Biochemistry and Biophysics Reports最新文献

{"title":"Towards precision epitopes based vaccine against Enterococcus faecalis by integrating vaccinomics, reverse vaccinology and biophysics approaches","authors":"Asad Ullah ,&nbsp;Sadiq Azam ,&nbsp;Sajjad Ahmad ,&nbsp;Ibrar Khan ,&nbsp;Dalia M. Alammari ,&nbsp;Sumra Wajid Abassi ,&nbsp;Dong-Qing Wei ,&nbsp;Fahad M. Alshabrmi ,&nbsp;Mohammad Abdullah Aljasir ,&nbsp;Eid A. Alatawi","doi":"10.1016/j.bbrep.2025.102082","DOIUrl":"10.1016/j.bbrep.2025.102082","url":null,"abstract":"<div><div><em>Enterococcus faecalis</em> is a Gram-positive bacterium and recognized as an etiological agent of different nosocomial infections. <em>E. faecalis</em> has developed resistance to several antibiotics. No licensed vaccine is available to prevent <em>E. faecalis</em> infections. A multi-epitopes-based vaccine construct may provide effective vaccine design foundation. In this study, an integrated bioinformatic approach was applied to design of a multi-epitopes-based vaccine construct against <em>E. faecalis</em>. In subtractive proteomics analysis, 10 proteins were prioritized as potential vaccine candidates based on several literature reported vaccine candidacy parameters. In immunoinformatics analysis, only two proteins (glucosaminidase domain-containing protein and serine protease) were found as promising vaccine targets. Both proteins were then subjected to epitopes mapping for screening of broad-spectrum antigenic epitopes. The predicted epitopes were further refined based on immunoinformatics filters and only six epitopes; DTSDHQKNNV, GMKKRKARY, SVFDESMALR, NLNQRIEKR, NVDKKIEEK, and TTTPSTDNSA were found as non-allergic, antigenic, water-soluble, non-toxic and DRB∗0101 good binders. The selected epitopes were fused via GPGPG linkers and additionally linked to an adjuvant molecule through EAAAK linkers to increase the immunogenicity and antigenicity of the vaccine construct. The net interactions energy of the vaccine and receptors was evaluated through molecular docking analysis, which predicted −833.0 kcal/mol and −1001.6 kcal/mol of binding energy for MHC-I and MHC-II, respectively. The values predict effective vaccine construct binding with host immune cell receptors and triggering of innate and adaptive immune responses. The dynamic behavior of the docked complexes was examined using molecular dynamics (MD) simulation technique on a time scale of 500 ns. The MD revealed minimal intermolecular conformational deviations and exposed presentation of the vaccine epitopes for immune cells recognition and processing. For MHC-I-Vaccine complex, the mean RMSD was found as 2.78 Å while MHC–II–Vaccine complex showed a mean RMSD value of 13.17 Å. The C-immune simulation predicted the formation of high titer humoral and cellular immunological responses against the vaccine antigen. The predicted IgG and IgM titer found against the antigen was 600000–650000 counts per milliliter. The interferon-gamma (IFN-γ) was predicted to be stimulated at 430000 ng per milliliter. Simulation trajectories based MMGB/PBSA binding energy was estimated as &lt; −250 kcal/mol for vaccine-MHC complexes, illustrating formation of robust interactions between the vaccine and MHC receptors. The study outcomes predicted the viability of the proposed epitope-based vaccine construct as a promising therapeutic approach for <em>E. faecalis</em> infections prevention, however, experimental confirmation is required.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"Article 102082"},"PeriodicalIF":2.3,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144253983","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":"Characterizing the expression profile of Dexras1 in human trabecular meshwork cells","authors":"ChihWei Chen ,&nbsp;Jiapeng Han ,&nbsp;Luis Sanchez ,&nbsp;Judy L. Chen ,&nbsp;Jie J. Zheng","doi":"10.1016/j.bbrep.2025.102077","DOIUrl":"10.1016/j.bbrep.2025.102077","url":null,"abstract":"<div><div>Corticosteroids are a mainstay therapy for the treatment of ocular and systemic inflammatory conditions but are associated with a significant risk of intraocular pressure elevation, or ocular hypertension. If intraocular pressure is inadequately