Search Results (16,313)

Mulberry, a plant highly valued for medicinal–edible features, was fermented with Lactobacillus plantarum M3 to enhance its bioactive profile. This study conducted a comprehensive evaluation of the antioxidant activity of fermented mulberry juice (FMJ) and identified key metabolites through an integrated approach involving non-targeted metabolomics, network pharmacology, RT-qPCR, and molecular docking. Under optimized conditions (28 °C, pH 5.5, 12°Bx initial sugar content, 48 h and 5% inoculum), fermentation significantly bolstered the antioxidant capacity of MJ. Specifically, superoxide dismutase (SOD) activity increased from 62.41 ± 0.11 to 84.99 ± 0.07 U/mL, while total phenolic content (TPC) surged from 1108.98 ± 2.90 to 2494.17 ± 7.05 mg GAE/L; DPPH radical scavenging activities were improved by 63.09%. Non-targeted metabolomics identified 195 secondary metabolites, primarily comprising alkaloids, flavonoids, and phenolic acids. Among these, protocatechuic acid, Albanin A, and apigenin exhibited significant dynamic shifts, indicating that they may play a pivotal role in regulating antioxidant capacity. Integrated network pharmacology, RT-qPCR validation, and molecular docking further elucidated that Albanin A and Moracin Q likely drive these enhanced antioxidant effects by activating the Nrf2 pathway, suppressing the NF-κB pathway, and upregulating SOD1 expression. These findings provide a theoretical basis for the development of high-potency functional mulberry products. Full article

To assess the therapeutic relevance of BRIP1 in gastric cancer (GC), we examine its functional role in conferring resistance to anoikis within GC cells and elucidate the oncogenic signaling pathways modulated by BRIP1. By integrating the Cancer Genome Atlas (TCGA) and Gene Set Enrichment Analysis (GSEA) databases with Least Absolute Shrinkage and Selection Operator (LASSO) regression, a novel risk score to stratify GC patients based on prognosis was generated, and a significantly differentially expressed gene, BRIP1, was validated through reverse transcription quantitative polymerase chain reaction (RT-qPCR). Protein expression associated with apoptosis, cell cycle, and epithelial-mesenchymal transformation (EMT) was quantified via RT-qPCR and Western blot (WB). 5-Ethynyl-2′-deoxyuridine (EdU) and cell counting kit-8 (CCK-8) assays were conducted to quantify proliferative activity. The protein level in axillary tumor tissues of nude mice was detected by immunohistochemistry (IHC). We established an eight-gene anoikis-related prognostic risk assessment model (DUSP1, VCAN, P3H2, TXNIP, BRIP1, FGD6, GPX3, and RLN2) for GC. Multivariate Cox regression confirmed the risk score as an independent prognostic factor. Among these genes, BRIP1 showed significant differential expression between tumor and normal tissues, as well as normal gastric mucosal epithelial cells and GC cells. Mechanistically, BRIP1 conferred anoikis resistance to GC cells by suppressing the generation of reactive oxygen species (ROS). We found that the PI3K inhibitor LY294002 counteracted BRIP1-driven oncogenic effects, which was evidenced by restored expression of key regulators governing apoptosis, cell cycle progression, and EMT, in addition to suppressed proliferation in GC cells. BRIP1 is postulated to function upstream of the PI3K/Akt signaling cascade. This study establishes a risk scoring model and identifies BRIP1 as a potential prognostic marker for GC. Full article

