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Jie Liu

Publications and source records attributed to Jie Liu.

17 recordsLinked to original sources
PubMed2026

Minimal Transport Units Govern Oxygen-Defect Stabilization and Transport for Lightweight Solid Electrolytes.

Solid electrolytes are central to electrochemical energy technologies, including fuel cells, sensors, catalysis, membrane separation, and electrolyser. However, most established oxide-ion solid electrolytes are built around heavy B-site cations embedded in rigid and highly connected coordination frameworks, leading to widespread high-weight and sluggish ionic transport that is strongly coupled to large-amplitude lattice relaxations. This intrinsic challenge hinders further performance optimization and constrains the rational design of lightweight electrolytes. Herein, we propose a minimal transport unit-based design paradigm that combines simplified structural motifs with light-element chemistry, enabled by the exceptional flexibility of B-O polyhedra in coordination, rotation, deformation, and connectivity. As a proof of concept, Sc1- xZnxBO3- x /2, constructed from isolated BO3 units, exhibits high oxide ion conductivity (σ(1000°C) ∼ 1.5 × 10-2 S/cm), alongside excellent thermo-mechanical stability. Oxygen vacancies are stabilized through the formation of B2O5 units rather than isolated BO2 species. Long-range oxide-ion migration is mediated by dynamic oxygen exchange between minimal BO3 and B2O5 units via continuous breaking and reforming of B2O5 units, with transient BO2 configurations as intermediates. This study demonstrates minimal transport units as a governing principle for defect stabilization and ionic conduction in lightweight solid electrolytes, offering a general design framework for portable and scalable high-temperature energy technologies.

NMR spectroscopy and variable‐temperature P↗
PubMed2026

Characterization of Dapalides D and E and Genomic Comparison of the Two Co-Occurring Dapalide-Producing Dapis spp.

Marine cyanobacteria are a rich source of diverse bioactive natural products, targeting proteins involved in many diseases. Here, we combined metagenomic analysis to enhance the structure elucidation process of two new cyclodepsipeptides named dapalides D (1) and E (2) from a collection of a cyanobacterial mat containing multiple Dapis species from Guam. Dapalides D/E are composed of 11 amino acids, including multiple identical units with different configurations. Enantioselective amino acid identification of the acid hydrolyzate established the identity of amino acids, including the configuration of α/β-stereogenic centers. Identification and analysis of the dapalides D/E biosynthetic gene cluster from a metagenome-assembled genome aided the elucidation of α-configuration and establishment of the order of individual building blocks, collectively revealing the total structure. Phylogenomic analysis indicates that the dapalides D/E producer belongs to Dapis sp. (Dapis sp. VPG23-80 MAG-2), which shares a 95.2% average nucleotide identity with Dapis sp. VPG23-80 MAG-1, the producer of dapalides A-C that cooccurs in the same assemblage. Dapalide D (1) showed moderate growth inhibitory activity against various cancer cell lines. This work expands the dapalide structure class and further highlights the use of combined chemical and metagenomic analyses for natural product structure elucidation.

Cyanobacteria↗
PubMed2026

Development and preliminary validation of plasma cell-free DNA methylation-based diagnostic prediction model for colorectal cancer detection.

BACKGROUND: Colorectal cancer (CRC) is a common malignancy associated with genetic and epigenetic alterations. Several methylation biomarkers have been investigated for non-invasive CRC detection; however, their reported performance varies across clinical settings, and the detection of early-stage or precancerous disease and discrimination from non-malignant colorectal conditions remain challenging. This exploratory study aimed to identify reproducible CRC-associated plasma cell-free DNA (cfDNA) methylation regions and to develop and preliminarily evaluate diagnostic prediction model for distinguishing CRC from healthy controls and benign samples. METHODS: Public CRC tissue methylation datasets from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were analyzed to identify reproducible CRC-associated methylation alterations. Plasma cfDNA methylation was profiled using methyl-CpG-binding-domain enrichment followed by paired-end sequencing in patients with CRC, patients with colorectal polyps, and healthy controls. After quality-control filtering, 30 CRC and healthy-control samples were randomly allocated at the participant level in a 7:3 ratio to a development set comprising 10 patients with CRC and 11 healthy controls and a held-out test set comprising 4 patients with CRC and 5 healthy controls. Hypermethylated regions were selected using least absolute shrinkage and selection operator (LASSO) logistic regression. The 12-region model was evaluated in the held-out test set and subsequently applied to 10 colorectal polyp samples without refitting or recalibration. RESULTS: Tissue methylation analysis identified reproducible CRC-associated alterations across independent datasets. In the plasma development set, 707 differentially methylated regions (DMRs) were identified between CRC and healthy-control samples, including 324 hypermethylated and 383 hypomethylated regions. LASSO regression selected a 12-region hypermethylation signature. In the held-out test set, the model achieved an area under the curve (AUC) of 0.85 [95% confidence interval (CI): 0.579-1.000]. At the development-set-derived threshold, sensitivity was 75.0% (3/4), specificity was 60.0% (3/5), and accuracy was 66.7% (6/9). When the original model was applied to colorectal polyp samples, model scores were significantly higher in both CRC and polyp samples than in healthy controls, while CRC samples showed a tendency toward higher scores than polyp samples. CONCLUSIONS: This exploratory study identified a 12-region plasma cfDNA hypermethylation signature associated with CRC and developed a LASSO-based diagnostic prediction model that showed preliminary discrimination between CRC and healthy controls in a small held-out test set. By integrating tissue methylation evidence with plasma cfDNA profiling, this study expands the repertoire of candidate region-level methylation markers for blood-based CRC detection.

