BANP ELISA kit
- Known as:
- BANP Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-BANP-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- BANP ELISA kit
Related genes to: BANP ELISA kit
- Gene:
- BANP NIH gene
- Name:
- BTG3 associated nuclear protein
- Previous symbol:
- -
- Synonyms:
- SMARBP1, SMAR1, FLJ20538, DKFZp761H172, FLJ10177, BEND1
- Chromosome:
- 16q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-07
- Date modifiied:
- 2016-10-05
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- There is compelling evidence that TNF preferentially activates and expands CD4Foxp3 regulatory T cells (Tregs) through TNFR2. However, the precise mechanisms underlying TNF-TNFR2 pathway-mediated Treg proliferation remain to be fully elucidated. In this study, using RNA-seq profiling of TNFR2 and TNFR2-deficient Treg cells, we identified that Trip13 is required for promoting TNF-TNFR2 pathway-mediated Treg expansion. Mechanistically, TRIP13 inhibited UBE4A-mediated ubiquitination degradation of HAT1 by directly binding to HAT1, thereby competing with UBE4A and promoting Treg expansion. In addition, TRIP13's ATPase activity was essential for its binding to HAT1, which promoted Treg expansion by increasing Foxp3 expression. In a mouse colitis model, TRIP13 overexpression markedly alleviated colon inflammation by enhancing Treg expansion, an effect that was reversed by HAT1 knockdown. Conversely, genetic ablation of TRIP13 substantially reversed the effects induced by HAT1 overexpression, including enhanced Treg expansion and attenuation of colitis. These findings illustrate the TRIP13/HAT1 axis-mediated mechanism for TNF-TNFR2-induced Treg expansion and indicate that targeting TRIP13 may offer therapeutic potential for autoimmune and inflammatory diseases. - Source: PubMed
Publication date: 2026/01/14
He TianzhenZhao LiwenFeng Chu-TingZhao Li-YaJing ShengnanYang HanWang KeYe SiyuZhao YingchunYu YingFu ZhutingChou Chon-KitChen XinGao Yong-Jing - Continuous abuse and overdose of aminophenone derivatives, a representative group of synthetic cathinones, are known to exhibit severe damage against neuronal cells, whereas little is known about their structure-toxicity relationship and cytotoxic mechanisms. Here, we newly synthesized eight α-aminononanophenone (ANP) derivatives bearing various N-alkyl side chains and measured sensitivity to toxicity elicited by treatment with the derivatives using six human cell lines. The sensitivity assay revealed a positive correlation between the length of substituted N-alkyl side chain and the strength of cytotoxicity of the ANP derivatives in all cell lines. In addition, treatment with butyl-ANP (B-ANP), one of the most potent cytotoxic ANP derivatives, markedly induced overproduction of reactive oxygen species (ROS) and 4-hydroxy-2-nonenal, mitochondrial membrane dysfunction and caspase-3/9 activation in neuronal SK-N-SH cells. Furthermore, the treatment resulted in the reductions of antioxidant capacity and 26S proteasome-based proteolytic activities and the significant formation of aggresome. These results indicate that exposure to the ANP derivatives provokes neuronal cell apoptosis through ROS overproduction and lowering of antioxidant properties. A measurement of ANP derivatives by liquid chromatography/mass spectrometry/mass spectrometry analysis revealed that cytochrome P450 (CYP) 3A4 metabolizes ANP derivatives with short N-alkyl chains (methyl and ethyl groups) in preference to ones with longer N-alkyl side chains (propyl and butyl groups) in liver HepG2 cells. Additionally, pretreatment with a CYP3A4 inhibitor augmented the cytotoxicity elicited by diethyl-ANP, not B-ANP. Therefore, it is inferred that CYP3A4-mediated metabolism is also a key factor involved in the reduction of neurotoxicity of ANP derivatives. - Source: PubMed
Publication date: 2025/11/14
