ArticleOncogene2001
The Mad1 transcription factor is a novel target of activin and TGF-beta action in keratinocytes: possible role of Mad1 in wound repair and psoriasis.
Article in Oncogene, 2001. 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, 45 citations in OpenAlex.
- MAD1 deficiency accelerates hepatocellular proliferation via suppressing TGF-β signaling.Heliyon · 2024Article
- Review
- OVOL1 Influences the Determination and Expansion of iPSC Reprogramming Intermediates.Stem cell reports · 2019Article
- TCP10L synergizes with MAD1 in transcriptional suppression and cell cycle arrest through mutual interaction.BMB reports · 2016Article
- Receptor-interacting protein kinase 4 and interferon regulatory factor 6 function as a signaling axis to regulate keratinocyte differentiation.The Journal of biological chemistry · 2014Article
- Radiation induces diffusible feeder cell factor(s) that cooperate with ROCK inhibitor to conditionally reprogram and immortalize epithelial cells.The American journal of pathology · 2013Article
- TGFβ1 enhances MAD1 expression and stimulates promoter-bound Pol II phosphorylation: basic functions of C/EBP, SP and SMAD3 transcription factors.BMC molecular biology · 2011Article
- The tumor suppressor activity of IKKalpha in stratified epithelia is exerted in part via the TGF-beta antiproliferative pathway.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- IKKalpha, a critical regulator of epidermal differentiation and a suppressor of skin cancer.The EMBO journal · 2008Review
- GLI2-specific transcriptional activation of the bone morphogenetic protein/activin antagonist follistatin in human epidermal cells.The Journal of biological chemistry · 2008Article
- Regulation of the MAD1 promoter by G-CSF.Nucleic acids research · 2008Article
- IKKalpha is a critical coregulator of a Smad4-independent TGFbeta-Smad2/3 signaling pathway that controls keratinocyte differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Activin type 2 receptor restoration in MSI-H colon cancer suppresses growth and enhances migration with activin.Gastroenterology · 2007Article
- Article
- Myc regulates keratinocyte adhesion and differentiation via complex formation with Miz1.The Journal of cell biology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activin A, a member of the transforming growth factor beta (TGF-beta) superfamily, affects keratinocyte proliferation and differentiation in vitro and in vivo. However, little is known about the mechanisms of activin action in keratinocytes, and its target genes have not been identified. In this study, we demonstrate that activin A and TGF-beta1 directly induce the expression and activity of Mad1, an antagonist of the c-Myc transcription factor, in the human HaCaT keratinocyte cell line. Expression and activity of Mad1 was strongly induced by both factors in keratinocytes, although the intensity of induction was different for activin A and TGF-beta1. To determine a possible role of activin and TGF-beta in the regulation of mad1 expression in vivo, we analysed its expression during cutaneous wound repair when high levels of these factors are present. Expression of mad1 mRNA and protein, but not of other mad genes, increased significantly after skin injury, particularly in polymorphonuclear leukocytes and in suprabasal keratinocytes of the hyperproliferative epithelium. Elevated levels of mad1 mRNA were also detected in the hyperthickened epidermis of psoriatic patients. Since Mad1 regulates proliferation and/or differentiation of various cell types, our results suggest that this transcription factor mediates at least in the part the anti-mitotic and/or differentiation-inducing activities of TGF-beta and activin in keratinocytes.
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.