controlled, steroid-induced glaucoma may develop, which can result in permanent vision loss and irreversible blindness. Pathological changes akin to fibrosis in the trabecular meshwork, the tissue responsible for intraocular pressure regulation, have been well described and contribute to the development of steroid-induced ocular hypertension and glaucoma. However, the molecular mechanisms driving these fibrosis-like changes in the trabecular meshwork following steroid treatment remain poorly understood. <em>RASD1</em> is a gene coding for Dexras1, a small G protein of the Ras family discovered based on its marked induction by the synthetic glucocorticoid dexamethasone. Accumulating evidence points to the role of glucocorticoids in alterations of trabecular meshwork cell morphology, growth, and cell-extracellular matrix interactions. Therefore, we sought to confirm and further characterize how glucocorticoid-induced Dexras1 expression may contribute to glaucoma pathology <em>in vitro</em>. In this study, we found that dexamethasone significantly upregulated the expression of Dexras1 in trabecular meshwork cells within 30 min to 1 h post treatment. In addition, we discovered two phenotypes of Dexras1 induction independent of glucocorticoid responsiveness: younger and older donors show significant upregulation of Dexras1, whereas middle-aged donors experience little to no changes in Dexras1 expression after dexamethasone treatment. This age-dependent Dexras1 response may provide a novel explanation for the greater prevalence of steroid-induced glaucoma observed in older and younger populations as opposed to middle-aged populations.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"Article 102077"},"PeriodicalIF":2.3,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144253986","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":"HUC-MSC-derived exosomal miR-16-5p attenuates inflammation via dual suppression of M1 macrophage polarization and Th1 differentiation","authors":"Yuanjing Zheng ,&nbsp;Yue Li ,&nbsp;Zhengyang Wei ,&nbsp;Yang Wang ,&nbsp;Yuanlin Liu ,&nbsp;Fengsong Liu ,&nbsp;Xue Li ,&nbsp;Yi Zhang","doi":"10.1016/j.bbrep.2025.102078","DOIUrl":"10.1016/j.bbrep.2025.102078","url":null,"abstract":"<div><div>Nowadays mesenchymal stem cell-derived exosomes (MSC-Exos) have emerged as a promising cell-free therapeutic alternative to MSC-based therapies, demonstrating efficacy in treating degenerative diseases, inflammatory disorders, and autoimmune diseases. MSC-Exos transport bioactive cargoes such as proteins, lipids, mRNAs, and microRNAs (miRNAs) to the recipient cells, mediating intercellular communication to regulate immunomodulation and tissue repair. However, the exosomal miRNA profile varies dynamically based on the culture conditions and tissue sources. Thus, elucidating the specific exosomal miRNA profile and regulatory targets is critical for the precise clinical applications and development of MSC-Exos-based cell-free therapies.</div><div>Here we established an optimized serum-free culture system for human umbilical cord-derived MSCs (hUC-MSCs) and determined the critical 48–72-h harvest window for exosome secretion. High-throughput sequencing identified miR-16-5p as the predominant exosomal miRNA, functioning as a core immunosuppressive effector by suppressing LPS/IFN-γ-induced M1 macrophage polarization and Th1 cell differentiation. Mechanistically, miR-16-5p was found to target key nodes in NF-κB and JAK-STAT pathways, validated via dual-luciferase assays. Additionally, miR-125b-5p and miR-34a-5p enhanced this immunosuppressive effect by co-targeting overlapping pathway components in NF-κB and JAK-STAT pathways, suggesting a multilayered regulatory network. Taken together, our findings highlight the potential of miRNA-engineered exosomes as standardized therapies for inflammatory disorders, emphasizing the importance of optimizing culture conditions and profiling miRNA expression over time in advancing clinical translation.