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
- MECP2 duplication syndrome (MDS) is a rare neurogenetic disorder characterized by neurodevelopmental delay, epilepsy, gastrointestinal dysfunction, and frequent infections. The broader spectrum of immune dysregulation remains poorly understood. We retrospectively reviewed four MDS patients with recurrent sterile polyserositis across multiple centers, analyzing clinical presentation, laboratory findings, treatment responses, and outcomes. All patients developed recurrent pleural and/or pericardial effusions of unclear etiology, with systemic inflammation (leukocytosis, elevated C-reactive protein, hyperferritinemia in some cases). Extensive workups were unrevealing. Patients also demonstrated evidence of immune dysregulation, including hypogammaglobulinemia, altered T- and B-cell populations, and abnormal immunoglobulin profiles. Effusions persisted despite antimicrobials and drainage, but resolved with immune-directed therapies. Earlier immunomodulatory therapy enabled faster recovery and reduced morbidity. One patient achieved sustained remission without recurrence with long-term immunomodulatory treatment. We identify recurrent sterile polyserositis as a previously unrecognized inflammatory manifestation of MDS, suggestive of an autoinflammatory mechanism given the systemic hyperinflammation, absence of infectious or oncogenic causes, and responsiveness to immunomodulatory therapy. Our findings highlight the importance of early immunophenotyping and targeted immunomodulation. Prospective studies are needed to define the prevalence, biology, and optimal management of this emerging inflammatory phenotype. - Source: PubMed
Publication date: 2026/08/28
Mendonca DanielleZinter Matt SDevarajan Sunjay RBoehme JasonSuter BernhardMaletic-Savatic MirjanaMuscal EyalPehlivan Davut - Obesity constitutes a significant worldwide health challenge and a primary risk factor for cardiovascular diseases. Diacerein, an anti-inflammatory medication approved for osteoarthritis, is being studied as a potential modulator of inflammatory signaling. However, its role in obesity-associated cardiovascular injury remains incompletely understood. In the present study, computational docking and 300-ns MD simulations supported preferential, stable binding of diacerein to the TLR4 complex through a deep, hydrophobic, solvent-shielded pose, consistent with coordinated protein dynamics. Then, the cardioprotective effects of diacerein were examined in a high-fat diet (HFD)-induced obesity model. Male Sprague-Dawley rats were divided into three groups: normal control, HFD, and HFD combined with diacerein (50 mg/kg/day) for 10 weeks. Metabolic parameters, lipid profile, serum troponin I, and C-reactive protein (CRP) were evaluated. A histopathological examination of the heart and aorta was conducted, and the tissue levels of TLR4, MyD88, IRAK1, TRAF6, NF-κB, and downstream pro-inflammatory cytokines (IL-6 and TNF-α) were assessed. Inflammatory cell infiltration was evaluated using CD45 immunohistochemistry. The HFD led to insulin resistance, dyslipidemia, increased troponin I and CRP levels, and significant histological alterations in cardiac and aortic tissues, accompanied by the activation of the TLR4/NF-κB inflammatory pathway and enhanced inflammatory cell infiltration. Diacerein treatment markedly alleviated metabolic abnormalities, diminished cardiac injury and systemic inflammation, improved histological features, and reduced tissue protein levels of the TLR4/NF-κB pathway and pro-inflammatory cytokines. In conclusion, diacerein provides marked protection against obesity-induced cardiovascular injury, at least partially, by inhibiting the TLR4/NF-κB inflammatory pathway, supporting its potential as a therapeutic strategy for obesity-related cardiovascular complications. - Source: PubMed
Publication date: 2026/08/20
