Expression of developmentally regulated endothelial cell locus 1 was induced by tumor-derived factors including VEGF
Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 333, Issue: 3, Page: 990-995
2005
- 19Citations
- 12Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations19
- Citation Indexes19
- 19
- CrossRef16
- Captures12
- Readers12
- 12
Article Description
Developmentally regulated endothelial cell locus 1 (Del1) is a new angiogenic molecules expressed specifically in early embryonic endothelial cells. We investigated the relationship between Del1 and tumor cell-derived vascular endothelial growth factor (VEGF). Dunn osteosarcoma cells and high- and low-metastatic murine sarcoma cells did not express Del1. However, the expression of Del1 was observed in these primary tumor tissues and the pulmonary metastatic tissues after subcutaneous inoculation in vivo. Every tumor cell-conditioned medium containing VEGF induced the expression of Del1 in murine lung microvascular endothelial (MLE) cells, although control MLE cells did not express Del1. The anti-mouse VEGF monoclonal antibody inhibited the induction of the Del1 expression. In addition, mouse recombinant interleukin-1α and tumor necrosis factor-α also induced Del1 in MLE cells. Del1 may play an important role in tumor angiogenesis through the effects of tumor-derived factors including VEGF.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006291X05012106; http://dx.doi.org/10.1016/j.bbrc.2005.06.009; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=20744451274&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/15964546; https://linkinghub.elsevier.com/retrieve/pii/S0006291X05012106; https://dx.doi.org/10.1016/j.bbrc.2005.06.009
Elsevier BV
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