ArticleThe American journal of pathology1999
Vascular smooth muscle cells express the transcriptional corepressor NAB2 in response to injury.
Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 48 citations in OpenAlex.
- A promising nucleic acid therapy drug: DNAzymes and its delivery system.Frontiers in molecular biosciences · 2023Review
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- Dynamics of Protein Expression Reveals Primary Targets and Secondary Messengers of Estrogen Receptor Alpha Signaling in MCF-7 Breast Cancer Cells.Molecular & cellular proteomics : MCP · 2016Article
- Egr-1 expression during neointimal development in flow-associated pulmonary hypertension.The American journal of pathology · 2011Article
- Time course analysis of gene expression identifies multiple genes with differential expression in patients with in-stent restenosis.BMC medical genomics · 2011Article
- EGR1, EGR2, and EGR3 activate the expression of their coregulator NAB2 establishing a negative feedback loop in cells of neuroectodermal and epithelial origin.Journal of cellular biochemistry · 2010Article
- Article
- FGFR1 forms an FRS2-dependent complex with mTOR to regulate smooth muscle marker gene expression.Biochemical and biophysical research communications · 2009Article
- Pitavastatin suppresses mitogen activated protein kinase-mediated Erg-1 induction in human vascular smooth muscle cells.European journal of pharmacology · 2009Article
- Lung EC-SOD overexpression attenuates hypoxic induction of Egr-1 and chronic hypoxic pulmonary vascular remodeling.American journal of physiology. Lung cellular and molecular physiology · 2008Article
- DNAzymes and cardiovascular disease.British journal of pharmacology · 2008Review
- Differential regulation of NAB corepressor genes in Schwann cells.BMC molecular biology · 2007Article
- Transcription factor and kinase-mediated signaling in atherosclerosis and vascular injury.Current atherosclerosis reports · 2006Review
- Article
- Egr-1 is a major vascular pathogenic transcription factor in atherosclerosis and restenosis.Reviews in endocrine & metabolic disorders · 2004Review
- Inhibition of human breast carcinoma proliferation, migration, chemoinvasion and solid tumour growth by DNAzymes targeting the zinc finger transcription factor EGR-1.Nucleic acids research · 2004Article
- Regulation of smooth muscle phenotype.Current atherosclerosis reports · 2003Review
- Catalytic DNAs as potential therapeutic agents and sequence-specific molecular tools to dissect biological function.The Journal of clinical investigation · 2000Review
- High-level expression of Egr-1 and Egr-1-inducible genes in mouse and human atherosclerosis.The Journal of clinical investigation · 2000Article
- NAB2: a transcriptional brake for activated gene expression in the vessel wall?The American journal of pathology · 1999Article
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6 authors at 4 institutions in 2 countries.
Funding
Abstract
The early growth response 1 (Egr-1 or NGFI-A) gene product is a zinc finger protein transcription factor which has been implicated in the regulation of genes differentially expressed during the development of vascular disease. Egr-1 activity is regulated by alterations in the amount of protein, as well as protein-protein interactions with positive and negative transcriptional cofactors. NGFI-A-binding protein 2 (NAB2) is an example of a negative transcriptional cofactor capable of binding directly to Egr-1 and repressing Egr-1-mediated transcription. In this study, we show that NAB2 is rapidly and transiently expressed in vascular smooth muscle cells (VSMC) in response to the model agonist phorbol 12-myristate 13-acetate (PMA). This induction occurs at the protein as well as mRNA level, and the time course of induction trails closely behind that of Egr-1. NAB2 expression in VSMC is capable of inhibiting Egr-1 dependent gene expression in response to either PMA or fibroblastic growth factor-2 (FGF-2). In an in vivo model of mechanical arterial injury NAB2 levels also increase transiently in VSMC at a time when Egr-1 is elevated. It is possible that NAB2 is part of a negative-feedback mechanism which serves to down-regulate Egr-1-mediated gene transcription in injured VSMC.
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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.