Biochemistry and Biophysics Reports最新文献

{"title":"Molecular identification and phylogenetic analysis of marmots in the Xinjiang's Altai Mountains, a newly discovered plague focus of China","authors":"Qiguo Wang ,&nbsp;Mailihaba Baikeli ,&nbsp;Yongjun Luo ,&nbsp;Xijiang Wang ,&nbsp;Yi Zhang ,&nbsp;Jun Zhao ,&nbsp;Remila Tuerhong ,&nbsp;Maidina Xiaokaiti ,&nbsp;Azhati Rehemu ,&nbsp;Xinhui Wang ,&nbsp;Wenting Mou","doi":"10.1016/j.bbrep.2026.102539","DOIUrl":"10.1016/j.bbrep.2026.102539","url":null,"abstract":"<div><div>The Altai Mountains in Xinjiang have been recognized as a new plague focus in China since 2023. Although previous morphological studies suggested that marmots in this region belong to <em>Marmota baibacina</em>, this classification remained unconfirmed at the molecular level. In this study, 37 marmot samples were collected: including 10 <em>M. baibacina</em> from the northern Tianshan Mountains, 9 <em>M. baibacina</em> from the southern Tianshan Mountains, and 18 unverified individuals from the Altai Mountains. The <em>COI</em>, <em>Cytb</em>, and <em>D-loop</em> gene fragments were sequenced and subjected to phylogenetic analysis. Homology comparisons revealed greater than 95% sequence identity across all samples, with all matches corresponding to marmot populations. Genetic distances between groups (1%–7%) exceeded those within groups (0%–2%). <em>F</em>_<em>st</em> values among populations ranged from 0.55780 to 0.98449, indicating significant differentiation, particularly between the southern Tianshan population and the other two groups. In contrast, genetic divergence between the Altai and northern Tianshan populations was minimal. Maximum likelihood trees based on <em>COI</em> and <em>Cytb</em> sequences strongly supported a close phylogenetic relationship between the northern Tianshan and Altai marmots, which clustered together, while the southern Tianshan population formed a separate clade. The <em>D-loop</em> region provided lower phylogenetic resolution. Based on these results, we confirm that the marmots in the Altai Mountains belong to <em>M. baibacina</em> and classify this plague focus as a <em>M. baibacina</em>–<em>Spermophilus undulatus</em> focus, given that <em>S. undulatus</em> is also a documented reservoir host in the area. These findings provide a molecular basis for targeted plague surveillance and control. The close genetic affinity between the northern Tianshan and Altai populations further suggests they may represent the same subspecies.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"46 ","pages":"Article 102539"},"PeriodicalIF":2.2,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147388237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fundamentals and emerging frontiers in p53-targeted drug development","authors":"Hui-Deng Long ,&nbsp;Ning Zhang ,&nbsp;Wen-Er Wang ,&nbsp;Yu-Shui Ma ,&nbsp;Fu-Xing Liu ,&nbsp;Zi-Yu Chen ,&nbsp;Cui-Ni Lu ,&nbsp;Xiao-Feng Wang ,&nbsp;Ning Han ,&nbsp;Yue-Feng Cai ,&nbsp;Chun Yang ,&nbsp;Xiao-Mei Tang ,&nbsp;Hong Yu ,&nbsp;Hong Jiang ,&nbsp;Da Fu ,&nbsp;Kai-Jian Chu ,&nbsp;Wen-Guang Wu","doi":"10.1016/j.bbrep.2026.102661","DOIUrl":"10.1016/j.bbrep.2026.102661","url":null,"abstract":"<div><div>As a key tumor suppressor protein, p53 plays a central role in biological processes such as cell cycle regulation, DNA repair, apoptosis, and metabolism. However, p53 gene mutations or functional inactivation are prevalent in over 50% of human cancers, leading to tumorigenesis, development, and drug resistance, making it an important target for anticancer drug development. Currently, p53-targeted therapy faces challenges such as diverse mutation types, insufficient drug specificity, and drug resistance. This article systematically reviews the fundamental theories and cutting-edge advances in the development of p53-targeted drugs. It elaborates on the structure and function of p53 and its mutation-induced carcinogenic mechanisms, then focuses on analyzing the research history and clinical translation status of small-molecule drugs (e.g., APR-246), discusses the application prospects of gene therapy and immunotherapy strategies, and introduces emerging therapies based on CRISPR and PROTAC technologies. By integrating the latest research findings, this article aims to provide theoretical basis and directional guidance for the precise development and clinical translation of p53-targeted drugs.