IRAK1 pSer376 antibody Ab
- Known as:
- IRAK1 pSer376 (anti-) Antibody
- Catalog number:
- 1488141
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- IRAK1 pSer376 antibody
Related genes to: IRAK1 pSer376 antibody Ab
- 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 pSer376 antibody Ab
Related articles to: IRAK1 pSer376 antibody Ab
- Dry eye disease (DED) is a highly prevalent ocular disorder affecting an estimated 5-50% of the global population. Despite its substantial clinical burden, effective therapeutic options remain limited owing to the multifactorial nature and complex pathophysiology of the disease. To simultaneously address the two principal pathological drivers of DED, oxidative stress and chronic inflammation, we engineered mRC@PAM, a polyamidoamine (PAMAM) dendrimer-based nanotherapeutic eye-drop system capable of co-delivering curcumin (Cur) and microRNA-146a (miR-146a) through hydrophobic encapsulation and electrostatic complexation, respectively. The resulting nanoformulation exhibited excellent physicochemical stability, high cargo-loading efficiency, outstanding biocompatibility, and prolonged retention on the ocular surface. Mechanistically, mRC@PAM effectively restored intracellular redox balance by preserving antioxidant defense capacity and maintaining mitochondrial membrane integrity. Simultaneously, it attenuated inflammatory responses through miR-146a-mediated suppression of interleukin-1 receptor-associated kinase 1 (IRAK1), leading to inhibition of the nuclear factor kappa B (NF-κB) signaling cascade and subsequent regulation of macrophage polarization. In vivo, treatment with mRC@PAM markedly reduced reactive oxygen species (ROS) accumulation and apoptotic cell death in corneal tissues, promoted recovery of the corneal epithelium and conjunctival goblet cells, diminished inflammatory cell infiltration, and significantly enhanced tear-film stability. Taken together, these findings highlighted mRC@PAM as a promising dual-action nanotherapeutic platform capable of concurrently mitigating oxidative and inflammatory damage, thereby offering a potential treatment strategy for DED and other ocular surface disorders characterized by intertwined oxidative stress and inflammatory pathologies. - Source: PubMed
Publication date: 2026/09/21
Chen DanSheng SitingLiu LiruiZhang YinZhao HuilingWang JingwenZhang MingxuanHan HaijieXu Wen - Chronic inflammation is involved in the pathogenesis of coronary artery disease (CAD). This case-control study investigated whether the systemic inflammatory response reflects the status of CAD by evaluating the expression of four genes in the IL-1R/TLR pathway (IRAK1, TRAF6, MAPK1, and CXCL8) in peripheral blood mononuclear cells (PBMCs). - Source: PubMed
Publication date: 2026/09/18
Subramanian VinodhiniKumar M JeevanMuralidharan T RVenkatesan Vettriselvi - Interleukin-1 receptor-associated kinase 1 (IRAK1) is a serine/threonine kinase that functions as a central transducer of Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) signaling, linking pathogen recognition to the activation of nuclear factor kappa B (NF-κB), mitogen-activated protein kinases (MAPK), and interferon regulatory factors (IRFs). Although the role of IRAK1 in innate immune signaling is well established, its regulatory complexity remains incompletely characterized, particularly regarding the dynamic phosphorylation landscape that governs activation, substrate specificity, and signal termination. This review presents a systematic phosphoproteomics map of IRAK1 phosphorylation, integrating 213 profiling and 33 differential mass spectrometry-based phosphoproteomic datasets from 56 studies. Eighteen phosphosites were identified in the profiling datasets and 16 in the differential datasets across independent expression and acquisition conditions. Among these, Ser131 (detected in 128 profiling and 26 differential datasets) and Ser110 (detected in 26 profiling and nine differential datasets) were the most frequently observed sites. Most high-frequency phosphosites are located within the serine/threonine kinase domain and the C-terminal proline/serine/threonine-rich (ProST) regulatory region of the protein. However, frequent detection does not necessarily indicate functional significance, and these sites