Biochemistry and Biophysics Reports最新文献

{"title":"Intrinsic clustering of flagellar basal body proteins in E. coli: A self-organization mechanism for assembly and regulation","authors":"Yun-Sing Sung,&nbsp;De-Fa Hong,&nbsp;Yi-Ren Chang","doi":"10.1016/j.bbrep.2025.102051","DOIUrl":"10.1016/j.bbrep.2025.102051","url":null,"abstract":"<div><div>The assembly and spatial organization of flagellar basal bodies in <em>Escherichia coli</em> are crucial for motility and chemotaxis. Using fluorescence and single-molecule microscopy, we demonstrate that key basal body proteins, FliF and FlhA, self-organize into clusters from low to high expression conditions. Rather than forming new basal bodies, excess proteins accumulate around pre-existing structures, suggesting an autocatalytic mechanism. It is confirmed that clustering occurs even at low protein levels, indicating an intrinsic organizational principle rather than an artifact of overexpression. Fluorescence recovery after photobleaching (FRAP) revealed dynamic protein exchange within clusters, supporting a diffusion-capture model. Single-molecule analysis showed that FlhA actively remodels clusters, while FliF stabilizes them. 3D imaging suggested that basal body positioning optimizes flagellar distribution for efficient motility. These findings highlight a robust mechanism that regulates basal body positioning and flagellar assembly, ensuring adaptability to varying cellular conditions.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102051"},"PeriodicalIF":2.3,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143942952","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":"β-suppressor protein 1 (ARRB1)-△exon13 modulates the progression of glioblastoma via combination with glycolysis-related proteins","authors":"Zi-Long Wei ,&nbsp;Shuo Han ,&nbsp;Dong-Hua Han ,&nbsp;Xue-Tao Li ,&nbsp;Yu-Lun Huang ,&nbsp;Zhi-Min Wang","doi":"10.1016/j.bbrep.2025.102048","DOIUrl":"10.1016/j.bbrep.2025.102048","url":null,"abstract":"<div><div>Glioblastoma multiform (GBM) constitutes approximately 14.7 % of all central nervous system tumors (CNSTs) and 45.2 % of primary malignant CNSTs. Extensive research has indicated that β-arrestin 1 (ARRB1) plays a significant role in tumor malignancy. In this investigation, we established GBM cell lines representing normal control (NC), overexpression (OE) and Δexon13 GBM variants (△exon13) of ARRB1. Our findings indicate that the ARRB1-OE isoform facilitated GBM cell proliferation and migration, with the ARRB1-△exon13 isoform further augmenting this effect. Notably, the isoform ARRB1-△exon13 binds to glycolytic proteins including ENO1 and ALDOA and regulates glycolysis. In vivo studies corroborate the tumor-promoting effects of ARRB1-Δexon13. Furthermore, we demonstrate that 2-DG effectively inhibits the malignancy-promoting capabilities of ARRB1-Δexon13 by reducing pyruvate levels. Our identification of alternative RNA splicing events of ARRB1 reveals a mechanism by which GBM cell malignancy is augmented through ARRB1-Δexon13, which mediates glycolysis-related pathways.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102048"},"PeriodicalIF":2.3,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936082","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":"Gene network changes after exposure to nanoliposomes containing antisense miR-21 and miR-373 in bladder cancer Cells: An in vitro model study","authors":"Omid Nikkhah ,&nbsp;Behzad Einollahi ,&nbsp;Mosa Asadi ,&nbsp;Mohammad Heiat ,&nbsp;Kiavash Hushmandi","doi":"10.1016/j.bbrep.2025.102041","DOIUrl":"10.1016/j.bbrep.2025.102041","url":null,"abstract":"<div><h3>Aims</h3><div>This study aimed to examine the changes in gene expression profiles of the bladder cancer cell line (HTB-9) after exposure with nanoliposomes (NLs) containing antisense miR-21, antisense miR-373, or a combination of both antisense miR-21 and antisense miR-373 oligonucleotides.</div></div><div><h3>Methods</h3><div>The sequence of miR-21 and miR-373 was obtained from the NCBI, and the optimal corresponding antisense oligonucleotides (ASOs) were selected and synthesized using the Oligowalk online server. After encapsulating the ASOs in liposomes and characterizing them, the liposomal ASOs were incubated with the target cells for 24 h at 37 °C. Following incubation, total RNA was extracted, and cDNA was synthesized. The expression levels of miR-21, miR-373, and eight additional core genes (<em>STK38L</em>: Serine/threonine-protein kinase 38-like; <em>PCDH19</em>: Protocadherin-19; <em>YOD1:</em> Ubiquitin thioesterase OTU1; <em>PRDM11:</em> PR domain-containing protein 11; <em>CROT:</em> Peroxisomal carnitine <em>O</em>-octanoyltransferase; <em>LATS2:</em> Serine/threonine-protein kinase; <em>ZNF845:</em> Zinc finger protein 845; <em>ZC3H6:</em> Zinc finger CCCH domain-containing protein 6) were then analyzed using quantitative Reverse Transcriptase - PCR (qRT-PCR).