ArticleMolecular and cellular biology2002
The response of c-jun/AP-1 to chronic hypoxia is hypoxia-inducible factor 1 alpha dependent.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 105 citations in OpenAlex.
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- Enhancement of melanoma aggressiveness via p38-MAPK, HIF-1α pathways, and metabolic reprogramming induced by Candida albicans.Scientific reports · 2025Article
- Mapping SET1B chromatin interactions with DamID using DamMapper, a comprehensive Snakemake workflow.BMC genomics · 2025Article
- Oxidative Stress and Inflammation in Hypoxemic Respiratory Diseases and Their Comorbidities: Molecular Insights and Diagnostic Advances in Chronic Obstructive Pulmonary Disease and Sleep Apnea.Antioxidants (Basel, Switzerland) · 2025Review
- Spatial epigenomic niches underlie glioblastoma cell state plasticity.bioRxiv : the preprint server for biology · 2025Article
- Hypoxia-induced conversion of sensory Schwann cells into repair cells is regulated by HDAC8.Nature communications · 2025Article
- A brain organoid/ALL coculture model reveals the AP-1 pathway as critically associated with CNS involvement of BCP-ALL.Blood advances · 2024Article
- The Relationship between Circadian Rhythm and Cancer Disease.International journal of molecular sciences · 2024Review
- Fusobacterium nucleatum infection modulates the transcriptome and epigenome of HCT116 colorectal cancer cells in an oxygen-dependent manner.Communications biology · 2024Article
- Hypoxia-induced activation of NDR2 underlies brain metastases from Non-Small Cell Lung Cancer.Cell death & disease · 2023Article
- Role of Interleukin(IL)-6 in NK Activity to Hypoxic-Induced Highly Invasive Hepatocellular Carcinoma(HCC) Cells.Journal of microbiology and biotechnology · 2023Article
- HIF activation enhances FcγRIIb expression on mononuclear phagocytes impeding tumor targeting antibody immunotherapy.Journal of experimental & clinical cancer research : CR · 2022Article
- Can We Predict Differentiated Thyroid Cancer Behavior? Role of Genetic and Molecular Markers.Medicina (Kaunas, Lithuania) · 2021Review
- Chronic and Cycling Hypoxia: Drivers of Cancer Chronic Inflammation through HIF-1 and NF-κB Activation: A Review of the Molecular Mechanisms.International journal of molecular sciences · 2021Review
- PERK-mediated expression of peptidylglycine α-amidating monooxygenase supports angiogenesis in glioblastoma.Oncogenesis · 2020Article
- Hypoxia-Induced Epithelial-Mesenchymal Transition in Cancers: HIF-1α and Beyond.Frontiers in oncology · 2020Review
- ERK Regulates HIF1α-Mediated Platinum Resistance by Directly Targeting PHD2 in Ovarian Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Functional cooperation between HIF-1α and c-Jun in mediating primary and acquired resistance to gefitinib in NSCLC cells with activating mutation of EGFR.Lung cancer (Amsterdam, Netherlands) · 2018Article
- Thyroid hormone and the brain: Mechanisms of action in development and role in protection and promotion of recovery after brain injury.Pharmacology & therapeutics · 2018Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Hypoxia (low-oxygen tension) is an important physiological stress that influences responses to a wide range of pathologies, including stroke, infarction, and tumorigenesis. Prolonged or chronic hypoxia stimulates expression of the stress-inducible transcription factor gene c-jun and transient activation of protein kinase and phosphatase activities that regulate c-Jun/AP-1 activity. Here we describe evidence obtained by using wild-type and HIF-1 alpha nullizygous mouse embryonic fibroblasts (mEFs) that the induction of c-jun mRNA expression and c-Jun phosphorylation by prolonged hypoxia are completely dependent on the presence of the oxygen-regulated transcription factor hypoxia-inducible factor 1 alpha (HIF-1 alpha). In contrast, transient hypoxia induced c-jun expression in both types of mEFs, showing that the early or rapid induction of this gene is independent of HIF-1 alpha. These findings indicate that the c-jun gene has a biphasic response to hypoxia consisting of inductions that depend on the degree or duration of exposure. To more completely define the relationship between prolonged hypoxia and c-Jun phosphorylation, we used mEFs from mice containing inactivating mutations of critical phosphorylation sites in the c-Jun N-terminal region (serines 63 and 73 or threonines 91 and 93). Exposure of these mEFs to prolonged hypoxia demonstrated an absolute requirement for N-terminal sites for HIF-1 alpha-dependent phosphorylation of c-Jun. Taken together, these findings suggest that c-Jun/AP-1 and HIF-1 cooperate to regulate gene expression in pathophysiological microenvironments.
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