Alatawi Shahad MAljadrawi Sara FAlanazi Layan SAljohani Yara AElsherbiny NehalAbo-Dya Nader EQushawy MonaAhmed Salwa Fares - Sensing of tissue injury or infection by Toll-like receptors (TLRs) must rapidly mobilize host defense, but that activation must also be terminated on an appropriate time scale to avoid sustained, tissue-damaging inflammation. The full network of molecular interactions that governs both the rapid onset and the properly timed shutoff of TLR signaling remains incompletely characterized at a deep mechanistic level. To this end, we built a rule-based model of mouse macrophage TLR4 signaling at the molecular-interaction level, parameterized with measured protein copy numbers, RNA-seq-based abundance estimates, literature- and structure-informed reaction rates, and 979 dynamic experimental constraints, achieving a level of granularity beyond that of prior TLR models. The trained model reproduced much of the TLR4-induced NF-κB and MAP kinase response, but it consistently failed to capture deactivation of MyD88, TRAF6-associated species, and IKKα/β. Rather than treating this as simple model error, we used the recurrent failure as a biological signal that localized missing regulation to the proximalMyD88-IRAK-TRAF6 module and motivated experimental evaluation of IKKε and its scaffold TANK. Loss of IKKε enhanced transcriptional, cytokine, MAP kinase, and NF-κB responses to MyD88-specific TLR ligands, and TANK deficiency produced a similar cellular phenotype while abolishing stimulus-induced IKKε phosphorylation. Deficiency of either protein increased IRAK1and TRAF6 ubiquitination without increasing MyD88 ubiquitination, placing the inhibitory checkpoint at or immediately downstream of the IRAK1-TRAF6 ubiquitin-signaling node. Overlapping but non-identical in vivo phenotypes further supported a shared regulatory axis with additional protein-specific functions. Together, these findings illustrate a model-experiment discovery cycle in which quantitative pathway discordance identifies missing biology, revealing a TANK-dependent IKKε checkpoint that restrains MyD88-driven inflammation. - Source: PubMed
Publication date: 2026/08/16
Manes Nathan PZhang FengkaiLin BinSun JingHassan Sergio AArmstrong Anthony AShao YutingCalzola Jessica MKaplan-Stafford Pauline RGottschalk Rachel AMarino Matthew JKim DoeunGermain Ronald NMeier-Schellersheim MartinFraser Iain D CNita-Lazar Aleksandra - An altered T-cell repertoire with aberrant immune activation is central to the pathogenesis of acquired aplastic anemia (aAA), and miRNAs are known to orchestrate T-cell activation; their relationship is, however, incompletely explored in aAA. The study aimed to validate specific miRNA-mRNA pairs involved in aberrant T-cell activation, differentiation, and cytokine levels in aAA. - Source: PubMed
Publication date: 2026/08/16
Sabereen GhazalaGupta RuchiSingh Manish KumarGupta KusumRahman KhaliqurChaturvedi Chandra PrakashChandra DineshKashyap Rajesh - Chronic atrophic gastritis (CAG) with intestinal metaplasia (IM) is a key precancerous lesion that may progress to intestinal-type gastric adenocarcinoma. Piwei Peiyuan Pill (PPP) has shown significant clinical efficacy in ameliorating CAG with IM, but its active components and underlying mechanisms remain unclear. High-performance liquid chromatography (HPLC) and ultra-high performance liquid chromatography coupled with high-resolution mass spectrometry (UHPLC-HRMS) were used to identify the components of PPP and the active ingredients in PPP-containing serum. The therapeutic efficacy and potential mechanisms of PPP were further investigated via transcriptomic sequencing and experimental validation. UHPLC-HRMS analysis of PPP-containing serum identified several bioactive components, including esculin, lithospermic acid, and atractylenolide III. In CAG rats, PPP significantly ameliorated gastric mucosal damage and reduced serum IL-6 and TNF-α levels. Transcriptomic results showed that IRAK1 was highly expressed in CAG patients with IM and associated with activation of the NF-κB pathway. PPP intervention dose-dependently suppressed hyperactivation of the Pellino1/IRAK1/NF-κB axis and decreased the expression of intestinal metaplasia markers CDX1 and MUC2. Additionally, PPP improved immune function by increasing the proportion of CD4 T cells and decreasing the proportion of CD8 T cells in CAG model rats. Taken together, these findings suggest that PPP mitigates CAG and attenuates IM at least in part by suppressing the Pellino1/IRAK1/NF-κB signaling pathway, indicating that it may serve as a promising therapeutic strategy for reducing inflammation-associated gastric carcinogenesis. - Source: PubMed
Zhang ChengLu FeiYe TingJin YuepingQin YunpengWu KairuiLiu KaiWang XuncuiSong HangLi Xuejun