IRAK3 Antibodies

Interleukin-1 receptor-associated kinase 3 (IRAK3)

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. .

Gene Information

Human
Gene Name:	IRAK3
Uniprot:	Q9Y616
Entrez:	11213

Family

Belongs to:
protein kinase superfamily

Alternative Names

ASRT5; EC 2.7.11.1; FLJ13601; IL-1 receptor-associated kinase M; interleukin-1 receptor-associated kinase 3; IRAK3; IRAK-3; IRAKM; IRAK-M

Molecular Weight

Mass (kDA):
67.767 kDA

Genomic Context

Human
Location:	12q14.3
Sequence:	12; NC_000012.12 (66189214..66254622)

Tissue Specificity

Expressed predominantly in peripheral blood lymphocytes.

Diseases

• Inflammation
• Inflammatory Response
• Innate Immune Response
• Malignant Neoplasms
• Systemic Infection
• Neoplasms
• Infective Disorder
• Pneumonia
• Asthma
• Respiratory Tract Infections
• Lung Injury
• Acute Lung Injury
• Tissue Adhesions

• Decreased Immunologic Activity [pe]
• Neoplasm Metastasis
• Injury To Liver
• Osteoporosis
• Bacterial Infections
• Leukemia
• Tumor Angiogenesis

Pathways

• Immune Response
• Inflammatory Response
• Cytokine Production
• Pathogenesis
• Innate Immune Response
• Rna Interference
• Secretion
• Virulence
• Sensitization
• Phagocytosis
• Bone Development
• Macrophage Activation
• Angiogenesis

• Cell Adhesion
• Osteoclast Differentiation
• Cell Activation
• Cell Migration
• Diapedesis
• Response To Virus
• Adaptive Immune Response

PTMs

• Phosphorylation
• Acetylation

• Cleavage
• Methylation

Research Areas

• Immunology
• Innate Immunity
• Protein Kinase

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/IRAK3

Boster Bio: Best Uses of the IRAK3 Marker

High-affinity primary antibodies are the first step to achieving these desired results. Boster has a variety of high-affinity primary antibody for your research needs. You can also apply for credits and submit your results for special samples or applications. This method is available to scientists around the world. Boster Bio: Best Uses for the IRAK3 Marker is a good option if you are looking for a high-affinity prima antibody.

Primary antibodies of high-affinity

Recent studies have shown IRAK3 inhibits TNFa and IL-6 protein expressions in mouse bone marrow derived macrophages. These findings are in contradiction to a meta-analysis that found that IRAK3 does no affect TNF-a expression in mouse cell lines at LT. However, these findings do not rule out other possibilities.

Researchers used human primary cell lines to detect IL-12p40, in the absence or presence IRAK3. The antibody was able to detect the endogenous levels of IRAK. Although it is not 100% specific, the antibody does identify an important target for in vitro inflammation detection. IRAK3 is involved the regulation of inflammation, and is a negative regulator inflammatory reactions.

IRAK3 plays a part in the pathophysiology for sepsis. This dysregulated immune response leads to organ damage, and dysfunction. The immune system becomes immune-suppressed over time, resulting in an immune response that is not responsive to pathogens. IRAK3 regulates sepsis by playing a critical role in regulating the immune system. In fact IRAK3 mRNA expression levels are elevated in blood from sepsis victims.

In this study, we used a 9-choice-three live-cell barcoding strategy to eliminate technical variability. We produced polyclonal antibodies using a restricted combinatorial nine-choice-3 live cells barcoding strategy. These antibodies were purified using protein A or peptide affinity chromatography. These antibodies are listed in Supplementary Tables 7 and 3.

The study of the effects that proteins have on gene expression can also be done using genetic tools, such as gene knockout or gene silencing. In the case IRAK3 mice, RNAi suppresses NFKB activity in the LT/IT, which is correlated IL-6 secretion. IRAK3 knockout mice are more likely to inhibit NFkB expression.

IRAK3Marker

A wide variety of tissues can express the IRAK3 gene, including bone marrow and lung. Many of its functions involve cell signaling. IRAK3 inhibits NFKB transcription when inducible in human tumors. It also decreases the expression of inflammatory mediators. There are some limitations to this drug, despite its many benefits.

IRAK3 (or pseudokinase) has many functions. It is an important negative regulator to Myddosome-signaling and is involved in allergic swelling and early asthma. It has a death and a Cterminal domain containing TRAF6-binding spots. It can therefore engage the Myddosome complex, suppress signaling through TRAF6 and is capable of doing so.

The gene silencing and knockout techniques are useful for studying the effects of proteins. Two studies with mouse cell line models produced contradictory results. One study found that IRAK3 had a decrease in NFKB-reporter gene transcription in the cell, while another showed a slight increase. This is good news to IRAK3 users.

IRAK3 also plays a role in the pathophysiology and treatment of sepsis. In this disease, dysregulated cytokine production responses lead to organ injury and dysfunction. These events are followed immunosuppression, which is characterized by irresponsiveness of pathogens. Numerous studies have shown increased levels of IRAK3 from blood samples taken from patients with severe sepsis.

IRAK is a fundamental part of the vertebrate innate defense system. This system evolved to protect against pathogens. Toll-like or TLRs are responsible for controlling IRAK signaling. TLRs recognize generic molecular structures. These receptors are converged on interleukin-1 receptor-associated kinases (TLRs), which coordinate multiple pathways of inflammatory response and priming the adaptive immune system. Evidence is mounting that IRAK signaling is involved with the development of nonsmall-cell lung carcinoma.

Future studies should address IRAK1 and IRAK4 scaffolding functions, refine the role of IRAK2 in human malignancy, and investigate IRAK degraders. These studies will ultimately inform and clarify the optimal target selection. These studies may also resolve the debate over IRAK degraders or IRAK family members. Further research is needed to identify which IRAK family members have signaling redundancy.