Colorectal cancer (CRC)↗
PubMed2026

Hypertensive mt. tRNAIle4263A>G mutation orchestrates vascular senescence and apoptosis by activation of mitochondria-ER interplay.

The pathogenic mechanism underlying diseases caused by mitochondrial DNA (mtDNA) mutation, including hypertension, persists as an unresolved global challenge. Although mutation-induced mitochondrial defects have been well characterized, how these mito-perturbations are converted into critical intermediary signaling cascades and contribute to diseases remain unknown. Here, using human induced pluripotent stem cell (hiPSC)-derived vascular organoids (VOs) and vascular cells, the hypertensive mt. tRNAIle4263A > G mutation was identified to induce vascular senescence, apoptosis and vascular-specific dysfunction through mitochondria-endoplasmic reticulum (ER) interaction. For the first time, this study mapped the transcriptional reprogramming landscape of human VOs carrying this mutation. Through systematic screening and functional validation, ER stress was screened out, together with downstream mitochondria-associated ER membranes-mitochondrial Ca2+ overload resulting in vascular abnormality. Pathological reactive oxygen species (ROS) elevation, driven by tRNAIle destabilization and bioenergetic failure, acts as the primary instigator of maladaptive ER stress activation in this cascade. Pharmacological targeting of this axis-using mito-Tempol (a mitochondria-targeted ROS scavenger), Tauro Ursodeoxycholic Acid (an ER stress inhibitor), or RU265 (a highly-selective mitochondrial calcium uniporter inhibitor)-rescues vascular abnormality. This study highlights mt. tRNAIle4263A > G mutation orchestrates vascular pathology through ROS induced activation of inter-organelle communication, resolving a long-standing knowledge gap between mtDNA mutations and diseases and establishing therapeutic nexuses for mtDNA mutation-related cardiovascular diseases.

Hypertension↗
PubMed2026

Inhaled vitamin A mitigates hyperoxia-induced acute and chronic lung damage in a neonatal rat model of bronchopulmonary dysplasia.

RATIONALE: Prevention of bronchopulmonary dysplasia (BPD) remains a critical unmet need. OBJECTIVES: We continued evaluating aerosolized vitamin A in a neonatal rat hyperoxia-injury model of BPD, testing whether lung-targeted inhalation yields superior outcomes compared to enteral or intramuscular (IM) delivery. METHODS: Rat pups were exposed to continuous 95% hyperoxia for seven days to induce lung damage. Vitamin A was administered from post-natal day (PD) 1-7 by inhalation, enteral or IM dosing. Persisting effectiveness of inhaled vitamin A was examined at PD 21, dwelling in normoxia after all interventions were discontinued at PD 7. MEASUREMENTS AND MAIN RESULTS: Comprehensive analyses include alveolar morphometrics, in vivo pulmonary function testing, assessment of hepatic vitamin A level, and quantitating gene and protein expression of relevant biomarkers of lung maturation, inflammation and damage/repair, employing singlex and multiplexed assays and whole-genome gene expression. CONCLUSIONS: Inhaled vitamin A suppressed hyperoxia-induced lung damage, with key hallmarks of BPD, including lung morphometrics and biomarkers associated with lung damage and inflammation, being effectively indistinguishable from healthy controls at both PD 7 and 21, Natural reparative processes were enhanced, with normal alveolarization and pulmonary function at PD 21. Despite raising hepatic vitamin A levels, enteral dosing was ineffective in restoring alveolar morphology at PD 7. Consistent with previous reporting, IM dosing yielded modest effect at PD 7 but with little evidence of benefit to pulmonary function at PD 21. Observation of dose-dependent effects with aerosolized vitamin A strengthens the evidence of the benefits of lung-targeted delivery, supporting further development of inhaled vitamin A as a BPD preventive strategy.