Background: LATERAL ORGAN BOUNDARIES DOMAIN (LBD/AS2) transcription factors integrate developmental and hormonal signals during organogenesis. As a high-value fruit tree crop, blueberries’ rooting ability underpins their vegetative propagation and field performance, yet a genome-wide view of the LBD repertoire and its roles in blueberry has been lacking. Results: We cataloged 153 non-redundant LBD genes (VcLBD) by homology search against the GDV RefTrans V1 genome and domain validation, substantially exceeding counts reported for other fruit crops. Phylogeny resolved the family into the canonical Class I/II and seven subclades, with extensive lineage-specific expansion supported by synteny: 72.31% of loci arose from whole-genome/segmental and tandem duplication. Gene structures were highly heterogeneous (2–24 exons) but conserved within clades; motif profiling (MEME/InterPro) recovered the signature LOB cysteine block, GAS module and a leucine-zipper-like motif with clade-specific combinations. Promoter scanning identified 38 cis-element types, including hormone- (auxin, cytokinin, GA, JA/MeJA, ABA, SA), stress- and meristem-associated motifs, indicating broad regulatory inputs. Public transcriptomes revealed pronounced tissue–stage specificity with a root-centered bias; qRT-PCR across eight organs/stages validated four archetypal expression programs (higher expression in roots, flowers, fruits in stage 1, or mature fruit, respectively), including floral/early-fruit enrichment (e.g., VcLBD39/40) and ripening-associated induction. Hormone assays demonstrated differential responsiveness: IAA up-regulated VcLBD6/16b/33c/40e/41, whereas 6-BA suppressed VcLBD16b/33c/39a/39c/40e and induced VcLBD41/46h; ACC and MeJA produced gene-specific induction or repression. During adventitious rooting (0/4/7/10 DAC), 30 VcLBDs were differentially expressed, forming three temporal patterns. VcLBD16b reaches its peak expression during the early stages of adventitious root development and exhibits a strong response to auxin. VcLBD11 shows dynamic changes synchronized with cytokinin activity, while VcLBD33/40 is associated with primordia growth and vascular-related processes. Conclusions: We identified and characterized 153 VcLBD genes, profiled their transcripts across multiple blueberry tissues, defined stages of adventitious root development, and evaluated hormone responsiveness for representative members. Together, these results establish a foundation for dissecting VcLBD regulatory mechanisms and functions, particularly in organ growth and adventitious rooting. Full article

Background: Brugada syndrome (BrS) is a genetic cardiac arrhythmia disorder inherited in an autosomal dominant manner, characterized by ST-segment elevation in the right precordial leads (V1–V3) on electrocardiograms (ECGs). This syndrome predominantly affects young individuals with structurally normal hearts and significantly increases the risk of ventricular arrhythmias and sudden cardiac death (SCD). The most common genotype found among BrS patients is caused by variants in the SCN5A gene, which lead to a loss of function of the cardiac sodium channel Nav1.5 by different mechanisms. Methods: Plasmids containing SCN5A were constructed using PCR and site-directed mutagenesis to create the D372H variant. HEK293 cells were cultured and transfected with the WT, D372H, or a combination of both plasmids. Patch-clamp recordings assessed sodium current characteristics. Confocal microscopy visualized channel localization. Quantitative RT-PCR was used to analyze mRNA expression levels, while Western blot evaluated protein expression using specific antibodies. Results: In HEK293 cells expressing the D372H mutant, functional assays revealed a near-complete loss of sodium currents. Co-transfection of WT and D372H plasmids resulted in a significant reduction in current density compared with WT alone, while activation, inactivation, and recovery kinetics were unaffected. In addition, both the mutant protein and protein expressed in co-transfected cells exhibited reduced fluorescence intensity, indicating decreased expression levels. These findings were further supported by Western blot and RT-qPCR analyses. Conclusions: In summary, our findings indicate that the D372H variant produces a marked reduction in Nav1.5 function through reduced sodium current density and decreased channel expression. Given its critical position within the DI-pore loop, this defect is expected to markedly diminish the inward sodium current necessary for normal depolarization. Such impaired excitability—particularly relevant in the right ventricular outflow tract—may accentuate regional differences in repolarization and create conditions that favor reentrant activity. These findings provide mechanistic insights into how the p.D372H variant alters Nav1.5 channel function in vitro and offer functional evidence that may assist in interpreting its potential relevance to Brugada syndrome. Full article

Patients with high-risk neuroblastoma (NB) continue to have long-term survival rates below 60%, with relapse occurring in more than half of patients, likely driven by chemoresistant minimal residual disease in the bone marrow (BM-MRD). Although several quantitative PCR (qPCR) and droplet digital PCR (ddPCR) assays measuring different but overlapping sets of NB-associated mRNAs (NB-mRNAs) have shown a significant prognostic value at various time points, the optimal combination of MRD markers (a set of NB-mRNAs) and evaluation timing remains unclear. In the present study, 89 bone marrow samples were collected from mostly overlapping 30 high-risk NB patients at four time points: diagnosis (Dx), end of induction (EOI), end of high-dose chemotherapy (EOH), and end of consolidation (EOC). BM-MRD was assessed with a 7NB-mRNAs ddPCR assay quantifying CRMP1, DBH, DDC, GAP43, ISL1, PHOX2B, and TH mRNAs. BM-MRD at EOH and EOC time points was significantly associated with relapse. Moreover, patients with higher BM-MRD levels at EOH (7NB-mRNAs ≥ 3.5) and EOC (7NB-mRNAs ≥ 3.5) time points had significantly inferior 3-year event-free survival (EOH, p = 0.003; EOC, p = 0.033). These results indicate that EOH and EOC are clinically informative evaluation time points for BM-MRD detected by 7NB-mRNA expression. Full article

