ArticleFEBS letters2009
Suppression of Tie-1 in endothelial cells in vitro induces a change in the genome-wide expression profile reflecting an inflammatory function.
Article in FEBS letters, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- FLI1 regulates radiotherapy resistance in nasopharyngeal carcinoma through TIE1-mediated PI3K/AKT signaling pathway.Journal of translational medicine · 2023Article
- Effect of Maternal Obesity in Mice on IL-6 Levels and Placental Endothelial Cell Homeostasis.Nutrients · 2020Article
- The Roles of H19 in Regulating Inflammation and Aging.Frontiers in immunology · 2020Review
- Therapeutic targeting of the angiopoietin-TIE pathway.Nature reviews. Drug discovery · 2017Review
- Tie1: an orphan receptor provides context for angiopoietin-2/Tie2 signaling.The Journal of clinical investigation · 2016Article
- Tie1 controls angiopoietin function in vascular remodeling and inflammation.The Journal of clinical investigation · 2016Article
- Tie-1: A potential target for anti-angiogenesis therapy.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015Review
- Tie1 deletion inhibits tumor growth and improves angiopoietin antagonist therapy.The Journal of clinical investigation · 2014Article
- Role of Tie1 in shear stress and atherosclerosis.Trends in cardiovascular medicine · 2011Review
- Tie1 attenuation reduces murine atherosclerosis in a dose-dependent and shear stress-specific manner.The Journal of clinical investigation · 2011Article
- Gene expression profiling identifies inflammation and angiogenesis as distinguishing features of canine hemangiosarcoma.BMC cancer · 2010Article
- XL-184, a MET, VEGFR-2 and RET kinase inhibitor for the treatment of thyroid cancer, glioblastoma multiforme and NSCLC.IDrugs : the investigational drugs journal · 2010Review
- Using transcriptomics to identify and validate novel biomarkers of human skeletal muscle cancer cachexia.Genome medicine · 2010Article
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 1 institution in 1 country.
Funding
Abstract
Tie-1 is an endothelial specific receptor tyrosine kinase that is upregulated in diseases such as atherosclerosis and rheumatoid arthritis. We recently demonstrated that Tie-1 induced a proinflammatory response when overexpressed in endothelial cells. Here, we used a complementary approach and suppressed endogenous Tie-1 expression in endothelial cells to examine its function by microarray analysis. Tie-1 appeared to govern expression of many genes involved in inflammation. Expression knockdown of Tie-1 significantly reduced endothelial conditioned medium ability to stimulate MCP-1 production in U937 cells. Collectively, our results support the notion that Tie-1 has an inflammatory function in endothelial cells.
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.