mProX™ Human IRAK4 Stable Cell Line

Sub Cat	Product Name	Target Protein Species	Host Cell Type	Assay Types	Inquiry	Datasheet
S01YF-1122-KX1173	Magic™ Human IRAK4 in Vitro Assay	Human		Kinase Assay

Product Information

Target Protein

IRAK4

Target Family

Kinases/Enzyme Drug Discovery Assays and Products

Target Protein Species

Human

Host Cell Type

Jurkat; CHO-K1; HEK293

Target Classification

Kinase Cell Lines

Target Research Area

Immunology Research

Related Diseases

Immunodeficiency 67 and Immunodeficiency 33. Among its related pathways are MyD88 dependent cascade initiated on endosome and Diseases of Immune System

Gene ID

51135

UniProt ID

Q9NWZ3

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

Within the IRAK family, IRAK-4 (interleukin-1 receptor-associated kinase 4) is a protein kinase that functions by using Toll-like receptors to signal innate immune responses. T-cell receptor signaling is also supported by it. Domain structures seen in IRAK4 are comparable to those found in IRAK1, IRAK2, IRAKM, and Pelle. In contrast to IRAK1, IRAK2, and IRAKM, IRAK4 functions upstream of the other IRAKs; nevertheless, Pelle is more comparable to IRAK4 in this regard. Important clinical uses exist for IRAK4. Animals lacking IRAK-4 are totally immune to LPS challenge, although they are more vulnerable to germs and viruses. The customized IRAK4 stable cell line can be used in antibody discovery and development, potential drug candidate screening and signaling pathway researches.

Protocols

Please visit our protocols page.

Customer Reviews

chat Helen

This IRAK4 KD cell line is the best choice for laboratories wishing to minimise troubleshooting time. Sep 12 2021

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chat David

The ideal IRAK4 cell line, often used in our laboratories. Mar 02 2021

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FAQ

Any questions about our products? Please visit our frequently asked questions page.

Published Data

Fig.1 IRAK4 inhibitor emavusertib as single agent in MZL models.

IC50 values, error bars, and dose-response curves (from three separate investigations) for emavusertib in parental cell lines Karpas1718 (K1718) and VL51, as well as resistance models to idelalisib (IDE-RES), ibrutinib (IBR-RES), or copanlisib (COP-RES).

Ref: Guidetti, Francesca, et al. "Targeting IRAK4 with emavusertib in lymphoma models with secondary resistance to PI3K and BTK inhibitors." Journal of Clinical Medicine 12.2 (2023): 399.

Pubmed: 36675328

DOI: 10.3390/jcm12020399

Research Highlights

Pharmacological inhibition of IRAK4 did not affect the IL-1-stimulated activation of IRAK1, nor did dephosphorylation or deubiquitylation reverse it. These findings imply that IRAK1 catalytic activity is triggered by an allosteric mechanism induced by its interaction with IRAK4, rather than by a covalent modification.
Vollmer, Stefan, et al. "The mechanism of activation of IRAK1 and IRAK4 by interleukin-1 and Toll-like receptor agonists." Biochemical Journal 474.12 (2017): 2027-2038.
Pubmed: 28512203 DOI: 10.1042/BCJ20170097

These results imply that inhibiting fibrogenesis and promoting regeneration in pericytes by disrupting this MyD88-dependent pathway may be a viable therapeutic strategy.
Leaf, Irina A., et al. "Pericyte MyD88 and IRAK4 control inflammatory and fibrotic responses to tissue injury." The Journal of clinical investigation 127.1 (2017): 321-334.
Pubmed: 27869651 DOI: 10.1172/JCI87532