Product nameRecombinant Human IRAK4 protein
See all IRAK4 proteins and peptides
Protein lengthProtein fragment
Amino Acid Sequence
SequenceMNKPITPSTYVRCLNVGLIRKLSDFIDPQEGWKKLAVAIKKPSGDDRYNQ FHIRRFEALLQTGKSPTSELLFDWGTTNCTVGDLVDLLIQNEFFAPASLL LPDAVPKTANTLPSKEAITVQQKQMPFCDK
Amino acids1 to 130
TagsGST tag N-Terminus
Our Abpromise guarantee covers the use of ab153334 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Additional notesProtein concentration is above or equal to 0.05 mg/ml.
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Preparation and Storage
Stability and Storage
Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.
Constituents: 0.31% Glutathione, 0.79% Tris HCl
- IL-1 receptor-associated kinase 4
- Interleukin 1 receptor associated kinase 4 mutant form 1
- Interleukin-1 receptor-associated kinase 4
FunctionRequired for the efficient recruitment of IRAK1 to the IL-1 receptor complex following IL-1 engagement, triggering intracellular signaling cascades leading to transcriptional up-regulation and mRNA stabilization. Phosphorylates IRAK1.
Involvement in diseaseDefects in IRAK4 are the cause of recurrent isolated invasive pneumococcal disease type 1 (IPD1) [MIM:610799]. Recurrent invasive pneumococcal disease (IPD) is defined as two episodes of IPD occurring at least 1 month apart, whether caused by the same or different serotypes or strains. Recurrent IPD occurs in at least 2% of patients in most series, making IPD the most important known risk factor for subsequent IPD.
Defects in IRAK4 are the cause of IRAK4 deficiency (IRAK4D) [MIM:607676]. IRAK4 deficiency causes extracellular pyogenic bacterial and fungal infections in otherwise healthy children.
Sequence similaritiesBelongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family. Pelle subfamily.
Contains 1 death domain.
Contains 1 protein kinase domain.
- Information by UniProt
ab153334 has not yet been referenced specifically in any publications.