IRAKM Recombinant Rabbit Monoclonal Antibody [SN64-07] (ET1611-11)

UNIPROT #

Q9Y616

PROTEIN NAME

IRAKM

SYNONYMS

ASRT5 antibody;IL 1 receptor associated kinase M antibody;IL-1 receptor-associated kinase M antibody;IL1 receptor associated kinase M antibody;Interleukin 1 receptor associated kinase 3 antibody;Interleukin 1 receptor associated kinase M antibody;Interleukin-1 receptor-associated kinase 3 antibody;IRAK M antibody;IRAK-3 antibody;IRAK-M antibody;Irak3 antibody;IRAK3_HUMAN antibody

SEQUENCE SIMILARITIES

Belongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family. Pelle subfamily.

TISSUE SPECIFICITY

Expressed predominantly in peripheral blood lymphocytes.

SUBCELLULAR LOCATION

Cytoplasm, Nucleus.

FUNCTION

The interleukin-1 receptor (IL-1R) associated kinase (IRAK) family plays a crucial role in the protective response to pathogens introduced into the human body by inducing acute inflammation followed by additional adaptive immune responses. IRAKs are essential components of the Interleukin-1 receptor signaling pathway and some Toll-like receptor signaling pathways. Toll-like receptors (TLRs) detect microorganisms by recognizing specific pathogen-associated molecular patterns (PAMPs) and IL-1R family members respond the interleukin-1 (IL-1) family cytokines. These receptors initiate an intracellular signaling cascade through adaptor proteins, primarily, MyD88. This is followed by the activation of IRAKs. TLRs and IL-1R members have a highly conserved amino acid sequence in their cytoplasmic domain called the Toll/Interleukin-1 (TIR) domain. The elicitation of different TLRs/IL-1Rs results in similar signaling cascades due to their homologous TIR motif leading to the activation of mitogen-activated protein kinases (MAPKs) and the IκB kinase (IKK) complex, which initiates a nuclear factor-κB (NF-κB) and AP-1-dependent transcriptional response of pro-inflammatory genes. Understanding the key players and their roles in the TLR/IL-1R pathway is important because the presence of mutations causing the abnormal regulation of Toll/IL-1R signaling leading to a variety of acute inflammatory and autoimmune diseases.