Morikawa YoshifumiAzuma NozomiSakai YujiTsuchimura SaekaMiyazono HidetoshiSuenami KoichiYanase EmikoEndo SatoshiIkari AkiraMatsunaga Toshiyuki - Cyclophosphamide (CTX)-induced ovarian dysfunction and infertility represent significant concerns for reproductive-age or younger female cancer patients. Although various fertility preservation techniques are currently accessible, there remains a pressing demand for an efficient, non-invasive strategy to protect ovarian function that can be employed concurrently with chemotherapy. Considering the significance of nicotinamide adenine dinucleotide (NAD+) in regulating DNA damage and apoptosis, we aimed to examine the protective effects of nicotinamide mononucleotide (NMN, an NAD precursor) on ovarian function against CTX-induced damage. - Source: PubMed
Publication date: 2025/08/23
Shen LinLi HemeiGong XueqiZhang HanwangZhao Yiqing - The inflammatory microenvironment (IME) is closely related to the progression of triple-negative breast cancer (TNBC). As an anti-inflammatory active compound, poor solubility and targeting limit the potential of baicalin (BA) to modulate IME in TNBC. In this study, BA loaded bifunctional albumin nanoparticles (BANP) with long circulation/acid-sensitive release and active targeting functions are developed to improve the delivery efficiency of BA. BANP have a spherical core-shell structure, with appropriate particle size (79.63 ± 1.91 nm), zeta potential (-33.7 ± 0.82 mV), and encapsulation efficiency (72.71%), and are released faster in an acidic environment. BANP can enhance the uptake by TNBC cells and "M2" macrophages, prolong circulation time in the blood, and increase accumulation at tumor sites in vivo. It induces cell cycle arrest and early apoptosis in MDA-MB-231 cells and inhibits tumor growth in 4T1 tumor-bearing mice. Additionally, BANP reduce tumor immune infiltration, promote macrophage recruitment and anti-inflammatory M2 polarization, and enhance the phagocytic activity of M2 macrophages. Transcriptome sequencing and cytokine profile analysis reveal that BANP regulate TNBC IME through multitarget mechanisms related to cell cycle, inflammatory response, metabolism, etc. In summary, this study provides a nanodelivery platform with broad application potential and a new strategy for the regulation of IME. - Source: PubMed
Publication date: 2025/08/22
Liu FengjieMeng FansuHong XiaoshanGiri Anil KAsim Mulazim HussainChen ZhongChen YiqiLin YixuanHe LuluBu QiaowenHuang YongSun XiaoliYang ZhenjiangCai Yu - Type-2 diabetes mellitus (T2DM) is a complex metabolic disorder that adversely affects various physiological systems, particularly male reproductive health. Research indicates that T2DM increases the risk of retrograde ejaculation, impairing sexual function and fertility. Dysregulation of lysyl oxidase (LOX) has been linked to diabetes-related complications in the male reproductive system. However, its role in seminal vesicle remains unclear. This study investigates LOX's involvement in diabetes-related seminal vesicle pathology using human and mouse models. We assessed LOX expression in the seminal vesicles of men with T2DM and created a T2DM mouse model to observe changes. Our findings revealed elevated LOX expression in the seminal vesicles of T2DM men, accompanied by epithelial atrophy and fibrosis. Similarly, T2DM mice displayed significant atrophy and fibrosis of the seminal vesicles, correlated with increased LOX levels. Treatment with the LOX inhibitor, β-aminopropionitrile (BANP), significantly improved extracellular matrix remodeling and normalized the architecture of the seminal vesicles. Besides, LOX inhibition led to a significant reduction in T lymphocyte infiltration and apoptosis in the seminal vesicle epithelium of T2DM mice.These results highlight LOX's critical role in seminal vesicle fibrosis associated with T2DM. Targeting LOX may provide a promising therapeutic strategy to alleviate reproductive complications and preserve reproductive health in men with T2DM. - Source: PubMed
Publication date: 2025/07/30
Yu YiLiu Peng-FeiZhan Ming-WeiChen Yao-QiLai Yu-QiWang LeiWu Jun-JieYao FanChen Xue-QinShang Xue-JunWu Ke-Rong