GKLF EMSA Kit
- Known as:
- GKLF EMSA Kit
- Catalog number:
- AY1314
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- GKLF EMSA Kit
Related genes to: GKLF EMSA Kit
- Gene:
- KLF4 NIH gene
- Name:
- Kruppel like factor 4
- Previous symbol:
- -
- Synonyms:
- EZF, GKLF
- Chromosome:
- 9q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-14
- Date modifiied:
- 2016-10-05
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- This study integrates epidemiological analysis and computational toxicology approaches to systematically investigate the association between cadmium (Cd) exposure and osteoarthritis (OA), as well as the underlying molecular mechanisms. Based on the data from the 2013-2018 National Health and Nutrition Examination Survey (NHANES), multivariate logistic regression models and forest plot analyses revealed that elevated blood cadmium levels were significantly associated with an increased risk of OA, with particularly pronounced effects observed among individuals with diabetes, hypertension, vitamin D deficiency, low income, and smokers. Further, potential cadmium-related targets were identified through network toxicology, and by integrating differentially expressed genes (DEGs) in OA, weighted gene co-expression network analysis (WGCNA), and protein-protein interaction (PPI) networks (STRING), a total of 113 intersection genes were obtained. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicated that cadmium may promote OA progression by regulating pathways, such as cellular senescence, FOXO signaling, and TNF signaling. Through Cytoscape MCC algorithm, forest plot, and Lasso regression analysis, six key hub genes-MYC, FOXO1, FOXO3, ZFP36, AIF1, and KLF4-were identified. Molecular docking simulations further validated the strong binding affinity between cadmium nitrate and these core targets. Overall, this study comprehensively delineates the molecular network by which cadmium exposure may contribute to OA, providing novel insights into the environmental heavy metal toxicity mechanisms and potential therapeutic interventions. - Source: PubMed
Publication date: 2026/09/24
Luo YingjinZhou DaqianZhou MingminZheng Qianghua - Metabolic kidney disease comprises renal disorders driven or worsened by systemic metabolic abnormalities, including diabetic kidney disease, obesity-related kidney injury, hyperuricemia-associated nephropathy, and metabolic syndrome-associated chronic kidney disease. Despite different triggers, these disorders share podocyte injury, glomerular endothelial dysfunction, tubular lipotoxicity, mitochondrial impairment, oxidative stress, inflammation, and tubulointerstitial fibrosis, indicating a common program of metabolic stress-induced renal cell reprogramming. Krüppel-like factors (KLFs) are zinc-finger transcription factors that regulate cell differentiation, metabolic homeostasis, redox balance, inflammation, vascular integrity, epithelial function, and tissue remodeling. Emerging evidence suggests that KLF family members function as cell-specific and disease-stage-dependent regulators linking metabolic disturbance to kidney injury and repair. KLF15, KLF2, and KLF4 generally maintain podocyte integrity, endothelial quiescence, tubular metabolic adaptation, mitochondrial homeostasis, and anti-inflammatory responses, whereas KLF5, KLF6, and possibly KLF10 promote tubular activation, immune recruitment, transforming growth factor-β signaling, fibroblast activation, and extracellular matrix deposition during chronic injury. This review summarizes current evidence on KLFs in metabolic kidney disease, highlights process-specific mechanisms across renal compartments, and discusses therapeutic opportunities, delivery challenges, and the potential value of KLF-related signatures as biomarkers. By integrating protective and pathogenic KLF programs, it provides a framework for understanding transcriptional control in metabolically stressed kidneys and progressive renal decline. - Source: PubMed
Publication date: 2026/09/17
