IL17A Antibody (AMM00030)
- Known as:
- IL17A Antibody (AMM00030)
- Catalog number:
- amm00030
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- IL17A Antibody (AMM00030)
Related genes to: IL17A Antibody (AMM00030)
- Gene:
- IL17A NIH gene
- Name:
- interleukin 17A
- Previous symbol:
- CTLA8, IL17
- Synonyms:
- IL-17A, IL-17
- Chromosome:
- 6p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-25
- Date modifiied:
- 2019-04-23
Related products to: IL17A Antibody (AMM00030)
Related articles to: IL17A Antibody (AMM00030)
- This study aims to isolate and extract Sanguisorbae Radix Carbonisata nano-components(SRC-NCs) from Sanguisorbae Radix Carbonisata(SRC) and investigate their protective effects against ulcerative colitis(UC) and the underlying mechanisms. The SRC-NCs were systematically characterized by nanomaterial characterization techniques to analyze their morphological structure, optical properties, and characteristics of functional groups on the surface. Meanwhile, a dextran sulfate sodium(DSS)-induced UC mouse model was established to evaluate the general condition, disease activity index(DAI) score, and pathological damage degree of the colon tissue of mice after SRC-NCs intervention. The level or activity of inflammatory factors(interleukin(IL)-17A, IL-6, IL-10, IL-2, tumor necrosis factor alpha(TNF-α), and IL-1β) and oxidative stress markers(myeloperoxidase(MPO), malondialdehyde(MDA), superoxide dismutase(SOD), glutathione(GSH), and nitric oxide(NO)) in the colon tissue was detected. The expression level of key proteins, such as Toll-like receptor 4(TLR4), myeloid differentiation primary response protein 88(MYD88), and nuclear factor-kappa B p65(NF-κB p65), in the colon tissue was detected by Western blot to provide key molecular evidence for revealing the intervention mechanism of SRC-NCs. The results showed that SRC-NCs were nearly spherical under transmission electron microscope(TEM), with a uniform particle size distribution(0.8-2.6 nm), a lattice spacing of 0.17 nm, and multiple active genes such as hydroxyl, amino, and carboxyl groups on the surface. In the UC model, SRC-NCs could slow down the weight loss and increase in DAI score of mice, and alleviate the shortening of the colon and the degree of tissue damage. SRC-NCs could down-regulate the levels of pro-inflammatory factors such as IL-17A, IL-6, IL-2, TNF-α, and IL-1β in the colon tissue, up-regulate the level of anti-inflammatory factor IL-10, reduce the activity of MPO and the content of MDA and NO, increase the activity of SOD and the level of GSH, and inhibit the expression of TLR4/MYD88/NF-κB p65 proteins. In conclusion, the study for the first time demonstrates that SRC-NCs are the key active components of SRC in exerting protective effects against UC, and the mechanism may be related to the inhibition of inflammatory responses of the TLR4/MYD88/NF-κB pathway and the reduction of oxidative stress. - Source: PubMed
Xia Min-LongHuang YanLi Xiao-PengJiang Ming-MinLi Hong-HuaZhao YunWang En-LiYao Jing-ChunCheng Guo-LiangQu Hui-HuaZhao YanKong Hui - PARP14, a pivotal mono-ADP-ribosyltransferase, has been reported to promote the development of inflammatory diseases via IL-4/STAT6/Th2 and IL-6/STAT3/Th17 signaling axes, making it an attractive therapeutic target for related disorders. Herein, we employed structure-based virtual screening and subsequent structural optimization to identify a series of novel PARP14 inhibitors featuring a phthalazinone scaffold. Among them, compound exhibited strong PARP14 inhibitory activity (IC = 3.03 nM), exceptional selectivity, and robust suppression of PARP14-mediated mono-ADP-ribosylation (MARylation) in cell-based assays. In a dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD)-like mouse model, significantly attenuated skin lesions and effectively decreased the expression of key inflammatory factors, including IL-4, IL-13, IgE, and IL-17A, demonstrating superior efficacy compared with RBN-3143 and Upadacitinib. In short, our findings establish as a novel and potent PARP14 inhibitor with promising therapeutic potential against AD. - Source: PubMed
Publication date: 2026/04/20
Wu ShiqiCong KaiyuanLiu JingQu LeZeng XiaorongKong XiangyingLi ZiyueLou ShaoxueWei PingShao LiGu HongfengZhao YanXu QinlongChu ZhaoxingHe GuangweiZhu QihuaXu YungenZou Yi - Recent studies have highlighted the critical role of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3) in inflammation, with inhibitors like 3PO showing therapeutic potential in various inflammatory diseases. However, its effect on asthma inflammation remains unclear. - Source: PubMed
Publication date: 2026/04/02
Huang SiqingWei ShunaLuo FangCheng Yuanxiong - Atrial fibrillation (AF) is the most common arrhythmia and is associated with high morbidity and mortality, particularly in the aging population. Current treatment and prevention strategies remain suboptimal, highlighting the urgent need to better understand the mechanisms underlying aging-associated AF. We recently reported a causal role of the stress-activated kinase JNK2 (c-Jun N-terminal kinase 2) in aging-associated AF pathogenesis, mediated by JNK2-driven sarcoplasmic reticulum Ca dysfunction. However, the mechanisms by which cardiac JNK2 is activated during aging to promote AF remain unclear. Emerging evidence suggests that interorgan crosstalk contributes critically to the development of cardiovascular diseases. A hyperpermeable gastrointestinal epithelial barrier ("leaky gut"), commonly observed in aged individuals, is associated with elevated levels of proinflammatory cytokines and an increased risk of AF. Although proinflammatory cytokines have been proposed as predisposing factors for AF, clinical and experimental studies have yielded inconsistent results, underscoring the complexity of inflammation-associated AF pathogenesis. Here, we investigated whether cardiac JNK2 integrates diverse stress stimuli, including proinflammatory cytokines and lipopolysaccharide, to drive AF pathogenesis. - Source: PubMed
Publication date: 2026/04/20
Yan JiajieCarrillo ElenaKohli AaryanKhanal SaugatRicchiuti NikolaDeSantiago JaimeWan XiaopingHan MeiRichardson AbigailYang MeiRondon JesusShen LeSun JunLiang QiangrongHund Thomas JMeller JarekDeschenes IsabelleBare Dan JAi Xun - Group 3 innate lymphoid cells (ILC3s) preserve intestinal barrier integrity by producing IL-22 and IL-17A, yet the molecular mechanisms that maintain these cytokines during inflammation are incompletely defined. Here, we identify DAB2IP as a cell-intrinsic regulator of ILC3 effector function. In human inflammatory bowel disease mucosa, DAB2IP expression is reduced and associated with transcriptional programs linked to impaired epithelial repair. In murine models, inflammatory cues dynamically modulate Dab2ip in ILC3s, and genetic loss of DAB2IP diminishes IL-22 and IL-17A, compromising host defense during Citrobacter rodentium infection, and exacerbates dextran sulfate sodium-induced colitis. Mechanistically, DAB2IP enables efficient NF-κB activation, promoting IκBα degradation, p65 nuclear accumulation, and thus transcription of Il22/Il17a and NF-κB targets. These results reveal a context-dependent role for DAB2IP as a positive regulator of NF-κB in ILC3s, highlighting its previously unknown function in mucosal immunity and epithelial repair, and suggesting that restoring DAB2IP signaling could enhance barrier protection during intestinal inflammation. - Source: PubMed
Liu LiangDavidorf BenjaminDong PeixianYu JohnHo DavidZhang BingHe Zhiheng