Target intelligence / Profile preview

Mitogen-activated protein kinase kinase 1 mRNA 3' untranslated region (MEK1 mRNA 3' UTR)

Target
MEK1 mRNA 3' UTR
Molecular classification
Nucleic acid, Messenger RNA (mRNA), Untranslated region (UTR)
01

Overview

The Mitogen-activated protein kinase kinase 1 (MEK1) mRNA 3' untranslated region (UTR) is a critical non-coding segment of the MAP2K1 transcript that governs the post-transcriptional fate of the message (NCBI Gene: 5604). This region contains specific binding sites for microRNAs, such as miR-424 and miR-1, as well as various RNA-binding proteins that collectively determine mRNA stability, localization, and translation efficiency (PubMed: 25613344, PubMed: 21822215). MEK1 is a central kinase within the MAPK/ERK signaling pathway, which is a primary regulator of cell proliferation, differentiation, and survival (UniProt: Q02750). Dysregulation or overexpression of MEK1 is a hallmark of many malignancies, including melanoma and colorectal cancer, and is also implicated in developmental disorders known as RASopathies. While traditional therapies focus on inhibiting the MEK1 protein's catalytic activity, targeting the 3' UTR with antisense oligonucleotides (ASOs) or miRNA mimics offers a strategy to reduce MEK1 protein synthesis at the source. This approach may help overcome resistance mechanisms associated with kinase domain mutations by inducing transcript degradation or blocking translation. Consequently, the MEK1 mRNA 3' UTR represents a high-value target for precision medicine in oncology and genetic disease management.

Other names
MAP2K1 mRNA 3' UTRMAP kinase kinase 1 mRNA 3' UTRMKK1 mRNA 3' UTRMAPK/ERK kinase 1 mRNA 3' untranslated region
02

Mechanism of action

Antisense-mediated mRNA degradation via RNase H recruitment or RNA interference-mediated translational repression and transcript decay by targeting regulatory motifs within the 3' UTR (PubMed: 25613344, PubMed: 21822215).

03

Biological functions

Regulation of mRNA stabilityRegulation of translationPost-transcriptional gene regulationSignal transduction regulation
04

Disease associations

CancerMelanomaColorectal cancerRASopathyCardiofaciocutaneous syndrome
05

Safety considerations

Off-target hybridization to homologous mRNA sequencesInnate immune activation via Toll-like receptorsSystemic delivery efficiency to target tissuesPotential hepatotoxicity associated with oligonucleotide therapies
06

Interacting drugs

Antisense oligonucleotides (experimental)

3 more in the full profile.

07

Biomarkers

MEK1 mRNA expression levelsMEK1 protein levelsPhosphorylated ERK1/2 (p-ERK1/2) levels

Beyond the preview

Go deeper on Mitogen-activated protein kinase kinase 1 mRNA 3' untranslated region (MEK1 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 Mitogen-activated protein kinase kinase 1 mRNA 3' untranslated region (MEK1 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