Ask about this productRelated genes to: KRT6B antibody
- Gene:
- KRT6B NIH gene
- Name:
- keratin 6B
- Previous symbol:
- KRTL1
- Synonyms:
- -
- Chromosome:
- 12q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-12
- Date modifiied:
- 2016-03-09
Related products to: KRT6B antibody
Related articles to: KRT6B antibody
- Lung adenocarcinoma (LUAD) exhibits high mortality and heterogeneity. While immune-related signatures show prognostic potential, robust models validated through both computational screening and experimental methods are lacking. - Source: PubMed
Publication date: 2026/02/25
Gu WeiweiWu YahuaJiang RongqiShi MingliangQi JiudeLai Jinhuo - Building on the identification of ABCB5 as a marker of limbal stem cells (LSCs), this study examines CD63, a newly identified molecule co-expressed with ABCB5 in limbal epithelial cells, to define its role in maintaining corneal epithelial cell identity. - Source: PubMed
Sasamoto YuzuruSuzuki KoseiSato ShinriLee Catherine A AMartin GabrielleKsander Bruce RFrank Markus HFrank Natasha Y - Risankizumab has demonstrated remarkable efficacy in the treatment of psoriasis; however, its long-term use faces multiple challenges, including high costs, reduced efficacy over time, and potential safety concerns, such as infections and malignancies. Therefore, identifying potential alternative or adjunctive therapies to risankizumab has significant clinical importance. - Source: PubMed
Publication date: 2026/01/14
Ma YupengZhang ShuminChen XinhongZhang XueZhang Denghai - The purpose of this paper is to explore the mechanism of 18β glycyrrhetinic acid (18β-GRA) in treating gastric cancer. Firstly, the toxicological effects of 18β-GRA were predicted using the ProTox3.0 database. Then, candidate biomarkers for the anti-gastric cancer of 18β-GRA were screened using the weighted gene co-expression network analysis (WGCNA), the least absolute shrinkage and selection operator (LASSO), the support vector machine (SVM), the random forest algorithm combined with the TMT proteomics methods. Additionally, we explored the potential upstream transcription factors and downstream interacting proteins of the biomarkers. The WGCNA method yielded 269 targets, while TMT proteomics analysis identified 6,273 genes. Among these, 12 targets were identical. Using LASSO, SVM, and random forest algorithms, three candidate markers were identified: insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3), keratin 6B (KRT6B), and E3 ubiquitin-protein ligase NEDD4-like (NEDD4L). Based on molecular docking and molecular dynamics results, NEDD4L is believed to be a 18β-GRA biomarker, while sodium channel protein type 5 subunit alpha (SCN5A) and early growth response protein 1 (EGR1) are the potential upstream and downstream regulatory proteins, respectively. These findings provide a theoretical basis for future experimental verification. - Source: PubMed
Publication date: 2026/01/06
Lu DoudouJia ShuminLi YahongWang ZhaozhaoZhou ZiyingLiu WenjingZhang LeiYuan LingNan Yi - Psoriasis, a chronic immune-mediated inflammatory skin disorder, is increasingly managed with anti-IL-23 biologics, such as guselkumab. Nevertheless, their rare adverse effects remain poorly understood. This study presents the case of a 78-year-old woman with moderate-to-severe psoriasis who presented with bullous pemphigoid (BP) 2 weeks after initiating guselkumab therapy. The clinical presentation was characterized by generalized bullae with epidermal-dermal separation and eosinophilic infiltration, despite negative anti-BP180 or BP230 antibodies. Single-cell RNA sequencing (scRNA-seq) of psoriatic versus BP lesions exhibited distinct cellular profiles: BP lesions were enriched in epidermal stem cells (44.32%) and endothelial cells (21.38%), in contrast to keratinocyte predominance (77.3%) noted in psoriasis. Differential gene analysis revealed the upregulation of keratinocyte stress markers (KRT6B and MMP7) and interferon-related genes (IFI6) in BP. Immune dysregulation was reflected in the activation of macrophages/T cells expressing pro-inflammatory factors (SPP1 and GZMB). Tissue stem cells demonstrated PTX3 upregulation, linking complement activation and extracellular matrix remodeling to epidermal damage. Collectively, these findings reveal dual mechanisms of guselkumab-induced BP: immune imbalance and defective epidermal repair. Future studies should validate these pathways in larger cohorts and investigate IL-23/interferon signaling crosstalk. - Source: PubMed
Publication date: 2025/12/18
Xi RongCao YiZhuang QianMa LiliTao MaocanLi Yuanyuan