Shi YuntianZhang KexinChen JinyanKan ChengxiaHan FangSun XiaodongGuo Zhentao - Cancer cells must deal with excessive reactive oxygen species (ROS) to survive severe hypoxia and anticancer therapy; however, anti-ROS mechanisms other than the well-known NFE2L2/NRF2 signaling pathway are poorly recognized. Here, we report a ROS scavenging mechanism mediated by HIF1α-KLF4-induced hemoglobin extraerythrocytically expressed in hepatocellular carcinoma (HCC). We found that the ROS pathway was aberrantly activated in HCC and was associated with hemoglobin upregulation, which independently predicts poor outcomes. Network analysis further identified heme binding as the top ROS-associated functional module, suggesting a previously unrecognized role of hemoglobin in maintaining redox homeostasis in HCC. Hemoglobin expression in cancer cells is transcriptionally controlled by HIF1α via KLF4 but not HIF2α or the recently identified KDM5A-KLF1 signaling. The upregulated hemoglobin counteracts the detrimental effects of oxidative stress by scavenging ROS, promoting sorafenib resistance, which could be effectively reversed by interfering with hemoglobin expression, leading to tumor suppression. Both in vitro and in vivo experiments consistently supported the functional importance of hemoglobin in regulating oxidative stress adaptation and therapeutic response. Overall, a previously unrecognized mechanism was identified for cancer cell survival under oxidative stress, where HIF1α-KLF4 signaling induces hemoglobin to scavenge ROS produced during hypoxia and anticancer therapy, providing a promising target of synthetic lethality for cancer therapeutics. - Source: PubMed
Publication date: 2026/09/16
Zhang BoLiu FeichangGao XinyueZhu YichaoChen TongHao JiahuiWei YuexianSun ZhuoranYang RuigangYang YalanRen HeLi YutongYu ChunxiaoRen TianyiHuang YinuoJiang HongMelino GerryMa LiHuang HongyanSun Qiang - Krüppel-like factor 4 (KLF4), a key transcription factor,plays an important role in cell proliferation, differentiation, and apoptosis. Here, we explored the prognostic value of KLF4 and its role in colorectal cancer (CRC) progression. We analyzed transcriptomic data and clinical information related to CRC from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) database. Immunohistochemistry was performed to evaluate KLF4 expression in CRC tissue samples. Additionally, we examined the relationship between clinicopathological factors and patient prognosis using Cox proportional hazards model analysis. Lentiviral transfection was used to create KLF4-knockdown HCT-116 cells. Analysis of the TCGA database and two GEO datasets (GSE21510 and GSE117606) revealed that KLF4 was expressed at low levels in CRC. Furthermore, reduced KLF4 levels correlated with lymph node metastasis, distant metastasis, and advanced TNM staging. ROC curve analysis indicated that KLF4 can effectively differentiate cancerous tissue from normal tissue. Functional enrichment analysis identified KLF4 as significantly linked to the glycoprotein metabolic pathway. Our detection of KLF4 expression in CRC tissue samples confirmed its decreased levels and their association with poorer patient survival. However, KLF4 was not identified as an independent prognostic factor. In vitro, KLF4 knockdown promoted HCT-116 cell migration and invasion and downregulated the mRNA expression of glycoprotein synthesis- and glycosylation-related genes. Conversely, KLF4 re-expression markedly reversed these effects. Our findings suggested that low KLF4 expression served as a predictor factor for disease progression in CRC patients. Furthermore, reduced KLF4 levels enhance the migration and invasion of CRC cells, which may be related to impaired glycoprotein metabolism. - Source: PubMed
Publication date: 2026/09/15
Zhang MengzheXiang FenfenQian JiawenChen ZixiLi XiaoxiaoSun GuotaiSun YipengWu Rong - Airway hillocks are specialized, stratified squamous epithelial structures featuring luminal barrier cells supported by a dedicated basal stem cell population. In this issue of Cancer Research, Izzo and colleagues identify a distinct population of slow-cycling KRT13+ hillock-like tumor cells in lung squamous cell carcinoma, a cell state conserved across multiple squamous cell carcinoma (SCC) models. Mechanistically, KLF4 drives KRT13 expression, correlating with enrichment of potential therapeutic targets and resistance to platinum-based chemotherapy. By linking the physiologic epithelial barrier to therapeutic resistance, this study unlocks a previously uncharacterized mechanism underlying SCC biology. See related article by Izzo et al., p. 4472. - Source: PubMed
Tong XinyuanJi Hongbin