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"46 ","pages":"Article 102661"},"PeriodicalIF":2.2,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148167381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Irisin promotes selective changes in hippocampal mitochondrial metabolism in mice.","authors":"Ariene S Fonseca, Marina S Chichierchio, Mariana G Chauvet, Guilherme B de Freitas, Andréa Tosta, Tiago Ferreira de Lima, Marcos A Formiga-Jr, Felipe C Ribeiro, Sergio T Ferreira, Fernanda G De Felice, Juliana Camacho-Pereira, Mychael V Lourenco","doi":"10.1016/j.bbrep.2026.102657","DOIUrl":"10.1016/j.bbrep.2026.102657","url":null,"abstract":"<p><p>Irisin, an exercise-induced hormone, exerts neuroprotective actions in neurological disease models, yet its effects on brain mitochondrial metabolism remain unclear. Here, we examined how irisin influences mitochondrial function and dynamics in the mouse hippocampus. Acute irisin exposure boosted ATP-coupled oxygen consumption without altering mitochondrial content or dynamics-related proteins. Furthermore, chronic irisin administration in vivo decreased hippocampal Opa1 and Drp1 levels, two key regulators of mitochondrial remodeling. These findings uncover selective actions of irisin on hippocampal mitochondrial homeostasis and identify prolonged irisin exposure as a potential regulator of mitochondrial dynamics in the brain.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"46 ","pages":"102657"},"PeriodicalIF":3.3,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13235361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"The role of γ-aminobutyric acid and its receptor in metabolicreprogramming and tumor progression\"[Biochem. Biophys. Rep. 46 (2026) 102611].","authors":"Yujie Wang, Junzhao Shao, Ming Wang, Zhenlong Sun, Nan Wang, Wei Li, Hong Luo","doi":"10.1016/j.bbrep.2026.102646","DOIUrl":"https://doi.org/10.1016/j.bbrep.2026.102646","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1016/j.bbrep.2026.102611.].</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"46 ","pages":"102646"},"PeriodicalIF":3.3,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148293262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic high-fat diet decreases global histone H4 acetylation and increases HDAC8 expression in mouse testes.","authors":"Shu Aizawa, Hikari Ohno, Yutaka Yamamuro","doi":"10.1016/j.bbrep.2026.102642","DOIUrl":"10.1016/j.bbrep.2026.102642","url":null,"abstract":"<p><p>Obesity is a major public health problem and a risk factor for metabolic disorders, including type 2 diabetes and cardiovascular disease. Additionally, accumulating evidence suggests that obesity impairs male reproductive capacity, potentially leading to infertility. However, molecular insights into the effects of obesity on the male reproductive system remain elusive. In this study, we examined the effects of diet-induced obesity on epigenetic marks-specifically histone acetylation-and the expression of epigenetic regulatory enzymes in mouse testes. C57BL/6 N male mice were randomly divided into two groups: a control group fed a control diet (10% kcal from fat) and a diet-induced obesity group fed a high-fat diet (HFD; 45% kcal from fat) for 8 weeks. Then, the acetylated histone H3 (K9 and K14) and histone H4 (K5, K8, K12, and K16) levels, as well as the expression of the histone deacetylase (HDAC) family, were investigated in the testes. We found that chronic HFD exposure decreased the acetylation levels of histone H4, but not histone H3, in the entire testis. We also observed the increased expression of HDAC8 at both the mRNA and protein levels in the testes of HFD-fed mice. HFD exposure did not affect the expression of other class I HDACs (HDAC1, HDAC2, and HDAC3) in the testes. These findings suggest that HFD-induced obesity disrupts epigenetic features in the testes, specifically through the modulation of HDAC8 and histone H4 acetylation, providing novel insight into obesity-induced male reproductive dysfunction.