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"Article 102078"},"PeriodicalIF":2.3,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144240808","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":"Combination of AURKA inhibitor and MEK inhibitor strongly enhances G1 arrest and induces synergistic antitumor effect on KRAS or BRAF mutant colon cancer cells","authors":"Masashi Sato ,&nbsp;Yoshiyuki Yamamoto ,&nbsp;Toshikazu Moriwaki ,&nbsp;Kuniaki Fukuda ,&nbsp;Kiichiro Tsuchiya","doi":"10.1016/j.bbrep.2025.102073","DOIUrl":"10.1016/j.bbrep.2025.102073","url":null,"abstract":"<div><div>In colorectal cancer, <em>RAS</em> and <em>BRAF</em> are major mutation points in the RAS-MAPK signaling pathway. These gene mutations are known to be important causes of resistance to anti-EGFR antibody therapies. Recently, it has been reported that Aurora kinase A (AURKA), one of the mitotic kinases, interacts with the EGFR-RAS-MAPK signaling pathway. In this study, we examined whether the combination of MK-5108 (AURKA inhibitor) and trametinib (MEK inhibitor) enhanced the antitumor effect for colon cancer cell lines. The combination of MK-5108 and trametinib showed synergistic enhancements of antitumor effect in three colon cancer cell lines harboring <em>KRAS</em> or <em>BRAF</em> mutation. Cell cycle analysis showed induction of G2/M and G1 arrests by MK-5108 and trametinib, respectively, and the potential enhancement of G1 arrest with the two drug combination. The addition of MK-5108 to trametinib enhanced the suppression of <em>p</em>-ERK and other G1/S progression-related proteins expression. In HCT116 cells, harboring wild-type <em>TP53</em>, the combination therapy induced more potent cell proliferation suppression and apoptosis induction than in <em>TP53</em> knockout cells. These were related to potential enhancement of p53 expression and caspase activation. In conclusion, the combination of MK-5108 and trametinib may synergistically inhibit tumor cell division with or without <em>TP53</em> mutation, and with either <em>KRAS</em> or <em>BRAF</em> mutation. Furthermore, the combination therapy could be more effective in wild-type <em>TP53</em> cells.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"Article 102073"},"PeriodicalIF":2.3,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144240806","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":"Blood perfusion through ventricular assist devices induces erythrocytes to interact with leukocytes","authors":"Kylie M. Foster ,&nbsp;Ahmed M. El Banayosy ,&nbsp;Zheila Azartash-Namin ,&nbsp;Phillip Coghill ,&nbsp;James W. Long ,&nbsp;Edgar O'Rear ,&nbsp;Hendra Setiadi","doi":"10.1016/j.bbrep.2025.102085","DOIUrl":"10.1016/j.bbrep.2025.102085","url":null,"abstract":"<div><div>Implantations of Ventricular Assist Devices (VADs) have significantly improved quality of life and life expectancy of end-stage heart failure patients. However, despite the advancements in the VAD designs and patient management protocols, the VAD recipients remain at risk of attaining bleeding, infection, pump thrombosis, and stroke. Although blood trauma has been suggested as a critical factor in development of these adverse events, its consequences in inducing interactions between different types of blood cells are largely unknown.</div><div>Following our recent findings on erythrocyte and leukocyte trauma in VAD recipients, we decided to explore interactions between erythrocytes and leukocytes by perfusing human whole blood through two different types of VADs, HeartMate II (HMII) and HeartMate 3 (HM3), concurrently in their respective Blood Circulatory Loop (BCL). By using a flow cytometry assay, we found increasing association between erythrocytes and leukocytes as VADs propelled blood through their BCLs. This time-dependent intercellular association was shown by increasing concomitant events of stained CD235a (specifically expressed on erythrocytes) and stained CD45 (specifically expressed on leukocytes) in the CD235a⁺ population. Compared to CentriMag (CM), which served as a control, VADs produced significantly higher concomitant signals. The findings described in this study have opened the need for further studies on a novel path for generation of adverse events that are commonly observed in VAD recipients, notably infection, pump thrombosis, and ischemic stroke.