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PubMed2026

Furmonertinib inhibits non-small cell lung cancer progression through ANGPT1-mediated regulation of cell migration and apoptosis.

BACKGROUND: Lung cancer remains one of the leading causes of cancer-related mortality worldwide, highlighting the urgent need for effective therapeutic agents. This study investigates the antitumor effects and underlying mechanisms of furmonertinib (FUR) in lung cancer cells. METHODS: Transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were utilized to identify FUR target genes, followed by functional enrichment, survival, and protein-protein interaction (PPI) network analyses. Human lung cancer cell line A549 was treated with FUR and/or ANGPT1-specific siRNA. Cell migration, apoptosis, and protein expression were assessed by wound healing, flow cytometry, and Western blotting. Cellular thermal shift assay (CETSA) and drug affinity response target stability (DARTS) assays were used to assess FUR-induced stabilization of angiopoietin-1 (ANGPT1) protein. RESULTS: FUR treatment significantly inhibited cell migration and increased apoptosis in NSCLC cells. Bioinformatics analysis revealed 12 overlapping target genes of FUR from the PharmMapper and SwissTargetPrediction databases, with ANGPT1 emerging as a key candidate. ANGPT1 expression was downregulated in tumor tissues and positively correlated with patient survival. Western blotting confirmed that FUR upregulated ANGPT1 protein levels in a dose-dependent manner. Knockdown of ANGPT1 enhanced migration and suppressed apoptosis, while FUR reversed these effects. FUR treatment enhanced the stability of ANGPT1 under high-temperature conditions while reducing its sensitivity to protease. ANGPT1 may have affected tumor cell migration through cell adhesion and extracellular matrix (ECM) pathways. CONCLUSIONS: FUR suppresses lung cancer progression by upregulating ANGPT1, thereby inhibiting cell migration and promoting apoptosis. ANGPT1 is a potential therapeutic target and provides new insights into the anti-tumor mechanism of FUR in lung cancer.

Lung cancer↗

PubMed2026

PSMB8: an immune-related prognostic marker for low-grade gliomas.

BACKGROUND: Glioma is the most common primary intracranial tumor in adults. As a subunit of immune proteasome, proteasome subunit beta type-8 (PSMB8) may regulate the progression of glioma via participating in degradation and presentation of tumor antigenic peptides, but its prognostic and clinical applicant usage is under investigation. Therefore, this study aimed to comprehensively evaluate the prognostic significance of PSMB8 in low-grade glioma (LGG) and to elucidate its association with the tumor immune microenvironment and potential as a predictor for immunotherapy response. METHODS: Transcriptome data were downloaded from The Cancer Genome Atlas (TCGA), Chinese Glioma Genome Atlas (CGGA), Gene Expression Omnibus (GEO) repositories. The correlations between PSMB8 expression and the clinicopathological features of LGG were investigated in our study, and the prognostic role of PSMB8 in LGGs was assessed fully and comprehensively. Furthermore, we evaluated the correlation between PSMB8 expression and LGG immune environment via the experiments and bioinformatic analysis. RESULTS: Our results indicated that, PSMB8 were highly expressed in most tumor tissues, including LGG. Lower expression of PSMB8 was significantly correlated with lower World Health Organization (WHO) grade and isocitrate dehydrogenase (IDH) mutation status. Moreover, PSMB8 showed a promising prognostic ability for LGG patients via nomogram model and receiver operating characteristic (ROC) curves. Association analysis showed that PSMB8 expression was associated with immune cell infiltration in a variety of tumors, including LGG. Our experiments validated the positive correlation between PSMB8 expression and M2-macrophage infiltration level in clinical LGG tissues and invasive ability of LGG cell. CONCLUSIONS: PSMB8 could be used as one of the prognostic indicators of LGG and it could regulate the LGG cell migratory and invasive ability. Besides, PSMB8 is expected to be a promising biomarker of cancer immunotherapy.

