Nature. 2025 Feb 12. doi: 10.1038/s41586-024-08532-4. Online ahead of print.

ABSTRACT

UM171 is a potent agonist of ex vivo human haematopoietic stem cell self-renewal1. By co-opting KBTBD4, a substrate receptor of the CUL3-RING E3 ubiquitin ligase (CRL3) complex, UM171 promotes the degradation of the LSD1-CoREST corepressor complex, thereby limiting haematopoietic stem cell attrition2,3. However, the direct target and mechanism of action of UM171 remain unclear. Here we show that UM171 acts as a molecular glue to induce high-affinity interactions between KBTBD4 and HDAC1/2 to promote corepressor degradation. Through proteomics and chemical inhibitor studies, we identify the principal target of UM171 as HDAC1/2. Cryo-electron microscopy analysis of dimeric KBTBD4 bound to UM171 and the LSD1-HDAC1-CoREST complex identifies an asymmetric assembly in which a single UM171 molecule enables a pair of KELCH-repeat propeller domains to recruit the HDAC1 catalytic domain. One KBTBD4 propeller partially masks the rim of the HDAC1 active site, which is exploited by UM171 to extend the E3-neosubstrate interface. The other propeller cooperatively strengthens HDAC1 binding through a distinct interface. The overall CoREST-HDAC1/2-KBTBD4 interaction is further buttressed by the endogenous cofactor inositol hexakisphosphate, which acts as a second molecular glue. The functional relevance of the quaternary complex interaction surfaces is demonstrated by base editor scanning of KBTBD4 and HDAC1. By delineating the direct target of UM171 and its mechanism of action, we reveal how the cooperativity offered by a dimeric CRL3 E3 can be leveraged by a small molecule degrader.

PMID:39939761 | DOI:10.1038/s41586-024-08532-4

Sci Rep. 2025 Feb 12;15(1):5204. doi: 10.1038/s41598-025-89882-5.

ABSTRACT

Patients with triple negative breast cancer (TNBC) show only modest response rates to immune checkpoint inhibitor immunotherapy, motivating ongoing efforts to identify approaches to boost efficacy. Using an immunocompetent mouse model of TNBC, we investigated combination therapy with an anti-PD-1 immunotherapy antibody plus balixafortide, a cyclic peptide inhibitor of CXCR4. Cell-based assays demonstrated that balixafortide functions as an inverse agonist, establishing a mode of action distinct from most compounds targeting CXCR4. Combination anti-PD-1 plus balixafortide significantly reduced growth of orthotopic tumors and extended overall survival relative to single agent therapy or vehicle. Adding balixafortide to anti-PD-1 increased numbers of tertiary lymphoid structures, a marker of local tumor immune responses associated with favorable response to immunotherapy in TNBC. Single cell RNA sequencing revealed that combination anti-PD-1 plus balixafortide reduced T cell exhaustion and increased markers of effector T cell activity. Combination therapy also reduced signatures of immunosuppressive myeloid derived suppressor cells (MDSCs) in tumors. MDSCs isolated from mice treated with anti-PD-1 plus balixafortide showed reduced inhibition of T cell proliferation following ex vivo stimulation. These studies demonstrate that combining inhibition of CXCR4 with anti-PD-1 to enhances responses to checkpoint inhibitor immunotherapy in TNBC, supporting future clinical trials.

PMID:39939722 | DOI:10.1038/s41598-025-89882-5

Nat Methods. 2025 Feb 12. doi: 10.1038/s41592-024-02579-x. Online ahead of print.

ABSTRACT

The ideal technology for directly investigating the relationship between genotype and phenotype would analyze both RNA and DNA genome-wide and with single-cell resolution; however, existing tools lack the throughput required for comprehensive analysis of complex tumors and tissues. We introduce a highly scalable method for jointly profiling DNA and expression following nucleosome depletion (DEFND-seq). In DEFND-seq, nuclei are nucleosome-depleted, tagmented and separated into individual droplets for messenger RNA and genomic DNA barcoding. Once nuclei have been depleted of nucleosomes, subsequent steps can be performed using the widely available 10x Genomics droplet microfluidic technology and commercial kits. We demonstrate the production of high-complexity mRNA and gDNA sequencing libraries from thousands of individual nuclei from cell lines, fresh and archived surgical specimens for associating gene expression with both copy number and single-nucleotide variants.