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"Article 102085"},"PeriodicalIF":2.3,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144240933","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":"Cytoplasmic physicochemical factors drive malignant transformation by adapting bioenergetic settings","authors":"Tattym E. Shaiken","doi":"10.1016/j.bbrep.2025.102079","DOIUrl":"10.1016/j.bbrep.2025.102079","url":null,"abstract":"<div><div>While significant insights have been gained by a study of cancer genetics, the roles of the cytoplasm in regulating chemical processes during the transformation to malignancy are often less appreciated. The cytoplasm functions as a two-phase system consisting of an elastic solid phase (the cytomatrix) and a viscous liquid phase (the cytosol). This finding has led to the development of a tumor progression model based on a two-phase system that connects genetic alterations with the physicochemical processes necessary for sustaining and facilitating malignant growth. Here, we show that the energy required for tumor growth is, in part, required for the cytomatrix activity, which accelerates chemical reactions. The ability to regulate cytomatrix motor proteins provides a mechanism to control whether a genetic mutation is able to induce the energy needed for cancer to develop and offers innovative strategies for cancer treatment.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"Article 102079"},"PeriodicalIF":2.3,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144240932","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":"Engineering bacterial cell morphology for the design of robust cell factories","authors":"Maarten Lubbers,&nbsp;Nova Jaspers,&nbsp;Dennis Claessen","doi":"10.1016/j.bbrep.2025.102076","DOIUrl":"10.1016/j.bbrep.2025.102076","url":null,"abstract":"<div><div>Bacteria come in a wide variety of shapes, ranging from spherical or rod-shaped unicellular cells to complex multicellular structures. These shapes have evolved to benefit the organism in its natural environment. However, industry often takes such organisms from their natural environment to produce useful molecules that favor mankind. Their natural morphology is often far from optimal for use in an industrial setting. Filamentous bacteria, for instance, have a morphology that presents unique challenges for industrial settings. Therefore, various engineering approaches have been developed to optimize their morphology. This review explores a spectrum of successful engineering strategies, offering insights and providing inspiration for future advancements. It holds the potential to lead the way in optimizing morphology in challenging microorganisms and thus improve their exploitability in biotechnology.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"Article 102076"},"PeriodicalIF":2.3,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144231061","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":"Novel and efficient synthesis of 5-chloro-6-methoxy-3-(2-((1-(aryl)-1H-1,2,3-triazol-4-yl)methoxy)ethyl)benzo[d]isoxazole derivatives as new α-glucosidase inhibitors","authors":"Ram Reddy Mudireddy ,&nbsp;Rambabu Gundla ,&nbsp;Chandra Prakash Koraboina ,&nbsp;Vani Madhuri Velavalapalli ,&nbsp;Venkata Veernjaneya Sarma Dhulipalla ,&nbsp;Gowri Sankararao Burle ,&nbsp;Sreekantha B. Jonnalagadda ,&nbsp;Naresh Kumar Katari","doi":"10.1016/j.bbrep.2025.102074","DOIUrl":"10.1016/j.bbrep.2025.102074","url":null,"abstract":"<div><div>A new series of benzisoxazole derivatives (<strong>9a-o</strong>) were designed by using molecular hybridization approach and synthesized <em>via</em> click-chemistry. All the synthesized compounds were evaluated for their α-glucosidase enzyme inhibition and antibacterial activity. All tested compounds (<strong>9a-o</strong>) exhibited a promising α-glucosidase inhibitory activity with IC₅₀ range of 14.69–38.71 nmol in comparison with the positive drug <strong>Acarbose</strong> (IC₅₀ 35.91 nmol). Additionally, these compounds have found to be active against <em>B. cereus</em> and <em>E. coli</em>. The <em>in vitro</em> inhibition results supported to <em>in silico</em>. Additionally, the compounds were subjected to computational drug-likeness/ADME testing, which revealed that this all the compounds had good ADME profiles in addition to exhibiting drug-like qualities. SAR indicates that analysis revealed that electron-withdrawing substituents such as Br and CF₃ at specific positions significantly enhanced α-glucosidase inhibition, while unsubstituted and ortho-methoxy phenyl derivatives also showed potent activity, highlighting the benzo[d]isoxazole–triazole scaffold as a promising pharmacophore for developing novel anti-diabetic agents.