Low-grade glioma (LGG)↗

PubMed2026

Hypoxia-inducible factor-1α promotes the malignant progression of cervical cancer cells by regulating lactate dehydrogenase A-mediated glycolysis.

BACKGROUND: Enhanced glycolysis is a hallmark of metabolic reprogramming in cervical cancer and plays a key role in tumor progression. Hypoxia-inducible factor-1α (HIF-1α), a core regulator of glycolytic metabolism, remains incompletely characterized in cervical cancer. This study aimed to investigate the expression pattern and clinical significance of HIF-1α in cervical cancer, and to explore its association with malignant biological behavior and lactate dehydrogenase A (LDHA)-related glycolytic metabolism in cervical cancer cells. METHODS: The expression level, clinicopathological features, immune infiltration correlation, and prognostic value of HIF-1α in cervical cancer were analyzed based on the The Cancer Genome Atlas (TCGA) database. HIF-1α overexpression and knockdown models were established in HeLa and Caski cells. Cell viability and invasive ability were assessed by Cell Counting Kit-8 (CCK-8) and Transwell assays, respectively. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot were used to detect changes in LDHA expression. Lactate production was measured using a lactate assay kit, and intracellular reactive oxygen species (ROS) levels were determined by flow cytometry. RESULTS: Bioinformatics analysis showed that HIF-1α was highly expressed in cervical cancer and was closely associated with patient age, menopausal status, immune cell infiltration, and poor prognosis. Kaplan-Meier survival analysis demonstrated that patients with high HIF-1α expression had significantly worse overall survival (OS) than those with low expression. In vitro functional experiments further confirmed that HIF-1α overexpression significantly enhanced the viability and invasive ability of HeLa and Caski cells, whereas HIF-1α knockdown produced the opposite effects. HIF-1α overexpression was associated with increased messenger RNA (mRNA) and protein expression levels of LDHA, a key glycolytic molecule, along with increased lactate production and elevated intracellular ROS levels. CONCLUSIONS: HIF-1α is aberrantly highly expressed in cervical cancer and may enhance glycolytic activity by upregulating LDHA expression, thereby promoting the proliferation and invasion of cervical cancer cells. These findings suggest that HIF-1α could serve as a potential diagnostic, prognostic, and therapeutic target biomarker for cervical cancer.

Hypoxia-inducible factor-1α (HIF-1α)↗

PubMed2026

Gut microbiome in advanced non-small cell lung cancer: effect of chemotherapy and impact on efficacy.

BACKGROUND: While evidence linking the gut microbiome (GM) to cancer immunotherapy is growing, data regarding its role in chemotherapy remains limited. This study aims to investigate the effect of chemotherapy on GM composition and its potential as a predictive biomarker for treatment outcomes in advanced non-small cell lung cancer (NSCLC). METHODS: Advanced NSCLC patients treated with chemotherapy at Ramathibodi Hospital were prospectively enrolled. Clinical data and stool samples were collected at three time points: baseline, post-evaluation, and at progression of disease (PD). Fecal bacterial DNA was extracted, followed by PacBio Sequel II sequencing and comprehensive bioinformatic analysis. Clinical data were summarized using descriptive statistics. Progression-free survival (PFS) and overall survival (OS) were estimated by the Kaplan-Meier method, and predictive factors were identified using Cox-regression analysis. RESULTS: This study analyzed 54 stool samples from 27 NSCLC patients treated with platinum-doublet chemotherapy. The median PFS and OS were 5.3 months [95% confidence interval (CI): 2.4-8.4] and 13.8 months (95% CI: 5.2-not reached), respectively. Post-chemotherapy changes (n=20 paired samples) showed a significant decrease in microbial richness, as evidenced by reduced abundance-based coverage estimator (ACE) (P=0.02) and Chao1 (P=0.03) alpha diversity indices. Taxonomically, the relative abundance of Enterobacter was significantly decreased post-chemotherapy (P=0.03). Regarding treatment response (n=26 evaluable patients; 13 PD, 13 clinical benefit), baseline alpha diversity was not predictive of outcome. However, the relative abundance of Akkermansia was notably higher in the clinical benefit group, approaching statistical significance (P=0.07). CONCLUSIONS: Chemotherapy significantly reduced GM by decreasing species richness (as measured by the ACE and Chao1 index), while species diversity (as measured by the Shannon and Simpson index) remained unchanged. Therefore, confirming the definitive role of the GM as a predictive biomarker in chemotherapy-treated NSCLC patients necessitates further investigation in a larger, more robustly powered cohort.