PMID:39939719 | DOI:10.1038/s41592-024-02579-x

Nat Commun. 2025 Feb 12;16(1):1561. doi: 10.1038/s41467-025-56873-z.

ABSTRACT

Drug-resistant bacteria pose an urgent global health threat, necessitating the development of antibacterial compounds with novel modes of action. Protein biosynthesis accounts for up to half of the energy expenditure of bacterial cells, and consequently inhibiting the efficiency or fidelity of the bacterial ribosome is a major target of existing antibiotics. Here, we describe an alternative mode of action that affects the same process: allowing translation to proceed but causing co-translational aggregation of the nascent peptidic chain. We show that treatment with an aggregation-prone peptide induces formation of polar inclusion bodies and activates the SsrA ribosome rescue pathway in bacteria. The inclusion bodies contain ribosomal proteins and ribosome hibernation factors, as well as mRNAs and cognate nascent chains of many proteins in amyloid-like structures, with a bias for membrane proteins with a fold rich in long-range beta-sheet interactions. The peptide is bactericidal against a wide range of pathogenic bacteria in planktonic growth and in biofilms, and reduces bacterial loads in mouse models of Escherichia coli and Acinetobacter baumannii infections. Our results indicate that disrupting protein homeostasis via co-translational aggregation constitutes a promising strategy for development of broad-spectrum antibacterials.

PMID:39939597 | DOI:10.1038/s41467-025-56873-z

Nat Commun. 2025 Feb 12;16(1):1585. doi: 10.1038/s41467-025-56858-y.

ABSTRACT

Biophysical cues play a crucial role in T cell biology, yet their implications in adoptive T cell therapy (ACT) remain largely unknown. Here, we investigate the effect of electrical stimuli on CD8+ T cells using a charged substrate composed of electroactive nanocomposites with tunable surface charge intensities. Electrical stimuli enhance the persistence and tumor-suppressive efficacy of transferred T cells, with effects dependent on substrate charge. Single-cell RNA-sequencing analysis unveils a decrease in virtual memory T (Tvm) cells and an increase in proliferative potential T (Tpp) cells, which exhibit superior antitumor activity and metabolic adaptations relative to those treated with uncharged substrate. ATAC-seq profiling demonstrates heightened accessibility at upstream binding sites for EGR1, a transcription factor critical for Tpp cell differentiation. Mechanistically, the charged substrate disrupts ionic TCR-lipid interactions, amplifies TCR signaling, and activates EGR1, thereby impeding Tvm polarization during ex vivo culture. Our findings thus highlight the importance of extracellular electrical stimuli in shaping T cell fate, offering potential for optimizing ACT for therapeutic applications.

PMID:39939595 | DOI:10.1038/s41467-025-56858-y

Antiviral Res. 2025 Feb 10:106099. doi: 10.1016/j.antiviral.2025.106099. Online ahead of print.

ABSTRACT

The emergence of new human viruses with epidemic or pandemic potential has reaffirmed the urgency to develop effective broad-spectrum antivirals (BSAs) as part of a strategic framework for pandemic prevention and preparedness. To this end, the host nucleotide metabolic pathway has been subject to intense investigation in the search for host-targeting agents (HTAs) with potential BSA activity. In particular, human dihydroorotate dehydrogenase (hDHODH), a rate-limiting enzyme in the de novo pyrimidine biosynthetic pathway, has been identified as a preferential target of new HTAs. Viral replication in fact relies on cellular pyrimidine replenishment, making hDHODH an ideal HTA target. The depletion of the host pyrimidine pool that ensues the pharmacological inhibition of hDHODH activity elicits effective BSA activity through three distinct mechanisms: it blocks viral DNA and RNA synthesis; it activates effector mechanisms of the host innate antiviral response; and it mitigates the virus-induced inflammatory response. However, despite the spectacular results obtained in vitro, the hDHODH inhibitors examined as mono-drug therapies in animal models of human viral infections and in clinical trials have produced disappointing levels of overall antiviral efficacy. To overcome this inherent limitation, pharmacological strategies based on multi-drug combination treatments should be considered to enable efficacy of hDHODH-targeted antiviral therapies. Here, we review the state-of-the-art of antiviral applications of hDHODH inhibitors, discuss the challenges that have emerged from their testing in animal models and human clinical trials and consider how they might be addressed to advance the development of hDHODH inhibitors as BSA for the treatment of viral diseases.

