Ask about this productRelated genes to: KRT23 antibody
- Gene:
- KRT23 NIH gene
- Name:
- keratin 23
- Previous symbol:
- -
- Synonyms:
- K23, DKFZP434G032, HAIK1, CK23, MGC26158
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2016-03-09
Related products to: KRT23 antibody
Related articles to: KRT23 antibody
- The aim was to determine the transcriptomic features of tumor and stromal cells in direct contact within tumor nodules in luminal and triple-negative breast cancer. - Source: PubMed
Publication date: 2026/07/29
Kalinchuk Anna YuPatskan Ivan AGrigorieva Evgeniya STashireva Liubov A - This study aimed to identify candidate shared transcriptomic signals between major depressive disorder and dermatomyositis through an integrative bioinformatic reanalysis of public GEO datasets with single-cell contextualization. The analytical workflow included Weighted Gene Co-expression Network Analysis (WGCNA) for key module identification, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses for functional characterization, GeneMANIA- and a network visualization platform-based network analysis for candidate-gene prioritization, and evaluation of 113 machine-learning models combined with SHapley Additive exPlanations (SHAP) for diagnostic feature selection. Gene Set Enrichment Analysis (GSEA), immune infiltration analysis, and single-cell RNA-seq-based contextualization were subsequently performed to further characterize the immune-related cellular context of the identified signals. Integration of dermatomyositis-related GEO datasets identified 570 differentially expressed genes, from which 33 candidate shared genes were obtained via WGCNA. Functional enrichment and network analyses highlighted immune defense, cytotoxicity, and pathways including PPAR, IL-17, and antigen processing, with ELANE, PPBP, and CTSG emerging as highly connected nodes. Machine-learning-based feature prioritization retained 8 candidate model-selected genes, namely KIF4A, OLR1, KIR2DL4, KRT23, KIR3DS1, AZU1, SCG5, and LRRC37E. Immune infiltration analysis associated these shared genes with regulatory T cells (Tregs), resting mast cells, resting dendritic cells, and both classically activated (M1) and alternatively activated (M2) macrophages. Single-cell RNA-seq contextualization further suggested that CD8⁺ T-cell subsets with different candidate-gene score states showed distinct intercellular communication patterns. Among these, the MIF-(CD74+CD44) axis and signals from naive/central memory T cells were notable features requiring further validation. Overall, this study identified candidate shared transcriptomic signals between major depressive disorder and dermatomyositis and highlighted immune-related cellular contexts that warrant further validation in true comorbid cohorts. - Source: PubMed
Publication date: 2026/06/26
Teng FeiZheng SisiZhang XiatianLu ZhongwenWang PengruiWang PengYin Dongqing - Respiratory syncytial virus (RSV) causes millions of lower respiratory tract infections (LRTIs) in young children, older adults, and immunocompromised populations every year. RSV infection initiates in the upper respiratory tract and can progress to the lower airways, resulting in bronchiolitis, pneumonia, and even death. RSV primarily infects epithelial cells apically, but we hypothesized that basolateral exposure of the respiratory epithelium could provide an alternative mechanism of infection that contributes to LRTI development. Using a human nose organoid-air-liquid interface (HNO-ALI) model, we performed apical and basolateral inoculations with contemporaneous RSV strains (RSV/A/Ontario [RSV/A/ON] and RSV/B/Buenos Aires [RSV/B/BA]) representing the two RSV subgroups (A and B) in both adult- and infant-derived HNO-ALIs. Basolateral RSV exposure resulted in delayed viral replication and apical release compared to apical infection. A statistically significant difference in basolateral infection frequency was observed between RSV/B/BA and RSV/A/ON (81.3% versus 25%). Basolateral infection selectively targeted a rare basal cell population, while preserving epithelial integrity. Using undifferentiated HNO-ALIs, we determined for the first time that Krt23+ activated basal cells are uniquely susceptible to RSV infection, a finding we confirmed in fully differentiated HNO-ALIs. Together, our findings show that RSV can infect the respiratory epithelium from the basolateral side by initially