Target intelligence / Profile preview

Proto-oncogene c-Jun protein (c-Jun)

Target
c-Jun
Molecular classification
Transcription factor, Basic leucine zipper (bZIP) family, Activator protein-1 (AP-1) complex component
01

Overview

Proto-oncogene c-Jun protein (c-Jun) is a basic leucine zipper (bZIP) transcription factor and key component of the activator protein-1 (AP-1) complex. It regulates gene transcription in response to diverse extracellular stimuli, including growth factors, cytokines, cellular stress, and UV irradiation[1][2][3][7]. c-Jun forms homo- and heterodimers, most notably with Fos family proteins, to bind specific DNA sequences (AP-1 sites) and modulate genes involved in cell proliferation, apoptosis, and differentiation[1][3][4][6]. It is tightly controlled through phosphorylation by c-Jun N-terminal kinases (JNKs), linking it directly to key stress- and mitogen-activated pathways, with documented roles in oncogenesis and metabolic reprogramming in cancer[7][9]. c-Jun's frequent overactivity or dysregulation is implicated in numerous diseases, especially various cancers, making it a therapeutic target of major interest in cancer biology[1][9].

Other names
Jun proto-oncogeneAP-1 transcription factor subunitAP-1P39v-Jun avian sarcoma virus 17 oncogene homolog
02

Mechanism of action

Inhibition of upstream kinases (e.g., JNK) leads to decreased c-Jun activation/phosphorylation and transcriptional activity[8]. Targeting downstream metabolic pathways regulated by c-Jun, such as glutaminase inhibition, may selectively affect c-Jun-dependent tumors[9].

03

Biological functions

Regulation of gene transcriptionCell proliferationApoptosisCell survivalTumorigenesisDiferentiationSignal transduction
04

Disease associations

CancerInflammationNeurodegenerative diseaseOther (based on involvement in widespread signaling pathways)
05

Safety considerations

Broad involvement in cell survival and proliferation pathways presents risk for adverse effects such as impaired cell growth, differentiation, and tissue repair if completely inhibited[1][7].
06

Interacting drugs

Indirect: c-Jun is not a direct drug target for approved drugs, but its activity is modulated by inhibitors of upstream kinases such as JNK inhibitors[8].

1 more in the full profile.

07

Biomarkers

c-Jun expression levels (for cancer prognosis and therapy selection)[9]Phosphorylation status of c-Jun (for pathway activation)

Beyond the preview

Go deeper on Proto-oncogene c-Jun protein (c-Jun).

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 Proto-oncogene c-Jun protein (c-Jun).

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