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BRAND / VENDOR: Abcam

Abcam, ab8116, Anti-IRAKM antibody

CATALOG NUMBER: ab8116
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Product Description

Size: 100µg
Rabbit Polyclonal IRAKM antibody. Suitable for ICC, WB, IHC-P and reacts with Rat, Mouse samples. Cited in 16 publications. Immunogen corresponding to Synthetic Peptide within Human IRAK3 aa 550 to C-terminus.
Key facts
Host species:Rabbit,
Clonality:Polyclonal,
Isotype:IgG,
Carrier free:No,
Reacts with:Mouse, Rat,
Applications:IHC-P, WB, ICCSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Immunogen:Synthetic Peptide within Human IRAK3 aa 550 to C-terminus. The exact immunogen used to generate this antibody is proprietary information.Q9Y616,
Specificity:Anti-IRAK-M has no cross response to IRAK or IRAK2.

Product details:
Interleukin-1 (IL-1) and lipopolysaccharide (LPS)induces cellular response through IL-1 receptor (IL-1R) and Toll like receptors (TLR). IL-1 receptor associated kinase (IRAK and IRAK2) mediates the activation of NF-kB by IL-1/Toll receptors (Wesche H et al.1999,Muzio M et al.1997), which is a pivotal transcription factor mediating inflammatory and immune response. A novel member in theIRAK/Pelle family was recently identified and designated IRAK-M (Cao Z et al.1996). IRAKs associate with IL-1/Toll receptors after IL-1 or LPS stimulation and thedominant negative mutants of IRAKs inhibit IL-1 orLPS induced NF-kB activation. Members inIRAK/Pelle family play a central role in IL-1R/TLRmediated inflammatory responses to cytokine IL-1and LPS.

Properties and Storage Information:
Form-Liquid, Purification technique-Affinity purification, Purification notes-Purified IgG prepared by ion exchange chromatography.IRAK-M Antibody is affinity chromatography purified via peptide column., Storage buffer-pH: 7.2Preservative: 0.02% Sodium azide, Shipped at conditions-Blue Ice, Appropriate short-term storage duration-1-2 weeks, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle, Stable for 12 months at -20°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
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.
Biological function summary
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.
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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