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"46 ","pages":"102642"},"PeriodicalIF":3.3,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13214310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148051970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-fibrillation and trans-fibrillation activities of L-arginine modified magnetic nanoparticles on lysozyme.","authors":"Vahid Alimohammadi, Fatemeh Eshari, Faezeh Kashanian, Ali Akbar Moosavi-Movahedi, Seyd Ali Seyed-Ebrahimi, Mehran Habibi-Rezaei","doi":"10.1016/j.bbrep.2026.102551","DOIUrl":"10.1016/j.bbrep.2026.102551","url":null,"abstract":"<p><p>Over the last two decades, the application of nanoparticles (NPs) in the investigation of protein and peptide aggregation and amyloid-related diseases has been extensively studied. Here, we investigate anti-fibrillation and <i>trans</i>-fibrillation activities of L-Arginine modified Magnetic NPs (RMNPs, Fe₃O₄@Arg) on hen egg white lysozyme (HEWL) as a model protein and HEWL amyloid aggregate (HAA, i.e., aggregated HEWL fibrils). RMNPs were prepared by the co-precipitation method and subsequently characterized using X-ray diffraction (XRD), vibrating sample magnetometry (VSM), Fourier transform infrared spectroscopy (FT-IR), and scanning electron microscopy (SEM). The comparison was made among Arg, Magnetic NPs (MNPs), and RMNPs to explore their anti-fibrillation activities on HEWL. Using intrinsic tryptophan (Trp) and extrinsic thioflavin T (ThT) fluorescence assays, circular dichroism (CD) spectroscopy, and electron microscopy methods, for instance, we present the anti-fibrillation and <i>trans</i>-fibrillation activities of the RMNPs on HEWLs or HAAs. Accordingly, fibrillation was inhibited more than 80 percent, and fibrils were longitudinally rearranged to form late amyloid aggregates with a 57< nm diameter from early aggregates with a <14 nm diameter, respectively. The ability to inhibit HEWL amyloid formation highlights the concentration-dependent effects of the investigated NPs on HEWL at different stoichiometric ratios of MNPs and RMNPs. Moreover, RMNPs can interact with HEWL amyloids <i>in vitro</i> and alter the structure of the aggregates. Collectively, our findings shed light on the anti-fibrillation and <i>trans</i>-fibrillation effects of RMNPs on HEWL and HEWL amyloid aggregate (HAA), respectively. In this study, we aim to investigate the potential preventive effects of RMNPs on protein structural <i>trans</i>-formation and fibrillation, as well as their potential to promote the <i>trans</i>-fibrillation of resulting fibrils, representing a novel strategy to interfere with protein aggregation-related disorders.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"46 ","pages":"102551"},"PeriodicalIF":3.3,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148293195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Lactylation as a metabolic-epigenetic switch: Mechanisms and roles in cancer, sepsis, trauma, inflammation, and tissue repair\" [Biochem. Biophys. Rep. 45 (2026) 102507].","authors":"David Bar-Or, Kaysie Banton, David Acuna, Jason Williams, Carlos H Palacio, Christopher Zaw-Mon, Raymond Garrett, Tyler Crawley, Daniel Paredes","doi":"10.1016/j.bbrep.2026.102541","DOIUrl":"https://doi.org/10.1016/j.bbrep.2026.102541","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1016/j.bbrep.2026.102507.].</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"46 ","pages":"102541"},"PeriodicalIF":3.3,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148293209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of daily phase relations identified by multiomic analyses in acute pancreatitis.","authors":"Heather Waddell, Xiaozhong Zheng, Lucile Neyton, Tyler J Stevenson, Natalia Bochkina, Damian J Mole","doi":"10.1016/j.bbrep.2026.102533","DOIUrl":"10.1016/j.bbrep.2026.102533","url":null,"abstract":"<p><p>Acute pancreatitis (AP) is sudden inflammation of the pancreas which can cause organ failure and death, and with no targeted therapies in the clinic, there is an imperative to identify new potential avenues for therapeutics discovery. This exploratory study investigates the potential role of circadian rhythms in AP pathogenesis. We integrated and analysed multiomics data, including transcriptomics, metabolomics, and clinical laboratory measurements, synthesised from peripheral whole blood samples obtained from AP patients. Our exploratory findings identified a potential association between circadian rhythm dysregulation and disease severity. Specifically, we observed that the rhythmic expression of circadian genes across a 24-h period, such as the circadian locomotor output cycles kaput (<i>CLOCK</i>) and the brain and muscle ARNT-Like 1 (<i>BMAL1</i>) gene, and a specific subset of metabolites may be altered in AP. These exploratory results provide a foundation for future investigations into the potential therapeutic implications of targeting circadian rhythms in AP. Additional studies are required to validate these findings and to elucidate the specific mechanisms involved.