Gut microbiome (GM)↗

PubMed2006

New analytical tools for studying autoimmune diseases.

Protein microarrays with immobilised proteins on their surface are new analytical tools to overcome the current limits with respect to sample volume and throughput. They have a great potential as well with respect to multiplexing of complex samples, as a research tool and in diagnostics. Based on recent advances in this technology, new applications for protein microarrays in studying autoimmune diseases were described. Required tools for bioinformatical analysis of protein microarrays concerning normalisation, clustering and classification methods are discussed. The huge potential of this technology as well as future requirements such as protein microarray based diagnostics are presented.

Animals↗

PubMed2026

Co-expression of the Mammaglobin (SCGB2A2) Gene With hsa-miR-184 and hsa-miR-190b Indicates Its Possible Role in Oncogenic Pathways in Breast Cancer.

BACKGROUND/AIM: Breast cancer is the most common cancer in women worldwide, and early detection remains a significant challenge. Recent studies have identified increased expression of Mammaglobin A (Q13296, Gene: SCGB2A2) mRNA in breast cancer, suggesting its potential as a disease marker, although its function is not fully understood. To elucidate Mammaglobin's role, this study sought to identify co-expressed miRNAs and analyze the biological pathways they regulate. MATERIALS AND METHODS: Using TCGAbiolinks and Firebrowse, miRNA and gene expression data were collected from 86 patients, including tumor and normal tissue samples from the Cancer Genome Atlas (TCGA) Breast Cancer cohort. Transcriptomic data were analyzed with DESeq2, and a Spearman correlation was calculated for significant p-values, which were further explored using enrichment tools and target gene databases. RESULTS: DESeq2 was used to identify differential expression of miRNAs between normal and tumor breast tissues. Out of 782 miRNAs differentially expressed in breast cancer, hsa-mir-184 and hsa-mir-190b showed a significant positive correlation with SCGB2A expression. These markers were also upregulated in breast cancer tissues compared to normal tissues. Bioinformatics analysis revealed that hsa-mir-184 and hsa-mir-190b play important roles in cancer and cellular proliferation. These miRNAs target a wide range of genes, including sorting nexin 9 (SNX9) and annexin 6 (ANXA6), which are involved in membrane stability, vesicular trafficking, and cell mobility, and they contribute to cancer metastasis. CONCLUSION: The positive correlation among the expression of hsa-miR-184, hsa-miR-190b, and SCGB2A2 suggests that they may participate in shared biological pathways. These pathways govern critical cellular processes, such as membrane trafficking and cell signaling, which are frequently disrupted in cancer. Consequently, these findings enable a better understanding of the role of Mammaglobin in breast cancer signaling.

MicroRNAs (miRNAs)↗

PubMed2001

The gene causing the Best's macular dystrophy (BMD) encodes a putative ion exchanger.

Best's macular dystrophy (BMD), also known as vitelliform macular degeneration type 2, is an autosomal dominant disease that causes loss of vision. The causative gene encodes a 585 amino acids protein called bestrophin with unknown function. From bioinformatics analysis, a putative ion exchanger function for bestrophin can be suggested.

Bestrophins↗

PubMed2026

Impact of NR4A3 on wound healing in chronic venous ulcers and its association with the PI3K/Akt signaling pathway.

