ArticleProceedings of the National Academy of Sciences of the United States of America1993
Vascular cell adhesion molecule 1: contrasting transcriptional control mechanisms in muscle and endothelium.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 87 citations in OpenAlex.
- Late vs. Early Preeclampsia.International journal of molecular sciences · 2025Review
- High mobility group box 1 (HMGB1) is a potential disease biomarker in cell and mouse models of Duchenne muscular dystrophy.Biology open · 2024Article
- Genome reading by the NF-κB transcription factors.Nucleic acids research · 2019Review
- Increased expression of vascular cell adhesion molecule 1 in muscle biopsy samples from juvenile dermatomyositis patients with short duration of untreated disease is regulated by miR-126.Arthritis and rheumatism · 2012Article
- Human promoter genomic composition demonstrates non-random groupings that reflect general cellular function.BMC bioinformatics · 2005Article
- The POU transcription factor Oct-1 represses virus-induced interferon A gene expression.Molecular and cellular biology · 2005Article
- Hox genes and their candidate downstream targets in the developing central nervous system.Cellular and molecular neurobiology · 2005Review
- Human vascular adhesion protein-1 in smooth muscle cells.The American journal of pathology · 1999Article
- Interferon enhances tumor necrosis factor-induced vascular cell adhesion molecule 1 (CD106) expression in human endothelial cells by an interferon-related factor 1-dependent pathway.The Journal of experimental medicine · 1998Article
- Interferon regulatory factor-2 is a transcriptional activator in muscle where It regulates expression of vascular cell adhesion molecule-1.The Journal of cell biology · 1998Article
- Distamycin prolongs E-selectin expression by interacting with a specific NF-kappaB-HMG-I(Y) binding site in the promoter.Nucleic acids research · 1997Article
- Cold shock domain proteins repress transcription from the GM-CSF promoter.Nucleic acids research · 1996Article
- Is rheumatoid arthritis a failure of B cell death in synovium?Annals of the rheumatic diseases · 1995Review
- Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes.The Journal of clinical investigation · 1995Article
- VLA-4 and lymphocyte trafficking in immune-inflammatory states: novel therapeutic approaches in allograft arteriopathy.Springer seminars in immunopathology · 1995Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Interaction between vascular cell adhesion molecule 1 (VCAM-1), which appears on the surface of endothelial cells in response to inflammation, and its integrin counter receptor, alpha 4 beta 1, on immune cells is responsible for targeting these immune cells to cytokine-stimulated endothelium. In addition to its role in the immune system, VCAM-1 is also expressed in a developmentally specific pattern on differentiating skeletal muscle, where it mediates cell-cell interactions important for myogenesis through interaction with alpha 4 beta 1. In contrast to endothelium, there is high basal expression of VCAM-1 in skeletal muscle cells and the expression is not cytokine-responsive. Here, we examine the molecular basis for these contrasting patterns of expression in muscle and endothelium, using VCAM-1 promoter constructs in a series of transfection assays. In endothelial cells, octamer binding sites act as silencers that prevent VCAM-1 expression in unstimulated cells. Tumor necrosis factor alpha overcomes the negative effects of these octamers and activates the promoter through two adjacent NF-kappa B binding sites. In muscle cells, a position-specific enhancer located between bp -21 and -5 overrides the effect of other promoter elements, resulting in constitutive VCAM-1 expression. A nuclear protein binds the position-specific enhancer in muscle but not endothelial cells; thus the pattern of expression of this protein could control enhancer activity.
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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.