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AB216132

Anti-IRAKM抗体[5C3D6] - C-terminal

Anti-IRAKM antibody [5C3D6] - C-terminal

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(1 Publication)

Mouse Monoclonal IRAKM antibody. C-terminal. Suitable for WB, ICC/IF and reacts with Human samples. Cited in 1 publication. Immunogen corresponding to Recombinant Fragment Protein within Human IRAK3 aa 450-600.

查看别名

Interleukin-1 receptor-associated kinase 3, IRAK-3, IL-1 receptor-associated kinase M, Inactive IL-1 receptor-associated kinase 3, IRAK-M, IRAK3

3 Images
Immunocytochemistry/ Immunofluorescence - Anti-IRAKM antibody [5C3D6] - C-terminal (AB216132)
  • ICC/IF

Supplier Data

Immunocytochemistry/ Immunofluorescence - Anti-IRAKM antibody [5C3D6] - C-terminal (AB216132)

Immunofluorescent analaysis of A549 cells labeling IRAKM with ab216132 at 1/100 dilution (green). Blue : DRAQ5 fluorescent DNA dye. Red : Actin filaments have been labeled with Alexa Fluor- 555 phalloidin.

Western blot - Anti-IRAKM antibody [5C3D6] - C-terminal (AB216132)
  • WB

Supplier Data

Western blot - Anti-IRAKM antibody [5C3D6] - C-terminal (AB216132)

All lanes:

Western blot - Anti-IRAKM antibody [5C3D6] - C-terminal (ab216132) at 1/500 dilution

Lane 1:

non-transfected HEK293 cell lysate

Lane 2:

Human IRAKM (aa: 454-596)-hIgGFc transfected HEK293 cell lysate

Predicted band size: 68 kDa

false

Western blot - Anti-IRAKM antibody [5C3D6] - C-terminal (AB216132)
  • WB

Supplier Data

Western blot - Anti-IRAKM antibody [5C3D6] - C-terminal (AB216132)

All lanes:

Western blot - Anti-IRAKM antibody [5C3D6] - C-terminal (ab216132) at 1/500 dilution

All lanes:

Human IRAKM (aa: 454-596) recombinant protein

Predicted band size: 68 kDa

false

关键信息

宿主种属

Mouse

克隆

Monoclonal

克隆号

5C3D6

亚型

IgG1

不含载体蛋白

No

反应种属

Human

应用

ICC/IF, WB

applications

免疫原

Recombinant Fragment Protein within Human IRAK3 aa 450-600. The exact immunogen used to generate this antibody is proprietary information.

Q9Y616

反应性数据

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "WB" : {"fullname" : "Western blot", "shortname":"WB"}, "ICCIF" : {"fullname" : "Immunocytochemistry/ Immunofluorescence", "shortname":"ICC/IF"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Human": { "WB-species-checked": "testedAndGuaranteed", "WB-species-dilution-info": "1/500 - 1/2000", "WB-species-notes": "<p></p>", "ICCIF-species-checked": "testedAndGuaranteed", "ICCIF-species-dilution-info": "1/100 - 1/400", "ICCIF-species-notes": "<p></p>" } } }

性能和储存信息

形式
Liquid
纯化工艺
Affinity purification Protein G
纯化说明
Purified from tissue culture supernatant.
存储溶液
Preservative: 0.05% Sodium azide Constituents: PBS
运输条件
Blue Ice
推荐的短期储存时间
1-2 weeks
推荐的短期储存条件
+4°C
推荐的长期储存条件
-20°C
分装信息
Upon delivery aliquot
储存信息
Avoid freeze / thaw cycle

补充信息

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.

产品实验方案

For this product, it's our understanding that no specific protocols are required. You can visit:

靶点信息

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).
See full target information IRAK3

文献 (1)

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Applications

Unspecified application

Species

Unspecified reactive species

Tatiana S Usenko,Alena E Kopytova,Artem D Izyumchenko,Darya G Kulabukhova,Artemiy S Silantyev,Victoria D Kazakova,Katerina S Basharova,Anastasia I Bezrukova,Luiza A Garaeva,Evgeny B Pichkur,Alexandra V Artynyuk,Irina V Miliukhina,Alla A Timofeeva,Valentina V Miroshnikova,Stanislav N Naryzhny,Anton K Emelyanov,Natalya B Zakharzhevskaya,Andrey L Konevega,Tatiana A Shtam,Sofya N Pchelina
View all publications

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