ArticleMolecular and cellular biochemistry2010
c-Jun-NH2 terminal kinase (JNK)-mediates AP-1 activation by thioredoxin: phosphorylation of cJun, JunB, and Fra-1.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- JUNB and JUND in Urological Cancers: A Literature Review.Current issues in molecular biology · 2025Review
- Emerging Evidence of the Significance of Thioredoxin-1 in Hematopoietic Stem Cell Aging.Antioxidants (Basel, Switzerland) · 2022Review
- Capn4 is induced by and required for Epstein-Barr virus latent membrane protein 1 promotion of nasopharyngeal carcinoma metastasis through ERK/AP-1 signaling.Cancer science · 2020Article
- PCR array profiling of antiviral genes in human embryonic kidney cells expressing human coronavirus OC43 structural and accessory proteins.Archives of virology · 2018Article
- Role of MAPK/MNK1 signaling in virus replication.Virus research · 2018Review
- Role of Thioredoxin in Age-Related Hypertension.Current hypertension reports · 2018Review
- The AP-1 transcription factor FOSL1 causes melanocyte reprogramming and transformation.Oncogene · 2017Article
- Nuclear Localization Signal and p53 Binding Site in MAP/ERK Kinase Kinase 1 (MEKK1).Journal of cellular biochemistry · 2015Article
- Hydrogen peroxide - production, fate and role in redox signaling of tumor cells.Cell communication and signaling : CCS · 2015Review
- Thioredoxin Activates MKK4-NFκB Pathway in a Redox-dependent Manner to Control Manganese Superoxide Dismutase Gene Expression in Endothelial Cells.The Journal of biological chemistry · 2015Article
- Bacterial protein AvrA stabilizes intestinal epithelial tight junctions via blockage of the C-Jun N-terminal kinase pathway.Tissue barriers · 2015Article
- 17β-Estradiol alters oxidative stress response protein expression and oxidative damage in the uterus.Molecular and cellular endocrinology · 2014Article
- Novel roles of reactive oxygen species in the pathogenesis of acute myeloid leukemia.Journal of leukocyte biology · 2013Review
- MAP/ERK kinase kinase 1 (MEKK1) mediates transcriptional repression by interacting with polycystic kidney disease-1 (PKD1) promoter-bound p53 tumor suppressor protein.The Journal of biological chemistry · 2010Article
- Differential gene expressions of the MAPK signaling pathway in enterovirus 71-infected rhabdomyosarcoma cells.The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious DiseasesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Thioredoxin (Trx) is a small ubiquitous protein, which has been shown to be involved in redox-dependent cellular functions. In this article, we demonstrate that the increased level of Trx induces AP-1 DNA binding in a redox-dependent manner by activating JNK subgroup of MAPKs. The majority of AP-1 DNA binding complex was found to be composed of cJun, JunB, and Fra-1. Increased expression of Trx resulted in phosphorylation of cJun, Jun B, and Fra-1. Further, increased expression of Trx induced the phosphorylation of MKK4 and MKK7 which are upstream kinases of the JNK signaling cascade. In co-transfection studies, AP-1-dependent luciferase reporter vector and pcDNA3-Trx increased luciferase activity demonstrating that increased expression of Trx increases AP-1 transactivation. In addition, dominant-negative JNK kinase (dnJNK/MKK4) or dominant-negative JNK (dnJNK) inhibited Trx-mediated AP-1 transactivation, as well as AP-1 DNA binding. Furthermore, transfection of kinase-dead MEKK1, an initiating kinase of the JNK pathway inhibited Trx-mediated AP-1 transactivation and DNA binding, suggesting that MEKK1 may mediate Trx-induced AP-1 activation. In contrast, wild-type MEKK1 overexpression did not inhibit Trx-mediated AP-1 activation. Taken together, our data demonstrate that increased expression of Trx induces MKK4/MKK7-dependent JNK activation, resulting in enhanced DNA binding, and transactivation of AP-1 transcription factor.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.