Journal Article↗
PubMed2026

Yeast Rad55-Rad57-SHU paralog complex dynamically promotes Rad51 filament formation.

Homologous recombination (HR) is an important DNA repair pathway that safeguards genome integrity. During HR, the Rad51 nucleoprotein filaments catalyze strand invasion into a homologous duplex DNA. Filament formation requires a conserved family of Rad51 paralogs that act as tumor suppressors in humans. By capturing six distinct states using cryo-electron microscopy, we reveal that the Saccharomyces cerevisiae Rad51 paralog complex, composed of the Rad55-Rad57 heterodimer and the SHU (Psy3-Csm2-Shu1-Shu2) complex, selectively brings Rad51 to single-stranded DNA to seed filament formation. Rad51 itself is a transient yet integral component of this machinery which binds along the Rad57 subunit to complete a high-affinity DNA-binding site. We also uncover a dual-nucleotide regulatory mechanism: a structural ADP molecule stabilizes the complex, while a second, catalytic ATPase site at the Rad57-Rad51 interface promotes the release of the paralog complex. These structural and mechanistic features provide a blueprint for understanding the function of Rad51 paralogs across eukaryotes.

Saccharomyces cerevisiae Proteins↗
PubMed2026

Second Primary Malignancies in Patients With B-Cell Lymphomas Treated With Bruton's Tyrosine Kinase Inhibitors: A Systematic Review and Meta-Analysis.

OBJECTIVE: To evaluate the overall second primary malignancy (SPM) burden in patients with B-cell lymphomas treated with Bruton's tyrosine kinase (BTK) inhibitors and compare SPM risk versus non-BTK inhibitor or placebo controls. METHODS: We searched major databases from inception to September 30, 2025. The primary outcome was SPM incidence. Consistent treatment backgrounds were defined as comparable baseline clinical and treatment characteristics, with BTK inhibitor exposure as the main between-arm difference. RESULTS: Fifty-two studies involving 9337 patients were included, mainly CLL/SLL; MCL was the largest non-CLL/SLL subtype. Pooled SPM incidence was 8% (95% CI: 6%-11%) with a median follow-up of 31.5 months. Multivariable meta-regression identified follow-up duration as the only independent predictor, whereas disease subtype, inhibitor generation, prior therapy lines, study design, and age were not significant. Furthermore, SPM patterns were comparable between CLL/SLL and non-CLL/SLL cohorts. Compared with controls, BTK inhibitors did not significantly increase SPM risk (RR = 1.30, 95% CI: 0.95-1.78), a finding confirmed in analyses with consistent treatment backgrounds (RR = 1.03, 95% CI: 0.85-1.25). CONCLUSIONS: SPMs occur across disease backgrounds and are mainly influenced by follow-up duration. Current evidence does not establish a direct carcinogenic effect of BTK inhibitors.

Humans↗
PubMed2026

Comprehensive analysis suggests CRIF1 is a potential target in breast cancer associated with prognosis and immune infiltration.

BACKGROUND: CRIF1 is a multifunctional factor that regulates cell biological processes such as the cell cycle, cell proliferation, and energy metabolism, and it is a new molecule that contributes to the poor prognosis of many malignancies. However, its involvement in breast cancer development is not fully known. MATERIALS AND METHODS: To investigate the relationship between CRIF1 expression, prognosis, and clinical characteristics using The Cancer Genome Atlas (TCGA-BRCA). The relationship between CRIF1 expression and the immunological microenvironment was investigated using CIBERSORT, ESTIMATE. Breast tissue and CRIF1 expression were validated by IHC. A tiny interfering plasmid was designed to transiently transfect breast cancer cell lines, and proliferation-related functional tests were carried out. The effect of sh CRIF1 on tumor formation was confirmed using a subcutaneous tumor experiment in naked mice. RESULTS: We discovered that CRIF1 was highly elevated in breast cancer tissues and associated with a poor prognosis. CRIF1 stimulates breast cancer cell proliferation, migration, and invasion. Knockdown decreased PI3K/AKT/mTOR signaling, which boosted autophagy activity. Immune infiltration research revealed that patients with high CRIF1 expression had higher CD8+ T cell expression but reduced macrophage M2 expression. CONCLUSION: Upregulation of CRIF1 in breast cancer cells enhances malignant behavior, which may be mediated by PI3K/AKT/mTOR signaling and is linked to cellular autophagy.