PMID:39938808 | DOI:10.1016/j.antiviral.2025.106099

J Ethnopharmacol. 2025 Feb 10:119479. doi: 10.1016/j.jep.2025.119479. Online ahead of print.

ABSTRACT

ETHNOPHARMACOLOGICAL RELEVANCE: Huachansu (HCS), a traditional Chinese medicine (TCM), has been used as an adjuvant therapy for colorectal cancer (CRC). However, its underlying mechanisms for combating CRC require further investigation.

AIM OF THIS STUDY: To comprehensively evaluate the anti-CRC effects of HCS and elucidate its underlying mechanisms, with a focus on elucidating the key pathways and targets involved.

MATERIALS AND METHODS: A series of cell experiments and xenograft tumor models were used to evaluate the inhibitory effects of HCS. The key components and potential targets of HCS against CRC were identified through network pharmacology and molecular docking. To further investigate the mechanisms, transcriptomics and proteomics were integrated, and the findings were supported by systematic pharmacological validation. Finally, the efficacy of HCS was further confirmed in CRC Patients-derived organoid and orthotopic models.

RESULTS: HCS could inhibit proliferation, disrupt the cell cycle, induce apoptosis of CRC cells, and suppress the growth of CRC xenograft tumors. Then eight components and six proteins (PIK3CA, CTNNB1, TP53, AKT1, CCND1, and CDH1) were identified as critical for HCS's anti-CRC activity. Notably, HCS inhibited the PI3K/AKT signaling pathway and glycolysis in CRC cells, with these findings validated in both in vitro and in vivo models. Additionally, HCS reduced growth in CRC patient-derived organoids and orthotopic models.

CONCLUSION: This study elucidates the mechanisms of HCS to combat CRC, offering a valuable reference for future clinical applications. It also presents a distinctive strategy for exploring TCM formulations' active components and effective mechanisms.

PMID:39938766 | DOI:10.1016/j.jep.2025.119479

Cell Syst. 2025 Feb 6:101171. doi: 10.1016/j.cels.2025.101171. Online ahead of print.

ABSTRACT

Cells of the immune system operate in dynamic microenvironments where the timing, concentration, and order of signaling molecules constantly change. Despite this complexity, immune cells manage to communicate accurately and control inflammation and infection. It is unclear how these dynamic signals are encoded and decoded and if individual cells retain the memory of past exposure to inflammatory molecules. Here, we use live-cell analysis, ATAC sequencing, and an in vivo model of sepsis to show that sequential inflammatory signals induce memory in individual macrophages through reprogramming the nuclear factor κB (NF-κB) network and the chromatin accessibility landscape. We use transcriptomic profiling and deep learning to show that transcription factor and chromatin dynamics coordinate fine-tuned macrophage responses to new inflammatory signals. This work demonstrates how macrophages retain the memory of previous signals despite single-cell variability and elucidates the mechanisms of signal-induced memory in dynamic inflammatory conditions like sepsis.

PMID:39938520 | DOI:10.1016/j.cels.2025.101171

Immunity. 2025 Feb 11;58(2):265-267. doi: 10.1016/j.immuni.2025.01.012. Epub 2025 Feb 11.

ABSTRACT

Renowned for driving interferon responses, the cGAS-STING pathway reveals a surprising role: lysosomal biogenesis. In this issue of Immunity, Xu et al. uncover how STING activates the transcription factor TFEB, linking innate immune sensing to enhanced pathogen clearance through lysosomal activity.

PMID:39938477 | DOI:10.1016/j.immuni.2025.01.012

Physiology (Bethesda). 2025 Feb 12. doi: 10.1152/physiol.00045.2024. Online ahead of print.

ABSTRACT

Over the past several decades, physiological research has undergone a progressive shift toward greater-and-greater reductionism, culminating in the rise of 'molecular physiology.' The introduction of Omic techniques, chiefly protein mass spectrometry and next-generation DNA sequencing (NGS), has further accelerated this trend, adding massive amounts of information about individual genes, mRNA transcripts, and proteins. However, the long-term goal of understanding physiological and pathophysiological processes at a whole-organism level has not been fully realized. This review summarizes the major protein mass spectrometry and NGS techniques relevant to physiology and explores the challenges of merging data from Omic methodologies with data from traditional hypothesis-driven research to broaden the understanding of physiological mechanisms. It summarizes recent progress in large-scale data integration through: 1) creation of online user-friendly Omic data resources with cross-indexing across data sets to democratize access to Omic data; 2) application of Bayesian methods to combine data from multiple Omic data sets with knowledge from hypothesis-driven studies in order to address specific physiological and pathophysiological questions; and 3) application of concepts from Natural Language Processing to probe the literature and to create user-friendly causal graphs representing physiological mechanisms. Progress in development of so-called "Large Language Models", e.g. ChatGPT, for knowledge integration is also described along with a discussion of the shortcomings of Large Language Models with regard to management and integration of physiological data.