BACKGROUND: To investigate the role of NR4A3 in chronic venous ulcer (VU) wound healing and to explore its potential regulatory mechanism involving the PI3K/Akt pathway. METHODS: Differential expression and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using the GSE174661 dataset. DEGs were filtered by |log2FC| > 1 and adjusted P < 0.05, with KEGG significance set at P < 0.05. NR4A3 was identified as the core gene. NR4A3 knockdown and overexpression were established in HaCaT cells to evaluate proliferation, migration, and inflammatory cytokines. TNF-α was used to mimic the inflammatory microenvironment. Western blotting assessed phosphorylation of GSK3β, mTOR, PI3K, and Akt. PI3K/Akt agonist 740Y-P and inhibitor LY294002 were used in rescue experiments. RESULTS: Bioinformatic analysis revealed that NR4A3 expression was markedly downregulated in chronic venous ulcer (VU) tissues relative to normal skin and ordinary acute wound tissues. Differentially expressed genes were significantly enriched in the PI3K/Akt signaling pathway. TNF-α stimulation significantly upregulated NR4A3 expression and increased phosphorylation of GSK3β and mTOR in HaCaT cells. In cultured HaCaT keratinocytes, NR4A3 knockdown suppressed cell proliferation and invasion, enhanced cell migration, and elevated the expression and secretion of pro-inflammatory cytokines (IL-6, IL-8, CXCL5), accompanied by reduced phosphorylation of PI3K and Akt. Conversely, NR4A3 overexpression promoted cell proliferation and invasion, restrained migration, and dampened inflammatory responses, while increasing PI3K/Akt phosphorylation. Treatment with the PI3K/Akt agonist 740Y-P partially rescued the impaired proliferation, aberrant migration, and excessive inflammation caused by NR4A3 silencing, whereas PI3K/Akt inhibitor LY294002 aggravated pathway suppression. These findings suggest that NR4A3-associated changes in keratinocyte functions and inflammatory reactions are functionally linked to PI3K/Akt pathway activity, and inflammatory stimulation activates GSK3β/mTOR signaling accompanied by compensatory NR4A3 upregulation. CONCLUSION: These findings suggest that NR4A3 is associated with keratinocyte behavior and inflammatory responses via the PI3K/Akt pathway, potentially affecting chronic VU progression and healing. Reduced NR4A3 may impair wound repair through inflammation and abnormal cell migration, while TNF-α induces compensatory NR4A3 elevation.

NR4A3↗

PubMed2026

Development and validation of whole-genome SSR markers in sugar beet (Beta vulgaris L.).

Sugar beet (Beta vulgaris L.) is an important sugar and cash crop worldwide. To systematically characterize SSR (Simple Sequence Repeat) loci across sugar beet chromosomes and enable the precise identification of germplasm resources, this study conducted a genome-wide scan for SSR loci, analyzed their distribution patterns, and determined their genotypes using resequencing data from 123 sugar beet varieties. The results revealed an abundance of SSR loci in the sugar beet genome, with a total of 135, 379 identified, from which 135, 344 pairs of SSR primers were designed (135, 344 primer pairs successfully designed; 35 loci failed to meet design criteria). Specifically, 31, 748 primer pairs were designed based on SSRs located in unassigned scaffolds, and 103, 596 primer pairs from SSRs assigned to the nine chromosomes. Through bioinformatic analysis, we identified 28, 768 SSR primers located in multi-copy genes with PIC (Polymorphism Information Content) ≥ 0.5, and 2, 326 SSR markers located in single-copy genes residing in various genic regions (among which 543 had PIC ≥ 0.5, with the highest reaching 0.776). PCR (Polymerase Chain Reaction) validation confirmed 20 robust and polymorphic markers producing clear and reproducible bands. Among them, 10 SSR primers located in multi-copy genes exhibited three or more polymorphic types, and 10 markers located in single-copy genes displayed 2-3 polymorphic types. The most polymorphic marker, YCD-4-2, detected 11 polymorphic types across 48 varieties. Furthermore, to explore markers with potential functional significance, we annotated the genes harboring SSR markers located in single-copy genes. The results showed that 1, 264 SSRs located in single-copy genes were localized to 967 genes, which are significantly enriched in pathways related to carbohydrate metabolism, stress responses, and plant-pathogen interactions. The 20 validated markers and the 2, 326 SSRs located in single-copy genes provided in this study can be directly applied to fingerprinting of sugar beet varieties, seed purity testing, and marker-assisted selection, thus representing a practical resource for molecular breeding.

genome-wide↗

PubMed2026

Molecular epidemiological characteristics of H9N2 subtype avian influenza virus in the external environment of western Zhejiang, China, 2014-2025.

