IRAK-4 Antibody (YA4923)
IRAK-4 Antibody (YA4923) is a Rabbit-derived and non-conjugated recombinant monoclonal antibody, targeting to IRAK-4.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P
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Reactivity :
Human, Mouse, Monkey
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Formulation:
Supplied in 1*TBS (pH7.4), 0.05% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Conjugation:
Non-conjugated
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Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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|---|---|---|
| Dilution Ratio | 1:1000 | 1:1000 |
Product Details
IRAK-4 Antibody (YA4923) is a Rabbit-derived and non-conjugated recombinant monoclonal antibody, targeting to IRAK-4.
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Host Rabbit
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Clonality Monoclonal,Recombinant
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Species ReactivityHuman, Mouse, Monkey
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Calculated Molecular Weight Predicted band size: 52 kDa;
Purified recombinant fragment of human IRAK-4 expressed in E. Coli.
Endogenous
Protein A affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in 1*TBS (pH7.4), 0.05% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
Interleukin-1 receptor-associated kinase 4 (IRAK4) is a serine/threonine kinase that functions as a key mediator in Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) signaling pathways[1][2]. Mechanistically, IRAK4 initiates myddosome formation by recruiting and activating IRAK1, facilitating downstream NF-κB and MAPK signaling[2][3]. Compared with other IRAK family members, IRAK4 possesses both kinase activity and scaffolding functions, with its scaffold role being essential for myddosome assembly independent of catalytic activity[2][3]. Dysregulation or overexpression of IRAK4 contributes to inflammatory, autoimmune, and oncogenic processes, including rheumatoid arthritis, myelodysplastic syndromes (MDS), and acute myeloid leukemia (AML) [1][4][5]. In MDS and AML, long isoforms of IRAK4 (IRAK4-L) produced by spliceosome mutations such as SF3B1 or U2AF1 retain maximal functional domains, driving constitutive NF-κB activation and sustaining leukemic stem cell function[5][6][7]. Selective IRAK4 inhibitors, including DW18134, CA-4948, PF-06650833, and KME-0584, have demonstrated efficacy in preclinical models by reducing proinflammatory cytokines and suppressing leukemic progenitor proliferation[8][9][10]. Dual inhibition of IRAK4 and IRAK1 enhances therapeutic outcomes, as IRAK1 compensatory activation can limit the efficacy of IRAK4-selective agents[9]. Mechanistic studies also highlight that IRAK4 degraders, which eliminate both scaffolding and kinase functions, achieve broader suppression of TLR/IL-1R-induced NF-κB and p38 signaling compared with kinase inhibition alone[3].
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Subcellular Localization
Cytoplasm
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Subunit
Associates with MYD88 and IRAK2 to form a ternary complex called the Myddosome (PubMed:16951688, PubMed:24316379). Once phosphorylated, IRAK4 dissociates from the receptor complex and then associates with the TNF receptor-associated factor 6 (TRAF6), IRAK1, and PELI1; this intermediate complex is required for subsequent NF-kappa-B activation (PubMed:11960013, PubMed:12496252, PubMed:16951688). Direct binding of SMAD6 to PELI1 prevents complex formation and hence negatively regulates IL1R-TLR signaling and eventually NF-kappa-B-mediated gene expression (PubMed:16951688). Interacts with IL1RL1 (PubMed:16286016). Interacts (when phosphorylated) with IRAK1 (PubMed:33238146). May interact (when phosphorylated) with IRAK3 (PubMed:33238146)
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SwissProt ID
Documentation
References
[1]. Singer JW, et al. Inhibition of interleukin-1 receptor-associated kinase 1 (IRAK1) as a therapeutic strategy. Oncotarget. 2018 Sep 7;9(70):33416-33439. [Content Brief]
[2]. Feng Y, et al. Emerging interleukin-1 receptor-associated kinase 4 (IRAK4) inhibitors or degraders as therapeutic agents for autoimmune diseases and cancer. Acta Pharm Sin B. 2024 Dec;14(12):5091-5105. [Content Brief]
[3]. De Nardo D, et al. Interleukin-1 receptor-associated kinase 4 (IRAK4) plays a dual role in myddosome formation and Toll-like receptor signaling. J Biol Chem. 2018 Sep 28;293(39):15195-15207. [Content Brief]
[4]. Huang Y, et al. A Novel IRAK4 Inhibitor DW18134 Ameliorates Peritonitis and Inflammatory Bowel Disease. Molecules. 2024 Apr 16;29(8):1803. [Content Brief]
[5]. Yoon SB, et al. A novel IRAK4/PIM1 inhibitor ameliorates rheumatoid arthritis and lymphoid malignancy by blocking the TLR/MYD88-mediated NF-κB pathway. Acta Pharm Sin B. 2023 Mar;13(3):1093-1109. [Content Brief]
[8]. Choudhary SA, et al. A small molecule potent IRAK4 inhibitor abrogates lipopolysaccharide-induced macrophage inflammation in-vitro and in-vivo. Eur J Pharmacol. 2023 Apr 5;944:175593. [Content Brief]
[9]. Hao X, et al. Electromagnetic Functional Properties of Flexible Picosecond Laser-Induced Graphene Films Modified with Silver Nanoparticles. ACS Appl Mater Interfaces. 2026 May 27;18(20):28957-28968. [Content Brief]
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