ReviewFrontiers in microbiology2017
Hijacking of the AP-1 Signaling Pathway during Development of ATL.
Review in Frontiers in microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers, 1 of them a synthesis that pooled it.
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
153 citing papers in PubMed, 1 synthesis or guideline pooled it, 254 citations in OpenAlex.
- Response of osteoblastic cells to low-level laser treatment: a systematic review.Lasers in medical science · 2022Pooled it
- Comprehensive analysis of mRNA-microRNA-lncRNA expression profiles in post-traumatic elbow heterotopic ossification using RNA sequencing and experimental validation.Annals of medicine · 2026Article
- FOSL2 drives transcriptional activation of super‑enhancer-regulatedMolecular medicine reports · 2026Article
- Fra-2 controls the response to the KRAS inhibitor MRTX-1133 in pancreatic ductal adenocarcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Interplay of oxidative stress and antioxidant mechanisms in cancer development and progression.Archives of toxicology · 2026Review
- MAFF as a potential novel protective factor against Parkinson's disease: evidence from Mendelian randomization and single-cell RNA sequencing.Frontiers in aging neuroscience · 2026Article
- Article
- FOSL1-PRMT1 transcriptional-epigenetic circuit promotes glioblastoma radioresistance via calcyphosine-mediated DNA repair and invasion.Molecular biomedicine · 2025Article
- Viral oncogenes drive biphenotypic lymphoproliferative malignancy in transgenic mice.Scientific reports · 2025Article
- Review
- Tissue-Specific Chromatin Accessibility Regions and Transcription Factor Binding Sites in Pig Brain and Endocrine Tissues.Molecular neurobiology · 2025Article
- Updated insights on ASK1 signaling: mechanisms, regulation, and therapeutic potential in diseases.Molecular and cellular biochemistry · 2025Review
- High exposure variance enables candidate biomarker detection in a small EWAS of methylmercury-exposed Peruvian adults.BMC genomic data · 2025Article
- Integrating UHPLC-QE-MS and Bioinformatics with Experimental Validation Reveals MAPK/FOS-Mediated Podocyte Apoptosis as the Key Mechanism ofPharmaceuticals (Basel, Switzerland) · 2025Article
- Machine learning combined with omics-based approaches reveals T-lymphocyte cellular fate imbalance in abdominal aortic aneurysm.BMC biology · 2025Article
- Therapeutic insights and molecular mechanism linking melatonin signaling and membranous nephropathy (Review).Biomedical reports · 2025Review
- Single-cell atlas reveals heterogeneous response to FcRn blockade in anti-AChR antibody-positive generalised myasthenia gravis.Clinical and translational medicine · 2025Article
- Epidermal Resident Memory T Cell Fitness Requires Antigen Encounter in the Skin.bioRxiv : the preprint server for biology · 2025Article
- Functional and molecular single-cell analyses implicate PRDM14 in the initiation of B cell leukemia in mice.Scientific reports · 2025Article
93 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T-cell leukemia (ATL). One way to address the pathology of the disease lies on conducting research with a molecular approach. In addition to the analysis of ATL-relevant signaling pathways, understanding the regulation of important and relevant transcription factors allows researchers to reach this fundamental objective. HTLV-1 encodes for two oncoproteins, Tax and HTLV-1 basic leucine-zipper factor, which play significant roles in the cellular transformation and the activation of the host's immune responses. Activating protein-1 (AP-1) transcription factor has been linked to cancer and neoplastic transformation ever since the first representative members of the Jun and Fos gene family were cloned and shown to be cellular homologs of viral oncogenes. AP-1 is a dimeric transcription factor composed of proteins belonging to the Jun (c-Jun, JunB, and JunD), Fos (c-Fos, FosB, Fra1, and Fra2), and activating transcription factor protein families. Activation of AP-1 transcription factor family by different stimuli, such as inflammatory cytokines, stress inducers, or pathogens, results in innate and adaptive immunity. AP-1 is also involved in various cellular events including differentiation, proliferation, survival, and apoptosis. Deregulated expression of AP-1 transcription factors is implicated in various lymphomas such as classical Hodgkin lymphomas, anaplastic large cell lymphomas, diffuse large B-cell lymphomas, and adult T-cell leukemia. Here, we review the current thinking behind deregulation of the AP-1 pathway and its contribution to HTLV-induced cellular transformation.
Indexed as
Identifiers
What Socratic 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 Socratic graph.