Background: Metastatic melanoma is an extremely aggressive malignancy with limited therapeutic options, despite advances in targeted and immunotherapy. MicroRNAs are key post-transcriptional regulators of gene expression and play a critical role in tumor adaptation, invasion, and metastasis. The aim of our study was to identify dysregulated miRNAs which may serve as novel biomarkers and therapeutic targets. Materials and Methods: The study was conducted on FFPE samples from metastatic melanoma (n = 15), compared to healthy skin tissue (n = 6). BRAF V600E/Ec mutation status was established by Real-Time qPCR. Expression miRNA analysis was performed, using digital counting of 827 miRNAs on the NanoString platform, with data normalization and fold change calculations. Results: Following normalization and quality control metrics, 58 differentially expressed miRNAs were identified in BRAFwt melanoma samples: 6 overexpressed and 52 inderexpressed miRNAs. In BRAFmut melanoma, 37 microRNAs were differentially expressed: 11 overexpressed and 26 underexpressed. Four miRNAs showed elevated expression in both melanoma groups. Among them, miR-146a-5p and miR-4286 demonstrated the highest elevation, especially in BRAFmut tumors. We focused further on their targeted genes. Conclusion: This study demonstrates significant alterations in the miRNA expression profile in metastatic melanoma and highlights the potential of miR-146a-5p and miR-4286 as key regulators of tumor biology. Full article

To decipher the molecular response mechanism of melon to saline–alkaline stress, seedlings of the melon cultivar “Xikaixin” were treated with 50 mmol·L⁻¹ mixed solutions of NaCl and NaHCO₃ at ratios of 1:1, 1:2, and 2:1 to simulate saline–alkaline stress. Transcriptome sequencing of roots (four biological replicates per group, with each replicate consisting of one pot containing four robust seedlings as the experimental unit) yielded 78.98 Gb of clean data (≥6.02 Gb per sample) with Q30 ≥ 96.61% and genome alignment rates of 97.00–98.02%, identifying 588, 686, and 1107 differentially expressed genes (DEGs) in the 1:1, 1:2, and 2:1 groups, respectively. Notably, the 1:1 treatment—mimicking the natural NaCl:NaHCO₃ ratio of saline–alkaline soil in southern Xinjiang—had 588 DEGs with the plant hormone signal transduction pathway as its most significantly enriched pathway, representing the core molecular response of “Xikaixin” to near-natural saline–alkaline stress. DEGs were significantly enriched in 50 pathways categorized into five major classes, with the plant hormone signal transduction pathway showing the highest enrichment across all treatments. A key observation from gene expression patterns is a potential auxin–ABA balance modulation, inferred from the differential expression of annotation-based auxin-related and ABA-related genes/pathways (no direct measurement of hormone levels or signaling was performed): two auxin-related genes (auxin-induced protein gene MELO3C013403 and auxin response factor gene MELO3C004381) were specifically upregulated (≥two fold vs. control) in the high-salt 2:1 group, while ABA-related genes were upregulated and auxin/jasmonic acid/gibberellin-related genes were downregulated in the 1:2 group, indicating a putative cultivar-specific hormone-related gene expression pattern associated with auxin–ABA crosstalk in “Xikaixin” under saline–alkaline stress. In contrast, photosynthesis-antenna protein genes (e.g., MELO3C021567) were significantly downregulated (to 32% of the control) under the 2:1 treatment. RT-qPCR validation confirmed the consistency of these candidate genes’ expression with transcriptomic data. Therefore, melon may respond to saline–alkaline stress by regulating the plant hormone signal transduction (especially auxin–ABA balance), photosynthesis, and carbon metabolism pathways. This study provides novel candidate genes and a theoretical basis for the genetic improvement of saline–alkaline-tolerant melon cultivars, with the unique auxin–ABA balance modulation as a key original contribution. Full article