</div></div><div><h3>Results</h3><div>ASOmiR-21 (AUCUCAUGGCAACACCAGU) and ASOmiR-373 (AAGUGCUUCGAUUUUGGGG) nucleotides were used in this study, respectively. Data analysis revealed that the expression levels of miR-21 and miR-373 were significantly reduced in HTB-9 cells exposed to nanoliposomal ASOs (NL-ASOs) with sizes ranging from 100 ± 5 to 260 ± 10 nm, compared to the control groups. Furthermore, HTB-9 cells exposed simultaneously to both liposomal ASOs (NL-ASOmiR-21+ASOmiR-373) exhibited a greater reduction in miR-21 and miR-373 expression. Additionally, all studied genes (<em>STK38L</em>, <em>PCDH19</em>, <em>YOD1</em>, <em>PRDM11</em>, <em>CROT</em>, <em>LATS2</em>, <em>ZNF845</em>, <em>ZC3H6</em>) showed significant decreases in expression in HTB-9 cells exposed to NL-ASOs across all experimental designs.</div></div><div><h3>Conclusions</h3><div>The results demonstrated that miR-21 and miR-373 play crucial roles in gene expression and that their inhibition can significantly impact the expression profile of a gene network in bladder cancer. Therefore, to regulate the expression of a gene network in bladder cancer, we can use antimir technology as an effective strategy.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102041"},"PeriodicalIF":2.3,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936081","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":"Effects of ibrutinib and venetoclax on the expression of immune checkpoint molecules in leukemic blasts of patients with acute lymphoblastic leukemia","authors":"Armin Dozandeh-Jouybari ,&nbsp;Fatemeh Mousavi-Mirkalaei ,&nbsp;Saeid Taghiloo ,&nbsp;Hossein Karami ,&nbsp;Mohammad Naderisorki ,&nbsp;Ehsan Zaboli ,&nbsp;Mohammad Eslami-Jouybari ,&nbsp;Tohid Kazemi ,&nbsp;Hossein Asgarian-Omran","doi":"10.1016/j.bbrep.2025.102045","DOIUrl":"10.1016/j.bbrep.2025.102045","url":null,"abstract":"<div><h3>Background</h3><div>In recent decades, targeted therapy using small molecule inhibitors (SMI) have been shown very promising results in the treatment of a variety of solid and hematopoietic malignancies. However, their exact mechanisms, especiallay on the evasion strategies of tumor cells from the host immune system are not fully understood. The current study investigates the effects of two SMIs, ibrutinib and venetoclax, on the expression of inhibitory immune checkpoint molecules in patients with acute lymphoblastic leukemia (ALL).</div></div><div><h3>Methods</h3><div>Leukemic cells were isolated from 20 patients with ALL by magnetic activated cell sorting (MACS) technique. Isolated leukemic cells were cultured and treated by ibrutinib and venetoclax for 48 h. Cell viability and apoptosis were monitored through MTT and flow cytometry assays, respectively. The mRNA expression levels of checkpoint molecules PD-L1, galectin-9, CD200, CD155, CD47, and anti-inflammatory cytokine TGF-β were determined by Real-Time PCR method.</div></div><div><h3>Results</h3><div>The purity of MACS-isolated ALL leukemic cells was &gt;98% as determined by flow cytometry. Following treatment, the proliferation of leukemic cells was significantly decreased and the apoptosis rate was significantly increased, which was more remarkable for venetoclax. Moreover, treatment of leukemic cells with ibrutinib and venetoclax showed alterations in the mRNA expression of immune checkpoint inhibitory ligands and TGF-β.</div></div><div><h3>Conclusion</h3><div>Our results indicated that small molecule inhibitors not only hinder proliferation and enhance apoptosis, but also affect the expression of inhibitory immune checkpoint ligands. By elucidating the precise underlying mechanisms, these drugs could emerge as promising therapeutic options, particularly in the context of combination therapy for ALL.