Target intelligence / Profile preview

Interleukin-1 receptor-associated kinase 1 messenger RNA 3' untranslated region (IRAK1 mRNA 3'-UTR) (IRAK1 mRNA 3'-UTR)

Target
IRAK1 mRNA 3'-UTR
Molecular classification
Messenger RNA regulatory region, RNA
01

Overview

The Interleukin-1 receptor-associated kinase 1 (IRAK1) mRNA 3'-untranslated region (3'-UTR) is a critical regulatory segment that controls the expression of the IRAK1 protein, a key mediator in the Toll-like receptor (TLR) and Interleukin-1 receptor (IL-1R) signaling pathways (Taganov et al., 2006, Nature Immunology). This region contains specific binding sites for microRNAs, most notably miR-146a, which functions as a negative feedback regulator to prevent excessive inflammatory responses by inducing mRNA degradation or translational repression (Boldin et al., 2011, Journal of Experimental Medicine). In various pathological states, such as myelodysplastic syndromes and certain solid tumors, the regulatory control exerted through the 3'-UTR is often lost or bypassed, leading to IRAK1 protein overexpression and constitutive activation of the NF-kappaB pathway (Starczynowski et al., 2010, Nature Medicine). Therapeutic strategies targeting this mRNA region involve the use of microRNA mimics or antisense oligonucleotides designed to restore normal regulation or silence IRAK1 expression (Saba et al., 2014, Blood). By modulating the stability and translation of IRAK1 mRNA, these interventions aim to dampen chronic inflammation and inhibit the progression of IRAK1-dependent malignancies. Consequently, the IRAK1 mRNA 3'-UTR represents a strategic target for precision RNA-based therapies in immunology and oncology.

Other names
IRAK1 3'-UTRIRAK-1 3'-UTRInterleukin-1 receptor-associated kinase 1 3'-untranslated regionIRAK1 mRNA regulatory region
02

Mechanism of action

Post-transcriptional gene silencing via microRNA-mediated mRNA degradation or translational inhibition.

03

Biological functions

Regulation of gene expressionmRNA stabilityTranslation regulationImmune response signalingNF-kappaB signaling pathway
04

Disease associations

InflammationCancerAutoimmune diseaseSepsisMyelodysplastic syndromes (MDS)Breast cancer
05

Safety considerations

Off-target effects of RNA-based therapeuticsPotential for systemic immune suppressionDelivery challenges to target tissuesInduction of innate immune responses by synthetic RNA
06

Interacting drugs

miR-146a mimics

2 more in the full profile.

07

Biomarkers

IRAK1 protein expression levelsmiR-146a expression levelsNF-kappaB activation status

Beyond the preview

Go deeper on Interleukin-1 receptor-associated kinase 1 messenger RNA 3' untranslated region (IRAK1 mRNA 3'-UTR) (IRAK1 mRNA 3'-UTR).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Interleukin-1 receptor-associated kinase 1 messenger RNA 3' untranslated region (IRAK1 mRNA 3'-UTR) (IRAK1 mRNA 3'-UTR).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call