Background: Cardiovascular diseases (CVDs) are the leading global cause of mortality, with vascular calcification (VC) as a major predictor of adverse outcomes. Although vascular smooth muscle cells (VSMCs) are established contributors, the role of endothelial cells (ECs), particularly via the endothelial–mesenchymal transition (EndMT) and exosome signaling, remains less defined. Objective: This study investigated whether the gut microbiota-derived metabolite Trimethylamine-N-oxide (TMAO) induces EndMT in ECs and whether exosomes from TMAO-treated ECs regulate the VSMC phenotype and calcification. Methods: Human umbilical vein endothelial cells (HUVECs) were exposed to TMAO at physiological and pathological levels (10–50 µM). EndMT markers were analyzed by Western blotting and qPCR. Exosomes were isolated, characterized, and applied to HAVSMCs in graded doses. Osteogenic and contractile markers, β-catenin signaling, and calcification were quantified. Exosomal miR-30 and miR-222 were studied. Results: TMAO triggered dose-dependent EndMT, decreasing CD31/VE-cadherin and increasing α-SMA, N-cadherin, and vimentin. Exosomes from TMAO-treated ECs reprogrammed VSMCs, downregulating contractile proteins and upregulating RUNX2, OPN, TNAP, and β-catenin, causing calcium accumulation. These exosomes displayed elevated miR-222 and reduced miR-30, changes that activated β-catenin signaling and promoted the osteogenic reprogramming of VSMCs. Conclusions: Pathophysiological TMAO levels induce EndMT and mediate the formation of exosomes, which drive the osteogenic reprogramming and calcification of VSMCs. Full article

Objectives: Dendrobine (DDB) is one of the active ingredients in Dendrobium and has been reported to have significant neuroprotective properties. Nevertheless, the precise mechanisms underlying its action have not been fully clarified. The microglial imbalance of polarization is regarded as one of the key determinants in the etiology of neurodegenerative conditions, in the contribution of neuroinflammation. The recovery of M1/M2 balance and the inhibition of over-production of the pro-inflammatory effects have become major topics in modern studies of preventing and treating neurodegenerative diseases. Methods: Therefore, the present study aimed to explore the effects of DDB on the Lipopolysaccharide (LPS)-induced neuroinflammatory model in BV2 microglial cells and the potential molecular mechanisms of microglial M1/M2 polarization. Result: The results showed that DDB significantly suppressed Nitric Oxide (NO) release and ROS levels in LPS-induced BV2 cells. ELISA, qPCR, Western blot, and immunofluorescence results indicated that DDB reduced pro-inflammatory mediators Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6), and nterleukin-1 beta (IL-1β) and increased anti-inflammatory mediators Interleukin-10 (IL-10) and Arginase-1 (Arg-1). Consistently, it decreased M1-like markers Inducible Nitric Oxide Synthase (iNOS) and Cluster of Differentiation 16/32 (CD16/32) while increasing M2-like/repair-associated markers (CD206 and Arg-1), suggesting a shift toward a more anti-inflammatory microglial activation profile based on the assessed marker pane. Conclusions: These results suggested that DDB can suppress the production of inflammatory cytokines and modulate microglial polarization, which indicated that DDB can be used as an effective compound in the prevention of neuroinflammation-related disorders. Full article

Environmental surveillance is important to monitor and mitigate antimicrobial resistance (AMR). In this context, sewage and its marine outfalls remain a hot spot for spreading AMR among pathogens. This study investigated the presence of drug-resistant Staphylococcus aureus in sewage effluent and marine sewage outfalls in Saudi Arabia. Water samples were collected from Jeddah’s southern and central marine outfalls and non-impacted sites. The isolates (n = 120) were identified through biochemical tests and MALDI-TOF. Resistance to antibiotics in the isolates was initially screened through phenotypic methods. Species-specific markers and antibiotic resistance genes (ARGs) were amplified through PCR. The presence of ARGs was also quantified in the isolates and in the environment through qPCR. The data indicated a higher prevalence of methicillin-resistant S. aureus (MRSA) in sewage effluent (63.3%) compared to marine water (50%). Sewage-borne MRSA exhibited higher resistance to various antibiotics. PCR detection confirmed the presence of mecA in MRSA isolates. Virulence genes encoding microbial surface components and recognizing adhesive matrix molecules (MSCRAMMs) were more prevalent in sewage isolates. Particularly, genes responsible for biofilm formation were more prevalent in the isolates from sewage samples. qPCR revealed a higher abundance of mecA, fnbB and bbp in sewage-derived isolates. Statistical analysis confirmed the strong influence of the sewage environment on the prevalence of drug-resistant isolates. Screening of environmental DNA further validated sewage as a reservoir of resistance and virulence determinants. These findings highlight the role of sewage outfalls in disseminating ARGs and virulent S. aureus strains, emphasizing the need to improve wastewater treatment and environmental surveillance strategies. Full article