PMID:39938090 | DOI:10.1152/physiol.00045.2024

Sci Adv. 2025 Feb 14;11(7):eads0760. doi: 10.1126/sciadv.ads0760. Epub 2025 Feb 12.

ABSTRACT

Defects in cell wall integrity (CWI) profoundly affect plant growth, although, underlying mechanisms are not well understood. We show that in Arabidopsis mur1 mutant, CWI defects from compromising dimerization of RG-II pectin, a key component of cell wall, attenuate the expression of auxin response factors ARF7-ARF19. As a result, polar auxin transport components are misexpressed, disrupting auxin response asymmetry, leading to defective apical hook development. Accordingly, mur1 hook defects are suppressed by enhancing ARF7 expression. In addition, expression of brassinosteroid biosynthesis genes is down-regulated in mur1 mutant, and supplementing brassinosteroid or enhancing brassinosteroid signaling suppresses mur1 hook defects. Intriguingly, brassinosteroid enhances RG-II dimerization, showing hormonal feedback to the cell wall. Our results thus reveal a previously unrecognized link between cell wall defects from reduced RG-II dimerization and growth regulation mediated via modulation of auxin-brassinosteroid pathways in early seedling development.

PMID:39937898 | DOI:10.1126/sciadv.ads0760

Mol Biol Rep. 2025 Feb 12;52(1):226. doi: 10.1007/s11033-025-10341-5.

ABSTRACT

Microsomal cytochromes P450 (micCYPs) are monooxygenases located in the endoplasmic reticulum and other endomembranes of human cells. micCYPs receive electrons from specific redox partners and perform enzymatic transformations of drugs and different endogenous substrates. The large biodiversity of micCYPs leads to the idea that protein-protein interactions (PPIs) involving micCYPs are not limited to classical redox partners. This review aims to perform a systems biology analysis of the complete set of PPIs for all 33 micCYPs studied, as well as to examine the subinteractome of each micCYP. We have retrieved 287 PPIs from interactomic databases, involving 246 unique protein interactors that share a similar profile of subcellular localization with micCYPs. The number of protein interactors per micCYP unevenly varies from one to 47. Interactors of micCYPs are involved in cellular metabolism, signal transduction, cell-cell junctions, cytoskeleton organization, and intracellular or transmembrane transport. Notably, up to one-third of all interactors belong to the latter group, half of which consists of membrane transporters of compounds, metabolites, and ions (e.g., CACNA2D1, ORAI1, SCN3B, SLC7A2, SLC19A3, and SLC11A2). The CYP2C8 subinteractome is enriched with proteins involved in autophagy; CYP2S1- ERBB2 and EPH-Ephrin signaling; CYP3A4- glucuronidation. Proteins UBC, PGRMC1, and FANCG are the most frequent common interactors across various micCYPs. Nine and 12 interactors of micCYPs are involved in phosphorylation and ubiquitination, respectively; 20 interactors are 'moonlighting' proteins that are represented in the CYP3A4 subinteractome. Furthermore, micCYPs such as CYP2C9, 3A5, 2E1, 2A6, 4F2, and 4A11 may be involved in potentially binary interactions with other micCYPs. The functional implication of these CYP-CYP pairs is likely associated with modulation of their activity. Analysis of transcriptomic data revealed that some micCYP/interactor pairs exhibit tissue-, time-, and disease-specific gene expression patterns. Drugs that are metabolized by micCYPs in some cases can influence the expression of corresponding interactors at the gene or protein levels. These findings suggest that micCYPs may play roles in functions beyond their monooxygenase activity, as indicated by the spectrum of PPIs analyzed.

PMID:39937310 | DOI:10.1007/s11033-025-10341-5

Microb Biotechnol. 2025 Feb;18(2):e70096. doi: 10.1111/1751-7915.70096.