OBJECTIVE: To elucidate the epidemiological distribution patterns of avian influenza virus (AIV) in the external environment of western Zhejiang from 2014 to 2025, analyze the molecular epidemiological characteristics of the H9N2 subtype, and assess its public health risks. METHODS: According to the Zhejiang Provincial Surveillance Program for Avian Influenza in Occupationally Exposed Populations and External Environments, real-time RT-PCR was used to detect AIV subtypes in environmental specimens. H9N2-positive samples with cycle threshold values <30 were inoculated into specific pathogen-free (SPF) embryonated chicken eggs for virus isolation, followed by whole-genome sequencing and bioinformatics analysis for phylogenetic and molecular characterization. RESULTS: A total of 7,762 specimens were tested from 2014 to 2025, with an overall positivity rate of 34.64% (2,689/7,762) for AIV. Significant differences in positivity rates were observed in seasons, regions, sampling sites, and specimen types (all p < 0.001). AIV activity peaked in winter and spring, with the highest rates detected in live poultry markets and chopping board swabs. The H9 was the predominant subtype, with co-circulation of multiple subtypes. All 48 H9N2 subtype isolates belonged to the G57 genotype, with the hemagglutinin (HA) and neuraminidase (NA) genes falling into the Y280-like branch, while the internal genes exhibited a mosaic pattern combining G1-like and F/98-like lineages. Molecular characterization analysis revealed multiple mammalian adaptive mutations, involving alterations in receptor-binding sites (T163N, H191N, T197D, T198V, Q234L, Q235M), antigenic epitopes (D280G, N285S), and glycosylation sites (218NRTF, 313NCSK). NA stalk deletion (62-64 aa), along with multiple mutations in the hemadsorption site (E/K368N, D369S/G, D401G/V, N402D, W403L/R, Q432H). Additionally, multiple key amino acid substitutions were also identified in the internal proteins. CONCLUSION: The external environment in western Zhejiang exhibits a high prevalence of AIVs with pronounced spatiotemporal clustering. H9 was the dominant subtype and co-circulated with multiple subtypes, with live poultry markets and slaughterhouses identified as high-risk settings. The H9N2 subtype AIV has accumulated multiple mammalian adaptive mutations, and exhibits genetic linkages across eastern Chinese provinces. These findings collectively underscore the need for an integrated One Health surveillance and early-warning system to reduce the risk of human infections with avian influenza.

Influenza in Birds↗

PubMed2022

An Exosomal miRNA Biomarker for the Detection of Pancreatic Ductal Adenocarcinoma.

Pancreatic ductal adenocarcinoma (PDAC) remains a difficult tumor to diagnose and treat. To date, PDAC lacks routine screening with no markers available for early detection. Exosomes are 40-150 nm-sized extracellular vesicles that contain DNA, RNA, and proteins. These exosomes are released by all cell types into circulation and thus can be harvested from patient body fluids, thereby facilitating a non-invasive method for PDAC detection. A bioinformatics analysis was conducted utilizing publicly available miRNA pancreatic cancer expression and genome databases. Through this analysis, we identified 18 miRNA with strong potential for PDAC detection. From this analysis, 10 (MIR31, MIR93, MIR133A1, MIR210, MIR330, MIR339, MIR425, MIR429, MIR1208, and MIR3620) were chosen due to high copy number variation as well as their potential to differentiate patients with chronic pancreatitis, neoplasms, and PDAC. These 10 were examined for their mature miRNA expression patterns, giving rise to 18 mature miRs for further analysis. Exosomal RNA from cell culture media was analyzed via RTqPCR and seven mature miRs exhibited statistical significance (miR-31-5p, miR-31-3p, miR-210-3p, miR-339-5p, miR-425-5p, miR-425-3p, and miR-429). These identified biomarkers can potentially be used for early detection of PDAC.

