Rabbit Polyclonal IRAKM antibody. Suitable for ICC, WB, IHC-P and reacts with Rat, Mouse samples. Cited in 15 publications. Immunogen corresponding to Synthetic Peptide within Human IRAK3 aa 550 to C-terminus.
pH: 7.2
Preservative: 0.02% Sodium azide
ICC | WB | IHC-P | |
---|---|---|---|
Mouse | Expected | Tested | Tested |
Rat | Tested | Tested | Tested |
Species | Dilution info | Notes |
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Species Rat | Dilution info - | Notes - |
Species | Dilution info | Notes |
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Species Mouse | Dilution info Use at an assay dependent concentration. | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Mouse | Dilution info 0.5-1 µg/mL | Notes - |
Species Rat | Dilution info 0.5-1 µg/mL | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Mouse | Dilution info 2 µg/mL | Notes - |
Species Rat | Dilution info 2 µg/mL | Notes - |
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Putative inactive protein kinase which regulates signaling downstream of immune receptors including IL1R and Toll-like receptors (PubMed:10383454, PubMed:29686383). Inhibits dissociation of IRAK1 and IRAK4 from the Toll-like receptor signaling complex by either inhibiting the phosphorylation of IRAK1 and IRAK4 or stabilizing the receptor complex (By similarity). Upon IL33-induced lung inflammation, positively regulates expression of IL6, CSF3, CXCL2 and CCL5 mRNAs in dendritic cells (PubMed:29686383).
Interleukin-1 receptor-associated kinase 3, IRAK-3, IL-1 receptor-associated kinase M, Inactive IL-1 receptor-associated kinase 3, IRAK-M, IRAK3
Rabbit Polyclonal IRAKM antibody. Suitable for ICC, WB, IHC-P and reacts with Rat, Mouse samples. Cited in 15 publications. Immunogen corresponding to Synthetic Peptide within Human IRAK3 aa 550 to C-terminus.
pH: 7.2
Preservative: 0.02% Sodium azide
Anti-IRAK-M has no cross response to IRAK or IRAK2.
Purified IgG prepared by ion exchange chromatography.IRAK-M Antibody is affinity chromatography purified via peptide column.
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.
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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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Terms & Conditions.
ab8116 staining IRAKM in murine lung macrophages by Immunocytochemistry/ Immunofluorescence.<.br>
The cells were permeablized with a 1:1 mixture of methanol and acetone. After washing with PBS, ab8116 was applied and the cells incubated for one hour. After washing, antibodies against the primary antibody labeled with FITC were applied to the cells and incubated for one hour. The cell were then mounted in DAPI mounting media and viewed on the fluorescent microscope.
Western blot analysis of IRAKM in mouse spleen (M) and rat liver (R) tissue lysates with anti-IRAKM at 1 μg /ml.
All lanes: Western blot - Anti-IRAKM antibody (ab8116) at 1 µg/mL
Lane 1: Mouse spleen tissue lysates
Lane 2: Rat liver tissue lysate
Predicted band size: 68 kDa
Observed band size: 68 kDa
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) of A20 cells staining IRAKM with ab8116 at 20 µg/ml
Immunohistochemical staining of rat liver tissue using IRAK-M antibody at 2 μg/ml.
Immunofluorescence of IRAK-M in Rat Liver cells using ab8116 at 10 ug/ml.
ab8116 at 2μg/ml staining IRAKM in rat liver cells by IHC
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