ABSTRACT

The DnaK (Hsp70) protein is an essential ATP-dependent chaperone foldase and holdase found in most organisms. In this study, combining multiple experimental approaches we determined FliC as major interaction partner of DnaK in the opportunistic bacterial pathogen Pseudomonas aeruginosa. Implementing immunofluorescence microscopy and electron microscopy techniques DnaK was found extracellularly associated to the assembled filament in a regular pattern. dnaK repression led to intracellular FliC accumulation and motility impairment, highlighting DnaK essentiality for FliC export and flagellum assembly. SPOT-membrane peptide arrays coupled with artificial intelligence analyses suggested a highly dynamic DnaK-FliC interaction landscape involving multiple domains and transient complexes formation. Remarkably, in vitro fast relaxation imaging (FReI) experiments mimicking ATP-deprived extracellular environment conditions exhibited DnaK ATP-independent holdase activity, regardless of its co-chaperone DnaJ and its nucleotide exchange factor GrpE. We present a model for the DnaK-FliC interactions involving dynamic states throughout the flagellum assembly stages. These results expand the classical view of DnaK chaperone functioning and introduce a new participant in the Pseudomonas flagellar system, an important trait for bacterial colonisation and virulence.

PMID:39937155 | DOI:10.1111/1751-7915.70096

Cells. 2025 Jan 21;14(3):152. doi: 10.3390/cells14030152.

ABSTRACT

Calcium (Ca2+) signalling is a fundamental cellular process, essential for a wide range of physiological functions. It is regulated by various mechanisms, including a diverse family of Ca2+-binding proteins (CaBPs), which are structurally and functionally similar to calmodulin (CaM). The CaBP family consists of six members (CaBP1, CaBP2, CaBP4, CaBP5, CaBP7, and CaBP8), each exhibiting unique localisation, structural features, and functional roles. In this review, we provide a structure-function analysis of the CaBP family, highlighting the key similarities and differences both within the family and in comparison to CaM. It has been shown that CaBP1-5 share similar structural and interaction characteristics, while CaBP7 and CaBP8 form a distinct subfamily with unique properties. This review of current CaBP knowledge highlights the critical gaps in our understanding, as some CaBP members are less well characterised than others. We also examine pathogenic mutations within CaBPs and their functional impact, showing the need for further research to improve treatment options for associated disorders.

PMID:39936944 | DOI:10.3390/cells14030152

Microbiol Resour Announc. 2025 Feb 12:e0094124. doi: 10.1128/mra.00941-24. Online ahead of print.

ABSTRACT

Sneathia vaginalis, a fastidious pathogen of the female reproductive tract, is implicated in obstetric and gynecologic pathologies, including spontaneous preterm birth and bacterial vaginosis. Here, we report the successful cultivation and genomic sequencing of three Sneathia vaginalis isolates collected via a vaginal swab from a patient with bacterial vaginosis.

PMID:39936913 | DOI:10.1128/mra.00941-24

ACS Synth Biol. 2025 Feb 12. doi: 10.1021/acssynbio.4c00881. Online ahead of print.

ABSTRACT

1,6-Hexamethylenediamine (HMD) and 1,6-hexanediol (HDO) are pivotal C6 platform chemicals with extensive applications as key monomers in the synthesis of nylons, polyurethanes, and polyesters. The biological production of HMD and HDO from cheap and renewable bioresources represents an environmentally benign strategy for the sustainable chemical industry. Herein, we report the development of a novel biocatalytic route for the direct conversion of d-glucose to HMD and HDO in Escherichia coli. This was achieved through the integration of an adipic acid synthesis module with conversion modules tailored for HMD and HDO production. The study entailed a comprehensive optimization of pathway enzymes, protein expression, and precursor supply. Furthermore, a co-culture fermentation strategy was employed to enhance the efficiency of labor division, resulting in a two-strain cocultivation process that yielded 16.62 mg/L of HMD and 214.93 mg/L of HDO using glucose as the sole carbon source. This study establishes a foundational framework for the advancement of sustainable biological production processes for HMD and HDO from renewable resources.

PMID:39936844 | DOI:10.1021/acssynbio.4c00881

Bioinformatics. 2025 Feb 12:btaf070. doi: 10.1093/bioinformatics/btaf070. Online ahead of print.