Humans↗

PubMed2026

Papillary Thyroid Carcinoma with Terminal Immune Exhaustion Phenotype Correlates with Increased Risk of Lymph Node Metastasis: An Exploratory Study Combining Flow Cytometry and TCGA.

BACKGROUND: Papillary thyroid carcinoma (PTC) is the most common thyroid malignancy, with lymph node metastasis (LNM) being a key predictor of recurrence and poor prognosis. Preoperative detection of LNM remains challenging due to the limitations of imaging modalities, leading to inadequate surgical resection in 20-30% of patients. While immune checkpoint molecules have been implicated in PTC progression, the heterogeneity of CD8+ T cell exhaustion subsets and their specific association with LNM remain poorly defined. In this study, we aimed to perform an exploratory characterization of the distinct immune landscape of PTC prone to LNM, with a focus on terminal immune exhaustion, in order to generate hypotheses for improved risk stratification and therapeutic strategies. METHODS: Fresh PTC tissues from 40 patients (22 LNM-positive and 18 LNM-negative) were analyzed via flow cytometry (FCM) to quantify immune cell subsets, inflammatory cytokines, and chemokines. Immunohistochemistry (IHC) validated CD45+ immune cell infiltration. Transcriptomic and clinical data from 448 PTC patients in The Cancer Genome Atlas (TCGA-PTC) cohort were used for bioinformatic analysis consistent with the observed phenotype, including Gene Set Variation Analysis (GSVA) of terminal exhaustion gene signatures. RESULTS: LNM-positive PTC exhibited a unique inflammatory milieu with significantly elevated IL-6, IL-1ra, CCL5, and IL-9 levels (all p < 0.05) in tumor interstitial fluid. FCM analysis revealed that LNM-positive PTC had increased infiltration of total CD45+ immune cells, CD3+ T cells, and CD3+CD8+ T cells (all p < 0.05). Critically, terminally exhausted PD-1hiTIM-3+ CD8+ T cells were significantly enriched in LNM-positive PTC (p = 0.022) and positively correlated with extrathyroidal extension (p = 0.044). Additionally, LNM risk was associated with increased CD4+ regulatory T (Treg) cell frequency (p = 0.023) and elevated CTLA-4 expression on CD4+ T cells (p = 0.047). In TCGA-PTC validation, the terminal exhaustion gene signature was predominantly enriched in LNM-positive (p < 0.0001) and advanced-stage PTC (p < 0.001) and strongly correlated with BRAF mutation (predominantly V600E) (p < 0.0001)-the most common oncogenic driver in aggressive PTC. CONCLUSIONS: Our findings suggest a terminal immune exhaustion phenotype (characterized by PD-1hiTIM-3+ CD8+ T cells and Treg enrichment) as a potential key feature associated with LNM-prone PTC. This phenotype shows consistency across clinical samples and TCGA datasets, linking BRAF mutation (predominantly V600E) to immune suppression and metastatic potential. These insights provide a novel exploratory immune-based biomarker for LNM risk stratification and support the potential of combining anti-PD-1/TIM-3 therapy with BRAF inhibitors for high-risk PTC, which should be confirmed in future studies.

lymph node metastasis↗

PubMed2026

SLE-Associated rs2295613(A) Allele Strengthens a Predicted c-MYC Motif and Enhances SLAMF1 Promoter Reporter Activity in B Cells.

