IRAKM overexpression 293T lysate (whole cell) suitable for WB. View our extensive range of validated lysates from normal and diseased human, mouse and rat tissue.
ASRT5, IL-1 receptor-associated kinase M, IRAK3_HUMAN, Interleukin 1 receptor associated kinase M, Interleukin-1 receptor-associated kinase 3
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IRAKM overexpression 293T lysate (whole cell) suitable for WB. View our extensive range of validated lysates from normal and diseased human, mouse and rat tissue.
ab94127 is a 293T cell transfected lysate in which Human IRAKM has been transiently over-expressed using a pCMV-IRAKM plasmid. The lysate is provided in 1X Sample Buffer.
The IRAK-M protein also known as IRAKM or interleukin-1 receptor-associated kinase M is a member of the IRAK family and has a molecular mass of approximately 65 kDa. It plays an important role in the immune response regulation. This protein is expressed in monocytes and macrophages but it is also found in other immune cells. Unlike other IRAKs IRAK-M acts as a negative regulator helping to ensure the immune system does not overreact.
IRAK-M inhibits the signaling pathways that lead to the activation of inflammatory responses. It predominantly affects signaling initiated by toll-like receptors (TLRs) and interleukin-1 receptors (IL-1Rs) preventing excessive inflammatory cytokine production. IRAK-M lacks kinase activity unlike other IRAK family members so it functions as a regulatory molecule rather than participating in kinase-mediated catalysis. It does not form part of a larger complex but interacts directly with other signaling components in these pathways.
IRAK-M impacts TLR and IL-1 signaling pathways. These pathways are important in the innate immune system's response to pathogens and inflammation. IRAK-M interacts with proteins such as MyD88 and TNF receptor-associated factor 6 (TRAF6) reducing the downstream production of pro-inflammatory cytokines. This modulation helps to maintain immune system balance and prevent chronic inflammation.
IRAK-M is involved in conditions such as sepsis and autoimmune diseases. In sepsis IRAK-M's alteration can lead to an inadequate immune response influencing the body's ability to control infection. In autoimmune diseases abnormal IRAK-M expression may result in regulatory failures leading to persistent inflammation and tissue damage. IRAK-M's interaction with other proteins like MyD88 suggests its pivotal role in these disorders where misregulated pathways can contribute to disease progression.
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ab94127 at 15µg/lane on an SDS-PAGE gel.
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