ABSTRACT

MOTIVATION: The Open Targets Platform (https://platform.opentargets.org) is a unique, comprehensive, open-source resource supporting systematic identification and prioritisation of targets for drug discovery. The Platform combines, harmonises and integrates data from >20 diverse sources to provide target-disease associations, covering evidence derived from genetic associations, somatic mutations, known drugs, differential expression, animal models, pathways and systems biology. An in-house target identification scoring framework weighs the evidence from each data source and type, contributing to an overall score for each of the 7.8M target-disease associations. However, the old infrastructure did not allow user-led dynamic adjustments in the contribution of different evidence types for target prioritisation, a limitation frequently raised by our user community. Furthermore, the previous Platform user interface did not support navigation and exploration of the underlying target-disease evidence on the same page, occasionally making the user journey counterintuitive.

RESULTS: Here, we describe "Associations on the Fly" (AOTF), a new Platform feature-developed with a user-centred vision-that enables the user to formulate more flexible therapeutic hypotheses through dynamic adjustment of the weight of contributing evidence from each source, altering the prioritisation of targets.

AVAILABILITY AND IMPLEMENTATION: The codebases that power the Platform-including our pipelines, GraphQL API, and React UI-are all open source and licensed under the APACHE LICENSE, VERSION 2.0.You can find all of our code repositories on GitHub at https://github.com/opentargets and on Zenodo at https://zenodo.org/records/14392214.This tool was implemented using React v18 and its code is accessible here: [https://github.com/opentargets/ot-ui-apps].The tools are accessible through the Open Targets Platform web interface [https://platform.opentargets.org/] and GraphQL API (https://platform-docs.opentargets.org/data-access/graphql-api).Data is available for download here: [https://platform.opentargets.org/downloads] and from the EMBL-EBI FTP: [https://ftp.ebi.ac.uk/pub/databases/opentargets/platform/].

CONTACT: Annalisa Buniello, European Molecular Biology Laboratory (EMBL-EBI), buniello@ebi.ac.uk.

SUPPLEMENTARY INFORMATION: Features walkthrough video: https://youtu.be/2A9bksboAag, https://www.youtube.com/watch?v=WQwQn6I4jkwExtensive documentation: https://platform-docs.opentargets.org/web-interface/associations-on-the-fly https://platform-docs.opentargets.org/target-prioritisation.

PMID:39936578 | DOI:10.1093/bioinformatics/btaf070

Front Plant Sci. 2025 Jan 28;16:1555255. doi: 10.3389/fpls.2025.1555255. eCollection 2025.

NO ABSTRACT

PMID:39935951 | PMC:PMC11810884 | DOI:10.3389/fpls.2025.1555255

Front Plant Sci. 2025 Jan 28;16:1533442. doi: 10.3389/fpls.2025.1533442. eCollection 2025.

ABSTRACT

INTRODUCTION: The genetic wealth present in pigmented rice varieties offer abundant variation in different sources of antioxidants to meet nutritional security targets among rice-consuming communities. There is limited knowledge of the dynamic changes in the lipidome of rice during germination and the corresponding genes associated with the antioxidant and anti-cancerous properties of lipophilic fractions of pigmented rice sprouts (PRS).

METHODS: In this study, we profiled the lipidome of diverse pigmented rice collections of germinated sprouts. Further, we employed Genome-wide association studies (GWAS), gene-set analysis, and targeted association analysis to identify the candidate genes linked to these lipids.

RESULTS: The genetic analyses revealed 72 candidate genes involved in the regulation of these accumulating lipids in PRS. Marker trait associations (MTA) analysis shown that the combination GGTAAC/ACAAGCTGGGCCC was associated with increased levels of unsaturated lipids and carotenoids, which likely underlie these beneficial effects. This superior MTA combination exhibited potent inhibitory activity against HCT116 and A549 cell lines, with average 1/IC50 values of 0.03 and 0.02 (mL/μg), respectively, compared to the inferior MTAs.

DISCUSSION: Collectively, our findings demonstrate that MTAs linked to selected GDSL esterase/lipase (GELP) genes, OsACP1, and lecithin-cholesterol acyltransferase significantly enhance antioxidant and anti-cancer properties, potentially through the mobilization of unsaturated lipids and carotenoids during germination. This study offers valuable insights into the health-promoting potential of germinated rice sprouts as a rich dietary source of antioxidants beneficial to human health.

PMID:39935946 | PMC:PMC11810972 | DOI:10.3389/fpls.2025.1533442

Front Genet. 2025 Jan 28;16:1547943. doi: 10.3389/fgene.2025.1547943. eCollection 2025.

NO ABSTRACT

PMID:39935834 | PMC:PMC11810898 | DOI:10.3389/fgene.2025.1547943