Current cancer treatments have significant limitations. Designing TPP⁺-modified, mitochondrial-targeted drugs can improve anticancer efficacy. Although wogonin exhibits antitumor activity, it has drawbacks, including poor solubility and limited distribution. This study designed and synthesized 27 derivatives, including nine novel wogonin triphenylphosphine derivatives that demonstrated in vitro antitumor activity. Mito-WO-8, one of these derivatives, exhibited potent activity against PC-3M cells (IC₅₀ = 3.19 μmol/L), demonstrating 15-fold higher potency than wogonin. Further analysis revealed that Mito-WO-8 accumulates more in mitochondria than wogonin and induces mitochondrial dysfunction, including increased reactive oxygen species, reduced membrane potential, and activation of the MPTP channel. Transcriptome and network analyses revealed that Mito-WO-8 activates the p38/MAPK pathway. Downregulation of p-MKK6 and p-p38, as well as upregulation of DDIT3 and cleaved caspase-3, were validated by Western blot (WB) and quantitative polymerase chain reaction (qPCR). Therefore, Mito-WO-8 enhances mitochondrial enrichment and induces mitochondrial damage. This process is associated with apoptosis and the activation of the ROS-p38/MAPK pathway. Additionally, the study found that Mito-WO-8 exhibits a stronger binding affinity for mitochondrial glycerol-3-phosphate dehydrogenase 2 (GPD2) than the parent compound (−9.6 kJ/mol vs. −6.6 kJ/mol), suggesting a potential interaction with GPD2. This finding establishes a foundation for further investigation into its targeted antitumor mechanism. Full article

The aim of this study was to investigate whether genotypes of HRG may modify the effect of Se(selenium) on all-cause mortality and cancer risk. The study was conducted on 2782 initially unaffected women from families with familial breast cancers, all registered at the Hereditary Cancer Centre in Szczecin. Participants were aged 40 years or older and were recruited between September 2010 and March 2024. Women carrying a BRCA1 mutation and those with a diagnosed cancer were excluded from the study. Blood Se levels were measured using inductively coupled plasma mass spectrometry, and molecular analyses of HRG (Histidine-rich glycoprotein) genotypes were performed using real-time PCR with TaqMan probes. After an average follow-up period of 6 years and 2 months, 89 deaths and 210 cases of cancer were identified. The study showed significant differences in the reference range of blood selenium levels, as well as its impact on all-cause mortality and cancer risk, depending on HRG genotype. The most striking finding regarding all-cause mortality risk was observed among women over 50 years of age, effect estimates are presented as hazard ratios (HRs) with 95% confidence intervals (CIs). Regardless of genotype, women with blood selenium (Se) levels in the lowest quartile (Q1) had a significantly higher all-cause mortality risk compared with those in the highest quartile (Q4), (HR = 3.07; 95%CI: 1.53–6.16; p = 0.001). Among women with the HRG non-TT genotype, the risk was even more pronounced—those with Se levels in Q1 had a significantly increased mortality risk compared with women in the higher quartiles (Q2–Q4) (HR = 7.68; 95%CI: 2.31–25.47; p = 0.0008). In contrast, for carriers of the HRG TT genotype, increased all-cause mortality risk was observed only when blood Se levels were in Q1 compared with Q4 (HR = 2.40; 95%CI: 1.09–5.31; p = 0.029). Important findings for any cancer risk have emerged in women below 50 years of age. Among women with the HRG TT genotype, the cancer risk was significantly increased in Q1 compared with women in Q2 (HR = 4.15; 95%CI: 1.55–11.06; p = 0.004). In contrast, the results for HRG non-TT carriers, regardless of genotype, were statistically insignificant. In summary, mortality and cancer risk appeared to be dependent on HRG genotype and blood Se levels. Full article