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"Article 102074"},"PeriodicalIF":2.3,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144220857","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":"Isolation, biochemical characterization, and primary structure and active site determination of Dioscorea opposita (‘Nagaimo’) oligopeptidase B","authors":"Sayaka Miyazaki-Katamura ,&nbsp;Mami Chosei ,&nbsp;Sota Tate ,&nbsp;Tomohisa Sakaue ,&nbsp;Takuya Yamane ,&nbsp;Junko Suzuki ,&nbsp;Shigeki Higashiyama ,&nbsp;Iwao Ohkubo","doi":"10.1016/j.bbrep.2025.102071","DOIUrl":"10.1016/j.bbrep.2025.102071","url":null,"abstract":"<div><div>A protease was purified to homogeneity from <em>Dioscorea opposita “</em>Nagaimo” using ion exchange, hydrophobic and gel filtration columns, and its biochemical characterization including molecular weight, substrate specificity and kinetic parameters were determined. Protease activity was strongly inhibited by AEBSF, DCI and TLCK. The enzyme moderately inhibited by NEM and HgCl₂. The enzyme activity inhibited by NEM and HgCl₂ was restored with the addition of β-ME. These findings suggest that the enzyme is a trypsin-like serine protease, which is regulated by SH compounds. The N-terminal amino acid of this protease is blocked in an unknown manner. We determined the structure of the cDNA and deduced amino acid sequence of the protease from <em>D. opposita</em>. The cDNA was composed of 2420 nucleotides and encoded 751 amino acids in the coding region. The results indicated that this enzyme is an oligopeptidase B (OPB), consisting of a N-terminal region (M¹ ∼ T4⁷), a N-terminal β-propeller domain (A⁴⁸∼ L⁴⁶⁵), a connecting domain (K⁴⁶⁶ ∼ D⁵²⁷), a peptidase_S9 domain (P⁵²⁸ ∼ D⁷⁴⁴) and C-terminal region (R⁷⁴⁵ ∼ S⁷⁵¹). The overall homology of amino acid sequences of <em>D. opposita</em> to <em>D. alata</em> and <em>D. rotundata</em> was 99.07 % and 97.07 %, respectively. The catalytically active amino acid sites [S⁵⁹⁹, D⁶⁸⁴, and H⁷¹⁹] among these yam species were found to be highly conserved. Site-directed mutagenesis confirmed that these three the active center.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"Article 102071"},"PeriodicalIF":2.3,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144204346","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 carminic acid on gene expressions under epigenetic regulation","authors":"Kei-ichi Sugiyama ,&nbsp;Petr Grúz ,&nbsp;Kaoru Sato ,&nbsp;Masamitsu Honma","doi":"10.1016/j.bbrep.2025.102070","DOIUrl":"10.1016/j.bbrep.2025.102070","url":null,"abstract":"<div><div>Carminic acid, which is an anthracene derivative, is a dye used as a food additive. Although anthracene is considered not to be epigenetic modifier, some anthracene derivatives affect yeast flocculation that is under the epigenetic regulation. FLO assay can detect the expression of <em>Saccharomyces cerevisiae FLO1</em> gene that mediates the flocculation phenotype influenced by epigenetic regulation. FLO reporter assays showed that 5–20 μM carminic acid induced the <em>FLO1</em> promoter in wild type yeast as well as in the yeast transformed with human DNA methyltransferase genes, in the absence of rat liver homogenates. Furthermore, in mouse embryonic stem cell line EB3, carminic acid decreased the expression of <em>Oct3/4,</em> which is also under epigenetic regulation, and induced slight morphological changes. These results suggest that carminic acid, but not its metabolites, has the potential to alter the epigenetic state of the genome.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"Article 102070"},"PeriodicalIF":2.3,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144204345","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}