targeting a rare subset of basal cells before spreading apically to ciliated cells. Moreover, RSV/B/BA may have an advantage over RSV/A/ON in utilizing the basolateral infection route. These findings highlight an alternative RSV infection pathway and could be a potential mechanism for RSV spread to the lower airways.IMPORTANCEUnderstanding the pathogenesis of respiratory syncytial virus (RSV) is essential to understanding and preventing acute and long-term sequelae from infection. The canonical understanding of RSV infection is that the virus infects and is restricted to the apical ciliated cells upon inhalation or fomite exposure. We demonstrate that an alternative route of infection-the basolateral route-can be utilized by RSV to infect the apical ciliated cells of the respiratory epithelium. We also show for the first time a novel difference in infectivity between the two contemporaneous RSV strains (RSV/A/Ontario and RSV/B/Buenos Aires). In addition, we describe a rare basal subset-the Krt23+ activated basal cells-that are uniquely susceptible to RSV, expanding the known cellular tropism of RSV. Infection of basal cells can impact airway differentiation, homeostasis, and remodeling. Overall, our findings expand on RSV pathogenesis and indicate there are alternative mechanisms of infection and cell populations that are susceptible to RSV. - Source: PubMed
Publication date: 2026/06/25
Murray AshleyNagaraj DivyaSchultz Emily MAloisio GinaNicholson ErinBlutt Sarah EAvadhanula VasanthiPiedra Pedro A - Sepsis is a persistent systemic inflammatory disease involving multiple organ failure caused by a dysregulated immune response to infection. As primary effector cells in innate immunity, neutrophils significantly contribute to combating infections and mediating inflammatory responses. The aim of this study was to evaluate the prognostic significance of neutrophil-related genes (NRGs) in sepsis and their relationship with the immune microenvironment. - Source: PubMed
Publication date: 2025/12/11
Sun FanShi MinLi XiaodongLiu XueyunWang Xiaowei - Colorectal cancer (CRC) represented a pervasive manifestation of malignant neoplasia within the digestive tract. Apigenin, exhibiting a multitude of physiological attributes and pharmacological actions, has undergone extensive scrutiny for its antitumor efficacy and benign toxicity profile. Cisplatin (DDP)-centered chemotherapy constituted a pivotal aspect of multidisciplinary therapeutic strategies. Nevertheless, resistance to DDP posed a considerable impediment to the efficacy of CRC chemotherapy. The aim of this investigation was to assess the impact of combining Apigenin with DDP on the proliferation and apoptotic processes of human CRC cells, while also delving into the underlying mechanisms. HCT116 and SW480 were cultivated and subjected to treatment with Apigenin (API) either as a monotherapy or in combination with cisplatin (DDP). Cell viability, proliferation, cycle distribution, apoptosis, migration, invasion and inflammatory factors were assessed. Western blot analysis was performed to detect the protein expression levels of Glut1, HK-2, KRT23, and β-catenin. In comparison to other treatment groups, the combined API and DDP group exhibited a more potent suppressive effect on cellular proliferation, migration, invasion, and glycolysis, while also enhancing apoptotic activity. Additionally, the combined API and DDP treatment group led to a reduction in the expression levels of KRT23, β-catenin, HK-2, and Glut1. Intriguingly, this combined treatment group demonstrated significantly elevated levels of TNF-α, IL-6, and IL-8 compared to the other groups. Notably, the overexpression of KRT23 was capable of reversing the changes induced by the combined API and DDP treatment. In vivo studies further validated that the combined API and DDP treatment suppressed tumor growth by inhibiting the expression of KRT23 and β-catenin. The present findings indicated that the combination of API with DDP has the potential to enhance colorectal cancer therapy through the modulation of the KRT23/Wnt/β-catenin signaling pathway. Our research may offer fresh perspectives and novel molecular therapeutic strategies for the treatment of colorectal cancer. - Source: PubMed
Publication date: 2025/11/28
Dong LeiYang FengWang XueZhang WeiSong JucaiJiao PanpanKang MengjieGuo QianqianSi LiangzhuZhang ShuhanHuang MeiLuo LinshanLi YongweiGong Yuesheng