TIE_1 Fc Chimera
- Known as:
- TIE_1 Fc Chimera
- Catalog number:
- RP17124730002
- Product Quantity:
- 2 µg
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- TIE_1 Chimera
Related genes to: TIE_1 Fc Chimera
- Gene:
- TIE1 NIH gene
- Name:
- tyrosine kinase with immunoglobulin like and EGF like domains 1
- Previous symbol:
- TIE
- Synonyms:
- JTK14
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-24
- Date modifiied:
- 2016-10-05
Related products to: TIE_1 Fc Chimera
Related articles to: TIE_1 Fc Chimera
- 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 - Cardiovascular diseases are increasingly recognized as immune-inflammatory disorders in which adaptive immunity shapes tissue injury, repair, and long-term remodeling. T cells are central to these processes because they integrate antigen recognition, lineage-defining transcriptional programs, tissue trafficking, cytokine production, and immunological memory. In this Review, we synthesize current evidence on the Krüppel-like factor (KLF) family as a transcriptional framework linking T-cell biology to cardiovascular disease. KLF2 primarily regulates T-cell quiescence and trafficking, KLF10 supports regulatory T-cell suppressive function and immune-metabolic fitness, KLF4 contributes to inflammatory effector differentiation, and KLF13 regulates delayed inflammatory chemokine expression and, in thymocyte models, exerts a survival-restraining effect through apoptosis-related pathways. Across atherosclerosis, myocardial infarction, myocarditis, hypertension, and heart failure, these KLF-dependent programs may influence the balance between pathogenic effector responses and protective regulatory mechanisms. The strongest direct disease-specific evidence currently supports a role for KLF10 within the CD4 T-cell lineage in experimental atherosclerosis, with complementary functional evidence implicating Treg-macrophage interactions, whereas the roles of KLF-dependent T-cell programs in other cardiovascular settings remain mechanistically compelling but less fully validated. Future progress will require disease-specific T-cell-restricted models, spatially resolved immune analyses, and cell-selective translational strategies to define the therapeutic relevance of the KLF-T-cell axis. - Source: PubMed
Publication date: 2026/08/24
Wang ShijiaZhu XiangbinLi NaOuyang KunfuLiao Zhiyong - As the leading histological form of lung cancer, lung adenocarcinoma (LUAD) displays considerable intratumoral heterogeneity, frequent therapeutic resistance, and an unfavorable clinical outcome. Although rewiring of mitochondrial energy metabolism is known to drive tumor progression and treatment failure, a comprehensive understanding of its dual role in LUAD drug resistance and prognosis has yet to be established. Here, we built a robust predictive signature that integrates mitochondrial metabolism with drug resistance through multi-omics integration and machine learning frameworks. - Source: PubMed
Publication date: 2026/07/31
Wu ChengyangJiao RuiYan HanyuSun YichenZhang TaoZhang YimengYan XiaolongWang Zhaoyang - 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 - Anxiety-depressive disorder (ADD) is one of the important subtypes of depression, which has been shown to be closely related to neuroimmune abnormalities. Currently, specific biomarkers have not been identified as diagnostic, differential, and therapeutic targets. This study aimed to explore the molecular mechanisms and diagnostic biomarkers of ADD and elucidate its association with neuroinflammation. - Source: PubMed
Publication date: 2026/08/10
Liu AnlanGuo WeifengLi JianxiangZhang TiangeXu Dan