are potential candidates for targeted validation. In addition to canonical phosphorylation, this review evaluates the coordinated interplay among phosphorylation, K63/K48-linked ubiquitination, and SUMOylation, which together determine whether signaling is propagated or terminated. We also discuss the non-canonical functions of IRAK1 in transcriptional regulation, antiviral defense, cytoskeletal organization, and oncogenic signaling, and evaluate current pharmacological inhibitors of IRAK1, including Pacritinib, JH-X-119-01, 1, 4-naphthoquinone, and rosoxacin. Overall, this review provides a systematic, data-informed framework for prioritizing phosphosite-specific functional studies to identify phospho-dependent interaction interfaces as potential targets for precision clinical interventions and biomarker development in inflammatory diseases and cancer. - Source: PubMed
Publication date: 2026/09/03
Suresh ManasaVaz Chrysilla EspyDcunha LeonaRaju RajeshPinto Sneha MKanekar Saptami - Activating MYD88 mutations promote pro-survival signaling through divergent HCK/BTK and IRAK1/IRAK4 pathways, and persistent IRAK signaling may contribute to incomplete responses to BTK inhibitors. Here, we show that IRAK1 or IRAK4 knockdown reduced NFKB signaling and impaired MYD88 mutant lymphoma cell survival but, unexpectedly, enhanced ERK1/2 signaling, which was blocked by HCK/BTK inhibition. Knockdown and replacement studies further supported kinase-independent scaffold functions for IRAK1 and IRAK4. These findings motivated development of JH-XIII-05-01, a first-in-class dual IRAK1/IRAK4 degrader designed to eliminate both catalytic and scaffold-dependent IRAK signaling. JH-XIII-05-01 retained potent IRAK1/IRAK4 biochemical activity, induced degradation of both targets, and showed superior antiproliferative activity compared with its nondegrading parental inhibitor JH-XI-82-01. JH-XIII-05-01 also enhanced apoptosis and synergized with covalent and noncovalent BTK inhibitors, BTK degraders, and the BCL-2 inhibitor venetoclax. These findings support dual IRAK1/IRAK4 degradation as a strategy for targeting MYD88 mutant lymphomas. - Source: PubMed
Publication date: 2026/08/26
Hatcher John MLiu ShirongLiu XiaKofides AmandaCanning Alexa GPizzarella DominicTsakmaklis NickolasGuerrera Maria LPatterson Christopher JGuijosa AlbertoGokhale PrafullaHunter Zachary RSarosiek Shayna RCastillo Jorge JWang JinhuaBuhrlage Sara JTreon Steven P - Non-small cell lung cancer (NSCLC) shows partial chemoimmunoresistance, driven by the upregulation of the drug efflux transporters ABCB1 and ABCC1 and the downregulation of the immunosensitizer protein ABCA1. To elucidate the molecular mechanisms underlying this chemoimmunoresistant phenotype, by performing a CRISPR-KO kinome screening, we identified interleukin-1 receptor-associated kinase 1 (IRAK1) as a key determinant of chemoimmunosensitive and chemoimmunoresistant phenotypes, defined as ABCB1/ABCC1ABCA1 and ABCB1/ABCC1ABCA1, respectively. IRAK1 expression was significantly associated with poor prognosis in the TCGA-LUAD cohort and in early-stage NSCLC patients. The IRAK1/ABCB1/ABCC1ABCA1 signature was predictive of poor response to chemotherapy and immunotherapy in advanced-stage patients. Mechanistically, IRAK1 silencing resensitized NSCLC cells to cisplatin by decreasing IL-1R/NFκB and IL-1R/AP-1 signaling, which in turn downregulated the drug efflux transporters ABCB1 and ABCC1. Concurrently, IRAK1 silencing activated the LXRα/ABCA1 axis, which enhanced Vγ9Vδ2 Tcell-mediated cytotoxicity and facilitated the recruitment of memory and effector CD4 and CD8 T cells in both ex vivo autologous cocultures and immunoxenografts, increasing the immuno-killing ability of tumor cells. Newly developed synthetic inhibitors of IRAK1 efficiently promoted chemo- and immunosensitization in immunoxenografts, resulting in good pharmacokinetic and safety profiles. These findings identify IRAK1 as a novel, druggable target that controls both chemoresistance and immune evasion in NSCLC. We suggest the pharmacological inhibition of IRAK1 as a future promising strategy to overcome resistance to chemotherapy and improve patient outcomes. - Source: PubMed
Publication date: 2026/09/15
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