I1654
Anti-IRAK2 (546-564) antibody produced in rabbit
~0.5 mg/mL, affinity isolated antibody
Synonym(s):
Anti-Interleukin-1 Receptor-Associated Kinase 2
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About This Item
MDL number:
UNSPSC Code:
12352203
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
mol wt
antigen 65 kDa
species reactivity
human
concentration
~0.5 mg/mL
technique(s)
western blot: 0.5-1 μg/mL using HeLa or K562 cell lysates
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
Gene Information
human ... IRAK2(3656)
General description
The gene IRAK2 (interleukin 1 receptor associated kinase 2) encodes a member of the IRAK/Pelle family. It is an important signaling molecule of the TLR (Toll like receptor)/IL1-R (interleukin 1 receptor) superfamily. The members of IRAK family are characterized by the presence of an N-terminal DD (death domain) and a C-terminal Ser/Thr kinase or kinase-like domain. The gene is mapped to human chromosome 3p25.3-3p24.1.
Immunogen
synthetic peptide corresponding to amino acids 546-564 of human IL-1 receptor-associated kinase 2 (IRAK2).
Biochem/physiol Actions
The members of this family activate the transcription factor NF-κB (nuclear factor κ B) via IL-R1 (interleukin receptor type 1) and TLR (Toll-Like Receptor) mediated inflammatory/immune response. The receptor IL-R1 binds to its ligand proinflammatory cytokine IL-1, and this binding facilitates the association of IL-R1 with IL-1 receptor accessory protein (IL-1RAcP). This complex then recruits myeloid differentiation protein (MyD88), an intracellular TIR-containing adaptor. MyD88, then recruits IRAK1, IRAK2, IRAK4 and IRAK-M. These kinases interact with TRAF6 (TNF receptor-associated factor 6), which in turn links to NFκB-inducing kinase (NIK). NIK activates the IκB kinase complex (IKKα and IKKβ), which in turn phosphorylates IκB. This final phosphorylation leads to ubiquitin-proteasome-mediated degradation resulting in the activation of NF-κB.
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Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Lu Gan et al.
Immunologic research, 35(3), 295-302 (2006-12-19)
The interleukin-1 receptor associated kinases (IRAKs) are critically involved in the IL-1R/Toll-like receptor (TLR)-mediated signal transduction processes and therefore regulate cellular innate immune responses. Four IRAK members have been identified in the human genome (IRAK-1, 2, M, and 4), which
H Wesche et al.
Immunity, 7(6), 837-847 (1998-01-16)
IL-1 is a proinflammatory cytokine that signals through a receptor complex of two different transmembrane chains to generate multiple cellular responses, including activation of the transcription factor NF-kappaB. Here we show that MyD88, a previously described protein of unknown function
Rainer Kaiser et al.
JCI insight, 6(18) (2021-08-18)
Neutrophils provide a critical line of defense in immune responses to various pathogens, inflicting self-damage upon transition to a hyperactivated, procoagulant state. Recent work has highlighted proinflammatory neutrophil phenotypes contributing to lung injury and acute respiratory distress syndrome (ARDS) in
Z Cao et al.
Nature, 383(6599), 443-446 (1996-10-03)
Many cytokines signal through different cell-surface receptors to activate the transcription factor NF-kappaB. Members of the TRAF protein family have been implicated in the activation of NF-kappaB by the tumour-necrosis factor (TNF)-receptor superfamily. Here we report the identification of a
K T Akama et al.
The Journal of biological chemistry, 275(11), 7918-7924 (2000-03-14)
In Alzheimer's disease, beta-amyloid (Abeta) plaques are surrounded by activated astrocytes and microglia. A growing body of evidence suggests that these activated glia contribute to neurotoxicity through the induction of inflammatory cytokines such as interleukin (IL)-1beta and tumor necrosis factor-alpha
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