in modulating cancer stemness. Among the fifteen CSM-circRNA-regulated proteins identified, ten are (post-)transcriptional or (post-)translational regulators, and five are signaling or structural proteins. The CRC CSM-circRNA-regulated proteins are dysregulated across multiple cancer types besides CRC, influencing key biochemical and signaling pathways. We propose that CSM-circRNAs constitute a novel class of post-transcriptional regulators that broadly activate cancer stem cells and driving malignant progression, highlighting their diagnostic and therapeutic potentials. It is anticipated that CSM-circRNAs in other cancers, and other functional circRNA categories across diseases, will be similarly categorized, providing systematic frameworks for organizing the rapidly expanding circRNA literature.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"803 ","pages":"Article 153343"},"PeriodicalIF":2.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146076720","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":"Mechanistic insights and therapeutic potential of E3 ubiquitin ligases in gastric cancer development","authors":"Yao Xiao ,&nbsp;Yalin Lei ,&nbsp;Qian He ,&nbsp;Tiebing Zeng ,&nbsp;Hui Ling","doi":"10.1016/j.bbrc.2026.153340","DOIUrl":"10.1016/j.bbrc.2026.153340","url":null,"abstract":"<div><div>The ubiquitin-proteasome system (UPS) is the primary pathway for protein degradation in eukaryotic cells. E3 ubiquitin ligases regulate protein homeostasis through substrate-specific ubiquitination and play a crucial role in the onset, progression, and therapeutic resistance of gastric cancer (GC). This article systematically reviews the classification, functions, and regulatory mechanisms of E3 ubiquitin ligases in gastric cancer, including their roles in cell proliferation, invasion and metastasis, apoptosis, autophagy, ferroptosis, as well as their relationship with the gastric cancer microenvironment. Furthermore, this article discusses the molecular mechanisms by which E3 ligases contribute to the progression of gastric cancer through the Akt, Wnt/β-catenin, and NF-κB signaling pathways. It also summarizes potential therapeutic strategies targeting E3 ligases, such as small molecule inhibitors, PROTAC technology, molecular glues, and immunotherapy. Finally, the article explores mechanism of treatment resistance and potential solutions of E3 ligases in gastric cancer, providing a theoretical foundation for the development of new targeted therapies for this disease.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"803 ","pages":"Article 153340"},"PeriodicalIF":2.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146049044","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":"ALB suppresses epithelial-mesenchymal transition and glycolysis via SPARC regulation in metastatic clear cell renal cell carcinoma","authors":"Wei Wang ,&nbsp;Liuyang Shu ,&nbsp;Sheng Xu ,&nbsp;Xudong Jiang","doi":"10.1016/j.bbrc.2026.153333","DOIUrl":"10.1016/j.bbrc.2026.153333","url":null,"abstract":"<div><h3>Background</h3><div>The most prevalent subtype of renal cell carcinoma is clear cell renal cell carcinoma (ccRCC). Approximately 20–30 % of ccRCC patients develop metastatic clear cell renal cell carcinoma (mccRCC), characterized by aggressive tumor behavior and resistance to conventional therapies. Identification of critical hub genes involved in mccRCC progression is essential for advancing clinical management.</div></div><div><h3>Methods</h3><div>Differentially expressed genes (DEGs) about ccRCC were identified by integrated analysis of four public datasets. Protein-protein interaction (PPI) network and topological analyses were executed to pinpoint hub genes. Functional assays, including quantitative real-time PCR, proliferation, Western blotting, transwell assays, and Seahorse metabolic flux analysis, were performed in ccRCC cell lines.</div></div><div><h3>Results</h3><div><em>Alb</em>umin (<em>ALB</em>) was recognized as a hub gene consistently downregulated in ccRCC and mccRCC cell lines. <em>ALB</em> expression proved a strong correlation with tumor stage, metastasis, and histological grade. Functional experiments demonstrated that <em>ALB</em> suppressed proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in primary and metastatic ccRCC. Mechanistically, <em>ALB</em> showed a negative association with <em>SPARC</em>, which could potentially influence EMT progression. Metabolomic and glycolytic flux analyses revealed that <em>ALB</em> overexpression reprogrammed glycolysis by reducing glycolytic intermediates, glucose uptake, and lactate production. Silencing <em>ALB</em> enhanced glycolysis and malignant phenotypes, which were reversed by glycolysis inhibition or <em>SPARC</em> knockdown.</div></div><div><h3>Conclusion</h3><div><em>ALB</em> is associated with reduced proliferation, EMT, and glycolytic activity in mccRCC, potentially through its negative association with <em>SPARC</em>. This study provides novel insights into mccRCC pathogenesis and identifies <em>ALB</em> as a potential diagnostic biomarker and therapeutic target.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"803 ","pages":"Article 153333"},"PeriodicalIF":2.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146076673","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}