Humans↗
PubMed2026

Plasma proteome profiling identifies XPNPEP3 as a novel biomarker associated with metabolic dysfunction-associated steatotic liver disease in patients with type 2 diabetes mellitus.

OBJECTIVE: To identify plasma protein differences between type 2 diabetes mellitus (T2DM) patients with and without metabolic dysfunction-associated steatotic liver disease (MASLD), and to evaluate the diagnostic potential of X-prolyl aminopeptidase 3 (XPNPEP3) for identifying MASLD in T2DM patients. METHODS: Twenty T2DM inpatients were categorized into groups with and without MASLD and their plasma samples were analyzed using data-independent acquisition mass spectrometry, followed by bioinformatics analysis to identify differentially expressed proteins. The cohort was then expanded to 84 patients, and plasma XPNPEP3 levels were validated by enzyme-linked immunosorbent assay. Correlation between XPNPEP3 and clinical indicators were evaluated, and diagnostic performance was determined via receiver operating characteristic (ROC) analysis. Immunohistochemistry was employed to compare hepatic XPNPEP3 expression between the two groups. RESULTS: Proteomic analysis identified 176 differentially expressed proteins, with XPNPEP3 exhibiting the most significant down-regulation by fold change. In the validation cohort, plasma XPNPEP3 was significantly lower in T2DM+MASLD versus T2DM alone. XPNPEP3 levels were negatively correlated with diabetes duration, liver function markers, and triglyceride levels, and was identified as an independent factor inversely associated with MASLD in T2DM.ROC analysis demonstrated strong diagnostic performance for XPNPEP3, further enhanced when combined with BMI and diabetes duration.  Immunohistochemistry confirmed reduced hepatic XPNPEP3 expression in T2DM+MASLD patients. CONCLUSIONS: Lower plasma XPNPEP3 is independently associated with MASLD in T2DM patients and demonstrates strong diagnostic potential, positioning XPNPEP3 as a promising biomarker for diagnosing MASLD in T2DM patients and a novel target for non-invasive diagnostic tool development.

Humans↗
PubMed2026

BCDX2-CX3 and DX2-CX3 complexes assemble and stabilize RAD51 filaments.

The repair of DNA double-strand breaks by homologous recombination is essential for genomic integrity, and its dysregulation is a hallmark of cancer1. Central to homologous recombination is the RAD51 recombinase, whose assembly into a nucleoprotein filament is governed by five RAD51 paralogues (RAD51B, RAD51C, RAD51D, XRCC2 and XRCC3)2. Mutations in any of these proteins predispose individuals to multiple cancers or genetic disorders3-6. These paralogues are thought to form two functionally separate complexes RAD51B-RAD51C-RAD51D-XRCC2 (BCDX2) and RAD51C-XRCC3 (CX3), that act independently at different stages of homologous recombination7-11. Here we demonstrate that all five paralogues can assemble into a single, ATP-dependent BCDX2-CX3-RAD51 supercomplex. The architecture of this assembly bound to single-stranded DNA reveals a contiguous filament where the CX3 module stacks atop BCDX2, creating a protofilament template for RAD51 filament formation. We further identify a novel, RAD51B-independent DX2-CX3 complex (RAD51D-XRCC2-RAD51C-XRCC3) functioning as a stable RAD51 anchor on single-stranded DNA, and we capture it in multiple states, including capping RAD51 filament segment. These distinct assemblies are differentially regulated by ATPase activity, defining a dynamic BCDX2-CX3 'loader' and a stable DX2-CX3 'anchor' that provide functional modularity to the homologous recombination machinery. This work provides a unifying mechanism for human RAD51 paralogue function and delivers an atomic blueprint for interpreting disease-causing mutations.

Rad51 Recombinase↗
PubMed2026

A nonlinear multi-omics data integration and classification model based on pathway self-attention and graph convolutional networks.

