IRAK1 Mouse Monoclonal Antibody
- Known as:
- IRAK1 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003654-M02
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- IRAK1 Mouse Monoclonal Antibody
Related genes to: IRAK1 Mouse Monoclonal Antibody
- Gene:
- IRAK1 NIH gene
- Name:
- interleukin 1 receptor associated kinase 1
- Previous symbol:
- -
- Synonyms:
- IRAK, pelle
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-22
- Date modifiied:
- 2017-07-12
Related products to: IRAK1 Mouse Monoclonal Antibody
Related articles to: IRAK1 Mouse Monoclonal Antibody
- Pulmonary fibrosis (PF) is a life-threatening interstitial lung disease characterized by scarring and inflammation in lung tissues. Aberrant activation of the JAK/STAT and NF-κB signaling pathways is critical in initiating and sustaining the inflammatory processes that drive fibrotic progression. In this study, we identify a novel small-molecule compound, T4015, a 4-indolyl-2-phenylaminopyrimidine derivative, as a dual-pathway inhibitor targeting both JAK/STAT and NF-κB signaling. Dual-luciferase reporter assays demonstrate the potent inhibitory activity of T4015 against these pathways. T4015 effectively suppresses the phosphorylation of STAT3, JAK1, and TYK2 induced by IL-6 and IFN-β, while suppressing LPS-induced NF-κB activation in macrophages. Transcriptome sequencing and pathway enrichment analyses further confirm that T4015 downregulates multiple inflammation-related signaling cascades, including the JAK/STAT, NF-κB, TNF, IL-17, and Toll-like receptor pathways. In a mouse model of bleomycin-induced PF, T4015 treatment significantly improves survival, attenuates collagen deposition, and reduces the expression of pro-inflammatory and profibrotic markers such as IL-6, CCL2, and COL1. Molecular docking and target prediction analyses suggest that T4015 exhibits strong binding affinity for multiple kinases within the JAK/STAT and NF-κB networks, including JAK1, TYK2, JAK2, JAK3, RIPK1, IRAK1/4, TAB1, and ZAP70. Collectively, these results highlight T4015 as a promising therapeutic candidate for PF through its simultaneous inhibition of the JAK/STAT and NF-κB signaling pathways. - Source: PubMed
Publication date: 2026/04/25
Zhang MinghuiXu HangLiu ShanXu XiaohanYin JiayiZhang XinxinZhang XiaonanYang XiaopingLiu XiaochunYin BinZhou MingmingWang LeweiZhang MengLiu HuiyingJiang WenqingSong QiaolingYang Jinbo - - Source: PubMed
Publication date: 2026/04/20
Li Lan-TingZhu Yan-XueZhao Dong-MeiZhang Jin-LeXia Lin-GuoLi Rui-Fang - Protein kinases are central to cell signaling and key drug targets in cancer. To inform potential repurposing of kinase inhibitors, we profiled 86 of the ~100 approved kinase inhibitors against 758 kinases, including 409 wild-type and 349 oncogenic variants using a biochemical kinase assay. Our results increase the number of druggable kinases from 89 to 235, revealing that 94% of mutations and 97% of fusions represented in our samples are inhibited by at least one existing drug. The dataset revealed mutation-specific selectivity, especially in tyrosine kinases FGFR and MET, highlighting gaps and repurposing opportunities. We experimentally validated several actionable findings, including tepotinib to target the IRAK1/4-cholesterol pathway in glioblastoma, brigatinib to target the MARK2/3-Hippo pathway in pancreatic cancer and gilteritinib to overcome MET mutation-driven drug resistance and metastasis. To facilitate exploration of our data, we provide KIRHub, a web-based tool that allows identification of existing inhibitors of wild-type and mutated kinases to guide precision oncology. - Source: PubMed
Publication date: 2026/04/20
Saifudeen MehlamZhu SongliLiang ShuguangEason MiaGoupil AlisonMische Deanna FLoch Christian MMa HaichingChan MarinaGujral Taranjit S - Myelodysplastic neoplasms (MDSs) are clonal disorders characterized by ineffective hematopoiesis, dysplasia, and a risk of transformation into acute myeloid leukemia. MDS is also associated with a higher incidence of osteoporosis, suggesting a complex interplay between hematopoiesis, the bone marrow (BM) microenvironment, and bone homeostasis. Targeting inflammation has emerged as a promising therapeutic strategy, particularly in lower risk MDS. Tasquinimod (TASQ) is a small-molecule inhibitor of the inflammatory alarmin S100A9, blocking its interaction with TLR4 and RAGE receptors. We investigated the efficacy of TASQ in modulating inflammation and improving disease phenotype using in vitro and in vivo MDS models. Immunofluorescence staining of human BM identified neutrophils and macrophages as primary S100A9 sources. Exposure of mesenchymal stromal cells (MSCs) to S100A9 induced Toll-like receptor 4 (TLR4) downstream signaling, resulting in increased expression of IRAK1, NF-κB-p65, interleukin-1β (IL-1β), IL-18, caspase 1, and PD-L1. These effects were effectively abolished by TASQ. Additionally, TASQ restored the disturbed MSC-mediated hematopoietic support, as demonstrated by increased numbers of cobblestone area-forming cells and colony-forming units. In NHD13 MDS mice, TASQ (30 mg/kg, 12 weeks) improved hemoglobin and red blood cell counts, but exerted no effect in wild-type (WT) mice. Additionally, TASQ improved bone microarchitecture by increasing trabecular number and bone volume, likely a result of reduced osteoclast activity. Our findings suggest that TASQ mitigates inflammasome activation in the MDS BM, improving erythropoiesis and bone health. These results provide a necessary preclinical basis for clinical trials in lower risk MDS patients, in whom anemia and osteoporosis often coexist. - Source: PubMed
Publication date: 2026/04/14
Wobus ManjaWeidner HeikeWehner RebekkaBaumann Anna-LenaMöbus KristinBalaian EkaterinaTörngren MarieVahtola ErikEriksson HelenaWinter SusannPlatzbecker UweChavakis TriantafyllosHofbauer Lorenz ChristianRauner MartinaBornhäuser MartinSockel Katja - Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease involving immune dysregulation, metabolic reprogramming, and multi-organ damage. The Jieduquyuziyin prescription (JP), a contemporary Chinese herbal formula based on the Traditional Chinese Medicine principle of "Jiedu Quyu Ziyin," has shown clinical efficacy in SLE. This review aims to synthesize clinical and preclinical evidence explaining how JP achieves systemic therapeutic effects by targeting interconnected pathological pathways in SLE. - Source: PubMed
Publication date: 2026/04/14
Gan YihongLiu JingqunZhou ShihuiLin KeWang XinchangFan YongshengXu LiBao Jie