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102045"},"PeriodicalIF":2.3,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936080","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":"Single-cell RNA-seq analysis reveals the multi-step process of cellular senescence","authors":"Minseo Ahn ,&nbsp;Junil Kim ,&nbsp;Jae Ho Seo","doi":"10.1016/j.bbrep.2025.102042","DOIUrl":"10.1016/j.bbrep.2025.102042","url":null,"abstract":"<div><div>Cellular senescence is a phenomenon marked by an irreversible growth arrest with altered physiological properties. Many studies have focused on the characteristics of cells that have already entered a senescent state. However, to elucidate the mechanisms of cellular aging, it is essential to investigate the gradual transition of proliferative cells into senescent cells. We hypothesized that cellular senescence is a complex, multi-step process in which each stage is characterized by distinct cellular features and transcription factor expression patterns. To test this hypothesis, we utilized publicly available single-cell RNA-Seq (scRNA-Seq) data from human umbilical vein endothelial cells (HUVECs) undergoing replicative senescence. We employed Seurat and Monocle 3 to capture the transition from proliferating to senescent states in HUVECs. Four clusters were identified, and each cluster displayed distinct expression patterns of cellular senescence markers and the senescence-associated secretory phenotypes (SASPs). We also employed SCENIC to identify the expression patterns of core transcription factors (TFs) during replicative senescence. While the majority of TFs exhibited a linear trend, HMGB1, FOSL1, SMC3, RAD21, SOX4, and XBP1 showed fluctuating expression patterns during replicative senescence. Furthermore, the expression of these TFs exhibited different patterns in the ionizing radiation (IR) model of senescence. Overall, our study unveils the distinct characteristics of each phase during replicative senescence and identifies expression trends in SASPs and TFs that may play pivotal roles in this process. Unlike previous bulk RNA-seq studies, this work uniquely integrates single-cell trajectory and transcription factor dynamics to decode phase-specific molecular signatures during replicative senescence. Here, we identify key transcription factors potentially involved in senescence induction and provide novel insights into the regulatory complexity of cellular aging.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102042"},"PeriodicalIF":2.3,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143931832","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":"High expression of THY1 is a prognostic marker for gastric Cancer: Deciphering its transcriptional regulation as a component of the Epithelial–mesenchymal transition","authors":"Paulo Rohan,&nbsp;Everton Cruz dos Santos,&nbsp;Pedro Leite Azevedo,&nbsp;Jessica Oliveira da Conceição,&nbsp;Eliana Abdelhay ,&nbsp;Renata Binato","doi":"10.1016/j.bbrep.2025.102050","DOIUrl":"10.1016/j.bbrep.2025.102050","url":null,"abstract":"<div><div>Gastric cancer (GC) remains one of the leading causes of cancer-related mortality worldwide, with high molecular heterogeneity contributing to its poor prognosis. Among potential biomarkers, <em>THY1</em> is associated with aggressive tumor behavior and poor patient outcomes. However, the transcriptional mechanisms governing <em>THY1</em> expression in GC remain largely unexplored. This study aimed to systematically investigate the upstream regulatory landscape of <em>THY1</em> and its role in tumor progression. By integrating multicohort transcriptomic data (n = 945), we inferred consensus transcriptional regulatory networks (TRNs) and identified six putative transcription factors (PRRX1, TWIST1, SNAI2, MEIS3, VENTX, and EGR2) as robust regulators of <em>THY1</em>. The functional enrichment analysis revealed that these regulators are involved in the epithelial–mesenchymal transition (EMT) and extracellular matrix remodeling, key processes associated with tumor invasion and metastasis. Experimental validation using chromatin immunoprecipitation (ChIP) assays indicated the direct and differential binding of TWIST1 and SNAI2 to the <em>THY1</em> promoter, supporting their roles as key regulators of <em>THY1</em> expression in GC. Our findings provide a mechanistic link between <em>THY1</em> expression and EMT transcriptional programs, offering insights into its association with a poor prognosis. By integrating bioinformatic predictions with experimental demonstration, this study not only improves our understanding of <em>THY1</em> regulation but also provides a framework for dissecting the transcriptional networks governing aggressive tumor phenotypes. These results contribute to a broader understanding of GC progression and may inform future therapeutic strategies targeting EMT-related pathways in <em>THY1</em>^high GC.