Low-temperature stress is a major factor limiting the development of the chrysanthemum industry. Chrysanthemum indicum L., wild germplasm with strong cold tolerance within the genus, is an ideal material for mining cold resistance genes. Through preliminary transcriptome analysis of C. indicum under low-temperature stress (PRJNA1391062), we found that multiple R2R3-MYB family members were significantly differentially expressed (|log₂FC| ≥ 1, p < 0.05), suggesting that this family may play important roles in cold stress responses. Within the C. indicum genome, we identified 63 R2R3-MYB members (CiMYBs) through HMMER and BLAST searches combined with domain validation. Phylogenetic analysis classified these genes into 19 subgroups, with most key nodes supported by bootstrap values > 80%. Promoter cis-element analysis revealed enrichment of elements related to light responsiveness, hormone signaling, and stress responses, including 41 low-temperature responsive elements distributed across 28 genes and 32 drought-induced MYB-binding sites present in 23 genes. Synteny analysis identified 13 duplicated gene pairs within the C. indicum genome and 41 collinear gene pairs between C. indicum and Arabidopsis thaliana L. Transcriptome data under low-temperature stress showed that 22 of the 63 CiMYB members were differentially expressed under 4 °C acclimation and −4 °C freezing stress, and they could be classified into three response patterns: acute stress-responsive (rapid upregulation upon initial stress), acclimation-induced (significant activation after 4 °C acclimation), and freezing-suppressed (downregulation after −4 °C freezing). Six differentially expressed genes were randomly selected for RT-qPCR validation, and the results showed consistent trends with the transcriptome data. This study provides a comprehensive identification of R2R3-MYB family members in C. indicum and reveals their expression divergence under low-temperature stress, offering candidate gene resources for deciphering the cold adaptation mechanisms of C. indicum and breeding new cold-resistant chrysanthemum cultivars. Full article

Central nervous system (CNS) evaluation for leukemic involvement is essential both at initial diagnosis and throughout relapse surveillance in childhood acute lymphoblastic leukemia (ALL). Accurate CNS risk classification is a cornerstone of individualized chemotherapy and has significantly advanced treatment strategies. However, detecting leukemic cells in the cerebrospinal fluid (CSF) is challenging, particularly when only a small number of cells are present. While cytomorphology remains a standard diagnostic method, it is limited by low sensitivity and interobserver variability, especially in low-cellularity or equivocal samples. Flow cytometry offers superior sensitivity and specificity and is increasingly recommended to confirm or clarify ambiguous findings. Current guidelines support the use of both cytomorphologic review and flow cytometry to maximize diagnostic accuracy. Evidence consistently demonstrates that any detectable CSF blasts—even in the setting of low WBC counts—are associated with increased risk of CNS relapse and poorer outcomes, underscoring the importance of risk-adapted CNS-directed therapy. Although the prognostic significance of isolated flow-only positivity remains under study, emerging data suggest that timely therapeutic intensification may mitigate adverse outcomes. Additional modalities, including advanced flow cytometry and molecular assays, may further refine CSF assessment in the future. This review summarizes current diagnostic approaches and highlights the need for standardized protocols for CSF evaluation in pediatric ALL. Full article

Isopentenyltransferase (IPT) is the rate-limiting enzyme in cytokinin biosynthesis and plays a critical role in plant acclimation to abiotic stress. To explore soybean IPT genes, we performed genome-wide identification, bioinformatics analysis, and molecular experimental validation to systematically characterize the features and functions of the soybean IPT (GmIPT) gene family. We identified 15 GmIPT genes in the soybean genome, which are unevenly distributed across 12 chromosomes; their evolutionary expansion is primarily driven by whole-genome duplication events. Phylogenetic analysis of soybean IPT proteins with those from Arabidopsis, rice and maize clustered them into four groups, exhibiting lineage-specific functional specialization. GmIPT genes exhibit significant variations in conserved motifs, gene structure, and cis-acting elements; their promoter regions are enriched in light-responsive, abiotic stress-responsive, and hormone-responsive elements, indicating their involvement in complex transcriptional regulatory networks. Tissue expression profiling revealed that GmIPT7 and GmIPT10 are highly expressed in various tissues, whereas GmIPT14 shows specific expression in flowers and the shoot apical meristem. Transcriptomic analysis and qRT-PCR validation demonstrated that GmIPT7, GmIPT10 and GmIPT15 respond differentially to drought, salt and low-temperature stress, with GmIPT15 exhibiting a transient upregulation at 3 h (p < 0.01) followed by a gradual decline to levels close to the pre-treatment control at 6–12 h under low-temperature stress. We further performed haplotype analysis of GmIPT15 and identified a putative elite haplotype (hap1) associated with cold tolerance based on low-temperature germination index assessment. This study provides useful insights for the future functional characterization of plant IPT genes and offers potential genetic resources and molecular markers that may support molecular-assisted breeding for soybean abiotic stress tolerance. Full article