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"102533"},"PeriodicalIF":3.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyaluronan induces ERK activation with minimal transcriptomic changes in pancreatic α-cells.","authors":"Suguru Sonoyama, Akiko Mizokami, Tomomi Sano, Eijiro Jimi, Masafumi Moriyama, Takashi Kanematsu","doi":"10.1016/j.bbrep.2026.102525","DOIUrl":"10.1016/j.bbrep.2026.102525","url":null,"abstract":"<p><p>Type 1 diabetes (T1D) is driven by the immune-mediated destruction of pancreatic β-cells. While β-cells are selectively targeted and depleted in T1D, α-cells that secrete glucagon are relatively spared from this autoimmune attack. Hyaluronan (HA), a glycosaminoglycan component of the extracellular matrix, accumulates within pancreatic islets in patients with T1D and in animal models, and has been implicated in promoting chronic inflammation. Given that surviving α-cells reside within this HA-rich microenvironment, we investigated whether HA contributes to molecular alterations in α-cells associated with the T1D phenotype. A murine α-cell line, αTC1-6, was stimulated with low-molecular-weight HA, which induced sustained extracellular signal-regulated kinase (ERK) phosphorylation upon HA stimulation, indicating activation of intracellular signaling. To assess whether this signaling response was accompanied by transcriptional changes, RNA sequencing was performed, and the resulting profile was compared with publicly available RNA-seq datasets from α-cells isolated from T1D donors. Despite robust ERK activation, HA stimulation elicited only minimal transcriptional changes relative to the T1D α-cell transcriptome. Gene set enrichment analysis further revealed a modest shift toward reduced peroxisome proliferator-activated receptor (PPAR) signaling in both HA-stimulated and T1D α-cells, suggesting a shared pathway-level signature. These findings indicate that HA alone does not fully recapitulate the extensive transcriptional remodeling observed in T1D α-cells, and that additional inflammatory or microenvironmental cues are required.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"102525"},"PeriodicalIF":3.3,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA GAS5 regulates osteogenic differentiation of human periodontal ligament stem cells through miR-23b-3p/STAT5B axis.","authors":"Qiufang Zhang, Yan Huang, Liping Huang, Zhisheng Zhang, Qiliang Zuo","doi":"10.1016/j.bbrep.2026.102516","DOIUrl":"10.1016/j.bbrep.2026.102516","url":null,"abstract":"<p><p>Periodontal ligament stem cells (PDLSCs) play a crucial role in alveolar bone regeneration due to their inherent osteogenic differentiation capacity. However, the molecular mechanisms regulating PDLSC osteogenic differentiation remain incompletely understood. In this study, human PDLSCs were isolated and characterized, revealing that the cytoplasmic long non-coding RNA GAS5 was significantly upregulated during osteogenic induction. Functional assays demonstrated that GAS5 overexpression markedly enhanced alkaline phosphatase (ALP) activity, mineralized nodule formation, and the expression of osteogenic marker genes (RUNX2, OCN, OPN). Conversely, GAS5 knockdown attenuated these osteogenic phenotypes. Mechanistically, GAS5 functioned as a competitive endogenous RNA (ceRNA) by directly binding to miR-23b-3p, thereby preventing miR-23b-3p-mediated post-transcriptional silencing of its target gene STAT5B. Rescue experiments confirmed that STAT5B silencing abolished the pro-osteogenic effects induced by GAS5 overexpression, while miR-23b-3p inhibition reversed the osteogenic impairment caused by GAS5 knockdown. Collectively, our findings reveal a novel regulatory axis (GAS5/miR-23b-3p/STAT5B) that modulates PDLSC osteogenic differentiation, offering a potential therapeutic target for periodontal tissue regeneration strategies.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"102516"},"PeriodicalIF":3.3,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12969340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}