The abundance of omics data has significantly advanced the development of multi-omics data integration techniques. Non-linear embedding approaches for data integration have gradually become the mainstream in multi-omics research, as these approaches can substantially improve cancer analysis by enhancing the quality of the embeddings. However, current multi-omics data integration methods are typically confined to omics measurements, neglecting domain-specific prior knowledge encompassing biological pathways. In this study, we proposed a multi-omics integrated classification model, PathTransGCN, based on pathway self-attention and graph convolutional networks (GCN). The model integrated biological pathway information into multi-omics data analysis with the aim of enhancing the accuracy of cancer classification. Multi-omics data for breast cancer (BRCA), non-small cell lung cancer (NSCLC), and low-grade glioma (LGG) were obtained from The Cancer Genome Atlas (TCGA) and UCSC Xena databases. These data included gene mutations, DNA methylation, copy number variations, and gene expression, and were used to assess the model's generalizability across different cancers. First, PathTransGCN employed a pathway self-attention module to learn latent representations of samples across different pathways, thereby obtaining multi-omics integration vectors. Concurrently, a patient similarity network (PSN) was constructed using the similarity network fusion (SNF) approach. Second, the integrated vectors and the PSN were jointly fed into a GCN for end-to-end training, enabling precise classification of cancer subtypes. Through multi-omics data analysis of the BRCA dataset, PathTransGCN outperformed several popular algorithms (such as MoGCN and DeePathNet) in the five-class classification of cancer subtypes, achieving an accuracy rate of 87.6% and an F1 score of 86.4%. Moreover, the model demonstrated robust generalization capabilities across both NSCLC and LGG datasets, while effectively identifying key disease-associated biomarkers at the pathway level. Experimental results demonstrate that PathTransGCN exhibits outstanding performance in integrating omics data and delivering interpretable classification outcomes, presenting significant potential for clinical applications.

Humans↗
PubMed2025

Detoxifying biotransformation of chloramphenicol by Exiguobacterium sp. CAP4 and its bioaugmentation of chloramphenicol biodegradation in simulated wastewater.

The extensive use of chloramphenicol (CAP) in livestock leads the accumulation of CAP in livestock manures, threatening environmental and human health. Therefore, eliminating or reducing CAP concentration in manures before its re-utilization and application through microbial remediation is necessary. Exiguobacterium sp. CAP4, isolated from the plastisphere in duck manures, was capable of degrading CAP with the biodegradation efficiency of 97.8 % at initial CAP concentration of 5 mg/L within 4 days. A total of twenty-four biotransformation products were determined, including two novel transformation products, TP166 and TP203, enriched the integrity of CAP biodegradation pathways. Furthermore, the biotransformation process was proposed as a detoxifying process through biotransformation products toxicity evaluation. Notably, Exiguobacterium sp. CAP4 successfully colonized in the cow manures after inoculation, and bioaugmented the biodegradation of CAP in virgin cow manures. This study significantly extended our understanding of the CAP biotransformation fate, and provided a promising bacterial strain for bioremediation of CAP containing wastewater in situ.

Chloramphenicol↗
PubMed2025

ChemPerturb-seq screen identifies a small molecule cocktail enhancing human beta cell survival after subcutaneous transplantation.

Traditional chemical screens have focused on a single assay per screen, making them labor intensive and costly. Here, we combined a chemical screen with single-cell RNA sequencing (scRNA-seq) to perform Chemical Perturb-seq (ChemPerturb-seq), enabling a systematic analysis of the molecular changes of human beta cells upon individual small molecule treatments. Using this platform, we performed an in vivo barcoded screen and discovered a small molecule cocktail, including beta-lipotropin 61-91, insulin growth factor-1, and prostaglandin E2, with which preconditioning human beta cells and primary islets significantly enhanced function and survival when transplanted subcutaneously to female, but not to male, mice. We identified two additional molecules, serotonin and histamine, that promote islet function when transplanted subcutaneously to male mice using ChemPerturb-seq. Such small molecule cocktails could be applied to improve the current FDA-approved islet transplantation procedure. Finally, we developed an artificial intelligence (AI)-powered website, ChemPerturbDB, which provides user-friendly open access analysis of the extensive ChemPerturb-seq dataset.

Humans↗
PubMed2025

Electrochemical sensor toolkit for simultaneous glutamate detection at edge of cleft and peri-soma.

Simultaneously monitoring glutamate (Glu) dynamic at edge of synaptic cleft and peri-soma is crucial for understanding Glu-related pathology. Here, we created an electrochemical Glu sensors toolkit with spatial resolution of ∼60 nm, combining biologically engineered Glu binding protein for specifically capturing Glu together with chemically designed ferrocene groups for signal labeling. Modulation conjugation approach between GluR and ferrocene significantly improved sensitivity up to 32-folds. More importantly, protein engineering of residue mutation and linker peptides flexibility expanded linear range from 10 μM to 6 mM, accelerated on/off times down to 35/40 ms. This toolkit realized real-time quantifying of Glu both at edge of cleft and peri-soma, we discovered that Glu was almost released through SLC7A11 channels in calyx of held synapse upon oxygen-glucose-deprivation, while Glu was mainly released through hemichannels upon β-amyloid42 stimulation. Our work provided a methodology for investigating Glu release and reuptake and offered insights for Glu related pathology.

Glutamic Acid↗