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102050"},"PeriodicalIF":2.3,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936078","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":"Recombinant human Neuritin protects cochlear ribbon synapses and hearing function via ERK1/2 activation post noise-induced injury","authors":"Haiyan Wang ,&nbsp;Jinchi Hu ,&nbsp;Shuangyan Liu ,&nbsp;Fei Gui ,&nbsp;Xiaopin Sun ,&nbsp;Rong Chen ,&nbsp;Guanwu Yin ,&nbsp;Xiaoming Song ,&nbsp;Yi Yang ,&nbsp;Yu Hong","doi":"10.1016/j.bbrep.2025.102044","DOIUrl":"10.1016/j.bbrep.2025.102044","url":null,"abstract":"<div><div>The preservation of synaptic integrity and physiological activity is pivotal for post-traumatic auditory rehabilitation following acoustic overexposure. Neuritin, a neurotrophic factor that facilitates synapse formation, maturation, and enhanced synaptic transmission, is essential for synapse development. In this study, we established a noise-induced cochlear synaptopathy model in CBA/CaJ mice, revealing a temporal association between endogenous Neuritin expression and synaptic density. Furthermore, administration of recombinant Human Neuritin (rhNeuritin) effectively preserves synaptic density in the cochlear basal turn at 7 days and 14 days following noise exposure. Importantly, it preserves the density of functional synapses (represented by overlapping CtBP2 and GluA2 puncta) and synapse function (indicated by ABR I wave amplitudes), thus diminishing the impairment of auditory function. In addition, rhNeuritin reverses the decrease in phosphorylated extracellular signal-regulated protein kinase 1/2 (<em>p</em>-ERK1/2) levels resulting from noise exposure. By primarily preserving both the number and functionality of synapses in the basal turn, potentially via the induction of ERK1/2 phosphorylation, rhNeuritin mitigated hearing loss. These findings underscore the protective efficacy of rhNeuritin against noise-induced synaptic injury.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102044"},"PeriodicalIF":2.3,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143931897","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":"Short communication: The effect of Propolis extract treatment on the Lee index and brain-body weight ratio in diet-induced obesity rats","authors":"Andreas Christoper ,&nbsp;Herry Herman ,&nbsp;Rizky Abdulah ,&nbsp;Felix Zulhendri ,&nbsp;Ronny Lesmana","doi":"10.1016/j.bbrep.2025.102039","DOIUrl":"10.1016/j.bbrep.2025.102039","url":null,"abstract":"<div><div>Obesity is a severe public health concern that can impair brain structure and function. The potential anti-inflammatory and anti-obesogenic properties of propolis extract are beneficial in preventing brain damage after diet-induced obesity. The purpose of the study is to investigate the role of propolis extract in high-fat diet-induced obesity rats using the Lee index and brain-body weight ratio (BBWR). We divided the rats into the experimental groups as follows: CD (normal chow diet), CP (normal chow diet with propolis treatment), FD (high-fat diet), and FP (high-fat diet with propolis treatment). We administered propolis extract in CP and FP for nine weeks during 21 weeks of diet. The rat's body weight and length were measured for obesity evaluation. The brain of all experimental rats was harvested and weighed at the end of the study. We found that a chronic high-fat diet significantly increased body weight and the Lee index (<em>p</em> &lt; 0.01). However, a high-fat diet significantly decreased brain weight and BBWR in rats (<em>p</em> &lt; 0.05). Nine weeks of propolis extract supplementation in the FP group reduced the Lee index (<em>p</em> &lt; 0.01) and slightly increased brain weight and BBWR compared to the FD group. We observed a negative correlation between brain weight and the Lee index (R = – 0.64). Therefore, we conclude that propolis extract has the potential to sustain brain health in obesity.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102039"},"PeriodicalIF":2.3,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143922570","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":"Paridis Rhizoma Saponins ameliorate CCl4-induced liver fibrosis via modulation of the Nrf2-HO-1/NQO-1 and TGF-β1/Smads signaling pathways","authors":"Yan Hong ,&nbsp;Shuang Geng ,&nbsp;Huihao Ao ,&nbsp;Mengya Fu ,&nbsp;Xiaojun Yang ,&nbsp;Gang Cao ,&nbsp;Yanquan Han","doi":"10.1016/j.bbrep.2025.102040","DOIUrl":"10.1016/j.bbrep.2025.102040","url":null,"abstract":"<div><h3>Objective/background</h3><div>Paridis Rhizoma is a common traditional Chinese medicine (TCM), possessing therapeutic effects including heat-clearing, detoxification, and liver calming effects. It is frequently applied in TCM prescriptions for the treatment of liver disease. Studies have shown that total saponins derived from Paridis Rhizoma (PRS) have potent anti-liver fibrosis effect, but its mechanism in treating liver fibrosis has not been clarified. This study aimed to explore the therapeutic effect of PRS on liver fibrosis and elucidate their potential underlying pharmacological mechanisms.