IRAK4 Antibody (YA4531)

(Synonyms: IPD1; REN64; NY-REN-64)
Customer Review

Based on 1 Customer Validation

IRAK4 Antibody (YA4531) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to IRAK4.

For research use only. We do not sell to patients.
  • Host:

    Mouse

  • Isotype:

    IgG

  • Application:

    WB, IHC-P, FC, ELISA

  • Reactivity :

    Human, Mouse, Rat, , Monkey

  • Formulation:

    Supplied in PBS with 0.05% sodium azide.

  • Conjugation:
    Non-conjugated

Applications

Application
WB Info
WB: Western Blot
IHC-P Info
IHC-P: Immunohistochemistry-Paraffin
FC Info
FC: Flow Cytometry
ELISA Info
ELISA: Enzyme Linked Immunosorbent Assay
Dilution Ratio 1:500-1:2000 1:200-1:1000 1:200-1:400 1:10000

Product Details

Description

IRAK4 Antibody (YA4531) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to IRAK4.

  • Host Mouse
  • Clonality Monoclonal
  • Species Reactivity
    Human, Mouse, Rat, , Monkey
  • Observed Molecular Weight
    Observed band size: 52 kDa Info
    Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
  • Calculated Molecular Weight Predicted band size: 52 kDa
Immunogen

Purified recombinant fragment of human IRAK4 aa 21-198.

Purification

affinity purified.

Conjugation

Non-conjugated

Modification

Unmodified

Isotype

IgG

Product Properties

  • Appearance

    Solution

  • Formulation

    Supplied in PBS with 0.05% sodium azide.

  • Concentration

    Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration

  • Storage & Stability

    Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.

  • Shipping

    Shipping with blue ice.

Verification Images

  • Experimental Validation Results for IRAK4 Antibody (YA4531)
    Flow cytometric analysis of 1X106 Jurkat cells labeling IRAK4 Antibody(HY-P84834, red). Cells were fixed with 4% paraformaldehyde and permeabilised with 90% methanol. Then stained with the primary antibody at 1/200 dilution for an hour at 4℃. AF488-conjugated Goat Anti-Mouse IgG H&L (HY-P8005) was used as the secondary antibody at 1/1,000 dilution for 30 minutes at 4℃. Mouse IgG Isotype Control (HY-P80757, blue) was used as the isotype control, cells without incubation with primary antibody were used as the unlabeled control (black).

Background

  • 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].

  • Subcellular Localization

    Cytoplasm

  • Isoforms & Post-Translational Modification

    Q9NWZ3 has 2 isomers: Q9NWZ3-1: 51530 Da (predicted); Q9NWZ3-2: 37674 Da (predicted).
    Phosphorylated

  • 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)

  • SwissProt ID

    Q9NWZ3

  • Gene ID
  • Synonyms

    IPD1; REN64; NY-REN-64

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]

[6]. Rosenbaum JS, et al. Inhibition of both IRAK1 and IRAK4 is required for complete suppression of NF-Kb signaling across multiple receptor-mediated pathways in MDS and AML. Blood. 2022;140(Suppl 1):5949.

[7]. Rosenbaum JS, et al. Kme-0584, a highly potent IRAK1/IRAK4/panFLT3 inhibitor, is a promising clinical candidate for hypomethylating agent plus venetoclax resistant AML/MDS patients. Blood. 2023;142(Suppl 1):4152.

[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]

[10]. Choudhary GS, et al. SF3B1 mutations induce oncogenic IRAK4 isoforms and activate targetable innate immune pathways in MDS and AML. Blood. 2019;134(Suppl 1):4224.

[11]. Skouras SM, et al. Selective IRAK4 degradation, not kinase inhibition, blocks TLR-activated NF-Kb and p38 signaling leading to broad cytokine inhibition. J Immunol. 2022;208(1 Suppl):111.13.

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IRAK4 Antibody (YA4531) Related Classifications

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