KLF6 antibody - N-terminal region (ARP35640_P050)
- Known as:
- KLF6 (anti-) - N-terminal region (ARP35640_P050)
- Catalog number:
- arp35640_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KLF6 antibody - N-terminal region (ARP35640_P050)
Related genes to: KLF6 antibody - N-terminal region (ARP35640_P050)
- Gene:
- KLF6 NIH gene
- Name:
- Kruppel like factor 6
- Previous symbol:
- BCD1, ST12, COPEB
- Synonyms:
- CPBP, GBF, Zf9, PAC1
- Chromosome:
- 10p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-16
- Date modifiied:
- 2016-10-05
Related products to: KLF6 antibody - N-terminal region (ARP35640_P050)
Related articles to: KLF6 antibody - N-terminal region (ARP35640_P050)
- Colorectal cancer (CRC) is a prevalent malignancy of the digestive system, originating from the epithelial cells in the colon or rectum and commonly arising from adenomatous polyps. Over time, CRC may progress to advanced disease and metastasis, resulting in limited therapeutic options and poor clinical outcomes. Biochanin A (BCA), a naturally occurring isoflavonoid, has been shown to possess a range of biological activities, including antioxidant and anti-inflammatory effects. However, the precise effects of BCA on colorectal cancer and the underlying mechanisms remain poorly understood. - Source: PubMed
Publication date: 2026/09/17
Zhang DaquanLuo BinyuZhang XiaoFeng Xuqin - 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 - It is well-known that the morbidity and clinical burden of type 2 diabetes mellitus (T2DM) are predominantly associated with its chronic complications, in which fibrosis is a significant contributor. Recently, sodium-glucose cotransporter 2 (SGLT2) inhibitors have made a pivotal advancement in the therapeutic landscape not only improving glycemic control, but also demonstrating high effectiveness in the prevention and treatment of T2DM complications. In this work, we aimed to assess the transcription factors (TFs) mediating the effects of SGLT2 inhibitor empagliflozin (EMPA) treatment by a comprehensive analysis of the allele-specific expression (ASE) events utilizing the RNA-seq data. Initial logistic regression analysis of the in vitro transcriptomic data for EMPA-treated peripheral blood mononuclear cells (PBMCs) of three healthy donors revealed a significant inter-individual variation in ASE for 240 genes linked to EMPA treatment beyond the glucose-lowering effects. Then, 146 TFs were predicted to regulate the expression of the corresponding targets using motifbreakR and DESeq2. Among these, multiple TFs (including ATF3, ATF4, E2F1, EGR1, FOS, JUN, JUNB, IRF8, KLF6, KLF11, SNAI1, TWIST1, and ZEB1) were involved in the TGF-β/SMAD3 canonical profibrotic signaling cascade, pertinent to diabetes-related fibrosis, playing a significant role in the development of diabetic complications. Further analysis of the in vivo data for the PBMCs from ten T2DM patients initiating EMPA therapy identified 98 TFs related to the ASE variation in both in vitro and in vivo cohorts. To conclude, our integrative allele-specific approach enables the prediction of novel EMPA-responsive regulatory interactions and suggests the important mediators of the mechanisms underlying the effects of EMPA on human PBMCs. - Source: PubMed
Publication date: 2026/08/12
Korbolina Elena EGubina MariaBryzgalov Leonid ODegtyareva Arina OEvseenko Anastasia AAntonseva Elena VKorbut Anton IRykova Elena YKlimontov Vadim VKzhyshkowska Julia GMerkulova Tatiana I - The Kruppel-like factor (KLF) family comprises transcription factors that share conserved zinc-finger domains and orchestrate key pathophysiological processes in the liver, including glucose and lipid metabolism, inflammatory responses, and fibrogenesis. In this review, we systematically dissect the roles of major KLF members-specifically KLF2-KLF10, KLF14, KLF15, and KLF16-in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD), liver fibrosis/cirrhosis, and hepatocellular carcinoma (HCC). We discuss several key findings. First, KLF16 drives fatty acid β-oxidation by activating peroxisome proliferator-activated receptor alpha (PPARα), whereas KLF4 and KLF2 suppress lipogenesis through the inhibition of SREBP-1c. Second, with respect to hepatic stellate cell activation, KLF6 and KLF5 promote fibrogenesis, whereas KLF14 has anti-fibrotic effects through the upregulation of peroxisome proliferator-activated receptor gamma (PPARγ). Third, in HCC, KLF2, KLF4, and KLF6 act as tumour suppressors, and are frequently epigenetically silenced, whereas KLF5, KLF7, and KLF8 function as oncogene products, by modulating Wnt/β-catenin signaling, glycolysis, and immune evasion. Last, emerging modalities, such as proteolysis-targeting chimeras and cell type-specific nanoparticle delivery, are described. These represent potential new avenues for KLF-targeting therapy. By delineating these context-dependent mechanisms, we provide a theoretical framework for the development of KLF-based precision strategies for the treatment of major liver diseases. - Source: PubMed
Publication date: 2026/06/25
Chen HepuHuang ShushengZhou ZhigangLi JialinPeng QingTu Jian - Although PD-1/PD-L1 inhibitors are central to the management of advanced bladder cancer, most patients fail to achieve a meaningful response. While evidence ties MMT to fibrotic disease, its contribution to bladder cancer has yet to be examined. - Source: PubMed
Publication date: 2026/08/10
Chen YuwenWang ZihuanHe ChengwuYu ZheZhang JingeJiang FeifanZhang ZicaiLi TanghuaFu XinyangHou LinaLi Fei