SLAMF1 encodes CD150, an immunoregulatory receptor involved in lymphocyte activation, T-B-cell interactions, and humoral immune responses. The SLAMF1 promoter polymorphism rs2295613(G>A) was previously associated with systemic lupus erythematosus (SLE) susceptibility in a Chinese case-control cohort. Here, we investigated the regulatory activity of rs2295613 in the transformed B-cell lines Raji and MP1 and in primary human CD19+ B cells. The rs2295613(A)-containing reporter showed higher promoter activity than the rs2295613(G)-containing reporter in all three cellular systems. Bioinformatic analysis predicted that the G to A substitution strengthens a pre-existing MYC-compatible motif. Substitutions disrupting the motif-containing region attenuated the rs2295613(A)-associated increase in reporter activity and reduced enrichment of the promoter fragment in anti-c-MYC DNA pull-down assays. Partial siRNA-mediated reduction in MYC mRNA also decreased the activity of the rs2295613(A)-containing reporter in Raji cells. Together, these findings identify rs2295613 as a functional SLAMF1 promoter variant in B-cell reporter systems and support a contribution of c-MYC-associated regulation to the enhanced activity of the rs2295613(A)-containing promoter.

Humans↗

PubMed2026

Screening of Fermentative Strains for Reducing the Allergenicity of a Whey Protein-Soy Protein System and Genomic Characterization of the Selected Strain.

Dual-protein systems combining whey protein isolate (WPI) and soy protein isolate (SPI) offer complementary nutritional benefits but are limited by the presence of major allergens. Lactic acid bacteria (LAB) fermentation provides a promising strategy to mitigate this limitation. In this study, Lacticaseibacillus paracasei JM053, selected from 13 LAB strains based on phenotypic screening, significantly reduced the in vitro allergenicity of the dual-protein system, increasing the IgE-binding inhibition rate to 48.75%. Whole-genome sequencing and characterization of JM053 revealed a comprehensive proteolytic system, including the proline-specific peptidase genes pepX and pepQ, which may contribute to the degradation of allergenic peptide sequences. Combined with in silico bioinformatic analysis, potential cleavage sites within the linear epitopes of the dual-protein system were predicted based on the substrate specificity of the identified proteases, offering a testable hypothesis for the strain's mechanism of action. In addition, in vitro safety assessment and genomic analysis supported the safety potential, stress tolerance, and probiotic characteristics of JM053. Collectively, this study provides a valuable candidate strain for the development of hypoallergenic dual-protein products and offers preliminary genomic insights into LAB-mediated allergenicity reduction.

Lacticaseibacillus paracasei↗

PubMed2026

PtoeIF5A1: A Pleiotropic Regulator of Development, PCD, and Salt Tolerance in Populus tomentosa.

Eukaryotic translation initiation factor 5A (eIF5A) is a highly conserved protein family unique to eukaryotes, yet its functional characterization in woody plants remains limited. In this study, we identified four eIF5A genes (PtoeIF5A1-PtoeIF5A4) from the genome of Populus tomentosa, a fast-growing tree species indigenous to China, and characterized their expression patterns and functional roles through bioinformatics analysis, quantitative real-time PCR, stable overexpression in Arabidopsis thaliana, and transient expression in Nicotiana benthamiana leaves. Our results demonstrated that all PtoeIF5A proteins contain a conserved OB-fold domain and multiple phosphorylation sites, with PtoeIF5A1 showing predominant expression in roots and secondary xylem. Functional assays revealed that PtoeIF5A1 overexpression accelerated inflorescence stem elongation and early flowering in Arabidopsis, induced visible chlorosis and programmed cell death (PCD) in tobacco leaves, and significantly enhanced salt tolerance under NaCl treatment. Collectively, these findings establish PtoeIF5A1 in poplar as a pleiotropic regulator integrating developmental cues, programmed cell death, and stress responses; and as a valuable genetic resource for breeding stress-resilient woody plants.

Populus tomentosa↗

PubMed2025

Molecular Characterization and Epidemiology of Human Noroviruses in the Sverdlovsk Region, Russian Federation.

