TIE_1 Fc Chimera
- Known as:
- TIE_1 Fc Chimera
- Catalog number:
- RP17124660001
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- TIE_1 Chimera
Ask about this productRelated 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
- 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 - Glioblastoma (GBM) is the most common and aggressive primary malignant tumor of the adult central nervous system, with nearly 90% of cases recurring within two years despite standard surgery, radiotherapy, and chemotherapy. Tumor-associated macrophages (TAMs) play critical roles in GBM recurrence, but their characteristics in recurrent GBM remain insufficiently defined. Krüppel-like factor 10 (KLF10) regulates metabolism, mitochondrial function, proliferation, and apoptosis; however, its role in GBM-associated TAMs remains unclear. - Source: PubMed
Publication date: 2026/07/20
Zhang XiaodongChen CaipingFan QianyaChen ShengCao DuanzhengHu ZhonglinZhou YejunXu JinfangWang Delin - Metabolic dysfunction-associated steatotic liver disease (MASLD) is a worldwide disease characterized by hepatic steatosis. γ-glutamylcysteine (γ-GC), a non-protein thiol peptide with nontoxic side effects, can alleviate insulin resistance (IR) and alcoholic liver disease (ALD). However, the role of γ-GC in MASLD remains elusive. Herein, the aim of this study was to reveal the effects and underlying molecular mechanisms of γ-GC in the progression of MASLD. - Source: PubMed
Publication date: 2026/07/12
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