STAT3 Over-expression Lysate Product
- Known as:
- STAT3 Over-expression Lysate Product
- Catalog number:
- GWB-4C1781
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- STAT3 Over-expression Lysate Product
Related genes to: STAT3 Over-expression Lysate Product
- Gene:
- STAT3 NIH gene
- Name:
- signal transducer and activator of transcription 3
- Previous symbol:
- -
- Synonyms:
- APRF
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: STAT3 Over-expression Lysate Product
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(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: STAT3 Over-expression Lysate Product
- Esophageal squamous cell carcinoma (ESCC) patients carries a poor prognosis, with limited effective therapeutic targets. This study aimed to clarify the clinical significance of guanine nucleotide-binding protein like 3-like (GNL3L) protein expression in ESCC and its role in malignant progression. - Source: PubMed
Publication date: 2024/04/29
Yu ShaobinZhang PeipeiXu ShaojunXiang ZhangMadan AnkitEslick Guy DDayyani FarshidChen Shuchen - Myocardial ischemia and hypoxia may result in myocardial cell necrosis, scar formation, and hyperplasia. We aim to explore the differentially expressed genes (DEGs) in ischemic cardiomyopathy (ICM), construct and identify a clinical prognosis model using bioinformatics methods, so as to screen potential biomarkers of ICM to provide a basis for the early diagnosis and treatment of ICM. - Source: PubMed
Publication date: 2024/04/02
Wang JingTang LiyingBai YuzhiZhao XiaTian TianMihos Christos GDelmo Eva Maria JavierLi Pei - Lead (Pb) is a nonessential heavy metal, which can cause many health problems. Isochlorogenic acid A (ICAA), a phenolic acid present in tea, fruits, vegetables, coffee, plant-based food products, and various medicinal plants, exerts multiple effects, including anti-oxidant, antiviral, anti-inflammatory and antifibrotic functions. Thus, the purpose of our study was to determine if ICAA could prevent Pb-induced hepatotoxicity in ICR mice. An evaluation was performed on oxidative stress, inflammation and fibrosis, and related signaling. The results indicate that ICAA attenuates Pb-induced abnormal liver function. ICAA reduced liver fibrosis, inflammation and oxidative stress caused by Pb. ICAA abated Pb-induced fibrosis and decreased inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α). ICAA abrogated reductions in activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Masson staining revealed that ICAA reduced collagen fiber deposition in Pb-induced fibrotic livers. Western blot and immunohistochemistry analyses showed ICAA increased phosphorylated AMP-activated protein kinase (p-AMPK) expression. ICAA also reduced the expression of collagen I, α-smooth muscle actin (α-SMA), phosphorylated extracellular signal-regulated kinase (p-ERK), phosphorylated c-jun N-terminal kinase (p-JNK), p-p38, phosphorylated signal transducer and phosphorylated activator of transcription 3 (p-STAT3), transforming growth factor β1 (TGF-β1), and p-Smad2/3 in livers of mice. Overall, ICAA ameliorates Pb-induced hepatitis and fibrosis by inhibiting the AMPK/MAPKs/NF-κB and STAT3/TGF-β1/Smad2/3 pathways. - Source: PubMed
Publication date: 2024/05/09
Guo Jun-TaoLi Han-YuCheng ChaoShi Jia-XueRuan Hai-NanLi JunLiu Chan-Min - To investigate the involvement of the homeobox gene B5 (HOXB5) in the progression and metastasis of osteosarcoma. - Source: PubMed
Publication date: 2024/04/29
Ma QimingLi XingxingWang HumingXu ShenglinQue YukangHe PengYang RuiWang QiweiHu Yong - Using (S)-decursinol isolated from root of AGN, we semi-synthesized and evaluated a series of both enantiomerically pure decursin derivatives for their antiproliferative activities against A549 human lung cancer cells. All synthesized compounds showed a broad spectrum of inhibitory activities against the growth of A549 cells. Especially, compound (S)-2d with (E)-(furan-3-yl)acryloyl group showed the most potent activity (IC: 14.03 µM) against A549 cancer cells as compared with the reference compound, decursin (IC: 43.55 µM) and its enantiomer, (R)-2d (IC: 151.59 µM). Western blotting assays indicated that (S)-2d more strongly inhibited JAK1 and STAT3 phosphorylation than decursin in a dose-dependent manner, while having no effect on CXCR7 overexpression and total STAT3 level. In addition, (S)-2d induced cell cycle arrest at G1 phase and subsequent apoptotic cell death in A549 cancer cells. Our combined analysis of molecular docking studies and biological data suggests that the inhibition of JAK1 with (S)-2d resulted in loss of STAT3 phosphorylation and inhibition of cell growth in A549 cancer cells. These overall results strongly suggest that (S)-2d (MRC-D-004) as a novel JAK1 inhibitor may have therapeutic potential in the treatment of A549 human lung cancers by targeting the JAK1/STAT3 signaling pathway. - Source: PubMed
Publication date: 2024/05/11
Ahn JunseongHwang Hyun-HaJung Soo YeonLee Ja YeonKim ChoiChoi Hye MinGwon Min JuKim Min JiKwon YoungbinWoo JaehyukPark BongkyuKo Seong-GyuLee Jae Yeol