</div></div><div><h3>Methods</h3><div>The targets and pathways of Paridis Rhizoma Saponins on experimental liver fibrosis were analyzed using network pharmacology and molecular docking. PRS was administered to rats with CCL₄-induced liver fibrosis rats. Liver function, fibrosis, and inflammatory indicators were assessed using ELISA to measure serum AST and ALT, as well as liver tissue levels of HA, LN, Col IV, and PC-III fibrosis markers. Additionally, inflammatory markers IL-6, IL-β, and TNF-a were quantified. Liver morphological, H&amp;E, and Masson's staining were used to observe the degree of liver fibrosis. The mRNA and protein expressions of Nrf2-HO-1/NQO-1 and TGF-β1/Smads signaling pathways in liver tissues were detected using immunohistochemistry (IHC) staining, Western blot (WB), and RT-qPCR.</div></div><div><h3>Results</h3><div>Comprehensive network pharmacology and animal experiments show that PRS may act on STAT3, SRC, VEGFA, AKT1 and other targets through its polyphyllin I, polyphyllin II, polyphyllin VI, polyphyllin VII and other components.Analysis from ELISA showed that PRS could improve liver function, mitigate the progression of liver fibrosis, and regulate inflammatory responses in rats. Morphological, H&amp;E, and Masson's staining demonstrated that PRS significantly improved liver tissue immune response and necrosis. Additionally, IHC staining, WB results, and RT-qPCR results showed that PRS positively regulates the Nrf2-HO-1/NQO-1 and TGF-β1/Smads signaling pathways to counteract the development of pathological liver fibrosis in rats.</div></div><div><h3>Conclusion</h3><div>These findings indicate that PRS can mitigate the impact of CCl₄-induced liver fibrosis in experimental animals by upregulating the Nrf2-HO-1/NQO-1 and downregulating the TGF-β1/Smads signaling pathways.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102040"},"PeriodicalIF":2.3,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143907756","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":"Steroid hormone binding and modulation of Trichinella spiralis progesterone receptor: A computational approach","authors":"Muhammad Tahir Aleem ,&nbsp;Shakeel Ahmed Lakho ,&nbsp;Muhammad Mohsin ,&nbsp;Shahbaz Ul haq ,&nbsp;Ashiq Ali ,&nbsp;Danmei Huang ,&nbsp;Fenfei Gao","doi":"10.1016/j.bbrep.2025.102031","DOIUrl":"10.1016/j.bbrep.2025.102031","url":null,"abstract":"<div><div>Trichinellosis, caused by <em>Trichinella</em> species, including <em>Trichinella spiralis</em>, is a foodborne zoonotic disease. Upon ingestion, ML swiftly invade the intra-multicellular niche of the small intestine, undergoing four rapid molts to mature into adults. In general, the route of transmission for <em>T. spiralis</em> nematodes occurs through ingestion of pork. Therefore, it is crucial to develop a vaccine that can deal with trichinellosis, particularly for humans and pigs. In this study, homology modelling, molecular docking, simulations and molecular mechanics-based scoring (MM/GBSA) are used to investigate the interaction between <em>T. spiralis</em> membrane-associated progesterone receptor component 2 (<em>Ts</em>-MAPRC2) and different steroids hormones. In the most favorable region, 93 amino acid residues (92.1 %) are located, while 7 amino acids (6.9 %) are located in the allowed region, showing that the model with a 93.33 ERRAT quality factor is good quality. The MD simulations were conducted for 50 ns to explore the affinities and stability of four hormones chosen from the docking studies that showed similar binding poses to the control hormone Mifepristone. Simulations showed that the selected hormones were potent Ts-MAPRC2 binders and can act as leads to determine their activity by biophysical assays. Discovery of these five steroid hormones and interactions with Ts-MAPRC2 could lead to new therapies and vaccines for trichinellosis.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102031"},"PeriodicalIF":2.3,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143907903","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}