Human noroviruses (HuNoVs) stand as the primary cause of acute viral gastroenteritis outbreaks worldwide, particularly impacting children under the age of five. In Russia, reports of norovirus gastroenteritis have surged, especially in the post-COVID-19 era starting in 2022, with elevated infection rates reported into 2024. These viruses exhibit significant mutational variability, leading to the emergence of recombinant strains that can evade immune responses. A comprehensive examination of the complete genome is crucial for understanding the evolution of norovirus genes and for predicting potential outbreaks. This research focuses on analyzing the genotypic composition of HuNoVs circulating in the Sverdlovsk region during 2024, using Sanger sequencing and next-generation sequencing (NGS). Biological samples were collected (n = 384) from patients diagnosed with norovirus infection within the region. Bioinformatics analysis targeted the nucleotide sequences of the ORF1/ORF2 fragment and the assembly of complete genomes for the GII.4 and GII.7 genotypes. In total, 220 HuNoVs were characterized, representing 57.3% of the collected samples. The main capsid variants forming the predominant genotypic profile included GII.4 (n = 88, 40%), GII.7 (n = 86, 39%), and GII.17 (n = 14, 6%). Using NGS, we successfully assembled 8 out of 10 complete genomes for noroviruses GII.4[P16] and GII.7[P7]. Non-synonymous substitutions appeared at amino acid sites corresponding to the subdomains of VP1 in these strains. This molecular-genetic analysis provides contemporary insights into the genotypic composition, circulation patterns, and evolutionary dynamics associated with the dominant genovariants GII.4[P16] and GII.7[P7].

Norovirus↗

PubMed2005

Tumor necrosis factor-alpha-induced protein 1 and immunity to hepatitis B virus.

AIM: To compare the gene expression profile in a pair of HBV-infected twins. METHODS: The gene expression profile was compared in a pair of HBV-infected twins. RESULTS: The twins displayed different disease outcomes. One acquired natural immunity against HBV, whereas the other became a chronic HBV carrier. Eighty-eight and forty-six genes were found to be up- or down-regulated in their PBMCs, respectively. Tumor necrosis factor-alpha-induced protein 1 (TNF-alphaIP1) that expressed at a higher level in the HBV-immune twins was identified and four pairs of siblings with HBV immunity by RT-PCR. However, upon HBV core antigen stimulation, TNF-alphaIP1 was downregulated in PBMCs from subjects with immunity, whereas it was slightly upregulated in HBV carriers. Bioinformatics analysis revealed a K+ channel tetramerization domain in TNF-alphaIP1 that shares a significant homology with some human, mouse, and C elegan proteins. CONCLUSION: TNF-alphaIP1 may play a role in the innate immunity against HBV.

Adaptor Proteins, Signal Transducing↗

PubMed2006

Identification of differently expressed genes in human colorectal adenocarcinoma.

AIM: To investigate the differently expressed genes in human colorectal adenocarcinoma. METHODS: The integrated approach for gene expression profiling that couples suppression subtractive hybridization, high-throughput cDNA array, sequencing, bioinformatics analysis, and reverse transcriptase real-time quantitative polymerase chain reaction (PCR) was carried out. A set of cDNA clones including 1260 SSH inserts amplified by PCR was arrayed using robotic printing. The cDNA arrays were hybridized with fluorescent-labeled probes prepared from RNA of human colorectal adenocarcinoma (HCRAC) and normal colorectal tissues. RESULTS: A total of 86 genes were identified, 16 unknown genes and 70 known genes. The transcription factor Somult9 influencing cell differentiation was downregulated. At the same time, Heat shock protein 10 KDis downregulated and Calmoulin is up-regulated. CONCLUSION: Downregulation of heat shock protein 10 KD lost its inhibition of Ras, and then attenuated the Ras GTPase signaling pathway, increased cell proliferation and inhibited cell apoptosis. Down-regulated transcription factor Somult9 influences cell differentiation and cell-specific gene expression. Down-regulated Somult9 also decreases its binding to calmodulin, accumulates calmodulin as receptor-activated kinase and phosphorylase kinase due to the activation of PhK.

Adenocarcinoma↗