Potential Role for ADAM15 in Pathological Neovascularization in Mice

By K. Horiuchi, G. Weskamp, L. Lum, H. Hammes, H. Cai, T. Brodie, T. Ludwig, R. Chiusaroli, R. Baron, K. Preissner and 2 more. 2003

192 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. R. Khalil
2. S. Zhong
3. D. Edwards

In Molecular Biology

1. R. Khalil
2. S. Zhong
3. D. Edwards
4. S. Eguchi
5. H. Ohtsu
6. P. Dempsey
7. M. Handsley
8. C. Pennington

In Oncology

1. S. Zhong
2. R. Khalil
3. D. Edwards
4. S. Eguchi
5. H. Ohtsu
6. P. Dempsey
7. M. Handsley
8. C. Pennington

Citations in the corpus

• A Disintegrin and Metalloproteinase (ADAM) and ADAM with Thrombospondin Motifs (ADAMTS) Family in Vascular Biology and Disease (2019, background): “ADAM-15−/− mice have been developed, and while no overt phenotype is found, tumor cell migration and invasion are reduced in these mice [81].”
• Essential Role for ADAM19 in Cardiovascular Morphogenesis (2004, background): “ADAMs (mnemonic for a disintegrin and metalloprotease) are membrane-anchored glycoproteins with key roles in fertilization, neurogenesis, angiogenesis, Alzheimer’s disease, and the release of proteins such as epidermal growth factor (EGF) receptor ligands and tumor necrosis factor family members fro”
• Metalloprotease‐disintegrin ADAM8: Expression analysis and targeted deletion in mice (2005, background): “ADAM15 has a role in pathological neovascularization in mice (Horiuchi et al., 2003), whereas ADAM19 is essential for cardiovascular morphogenesis (Kurohara et al., 2004; Zhou et al., 2004).”
• A Disintegrin and Metalloprotease (ADAM): Historical Overview of Their Functions (2016, background): “Similarly, ADAM-15 depletion showed reduced pathological neovascularization and tumor metastasis [99,100].”
• ADAMs: key components in EGFR signalling and development (2005, background): “Regulation of ADAMs The central role of ADAMs in EGFR signalling, as well as their other known functions in development and diseas”
• ADAM15 contributes to atherosclerosis by mediating endothelial barrier dysfunction via Src family kinase activity (2012, background): “Since the initial report of ADAM15 expression in human endothelial cells (ECs)(10) and animal micro/macrovessels,(11) evidence has emerged for a role of this molecule in regulating cell–cell adhesion(12) and vascular functions.(8,9,11) In particular, ADAM15 supports lung cancer metastasis by promoti”
• ADAMs as mediators of EGF receptor transactivation by G protein-coupled receptors. (2006, background): “In ADAM15 / mice, the growth of implanted tumor cells was strongly inhibited, suggesting a role of ADAM15 in neovascularization (45).”
• Distinct roles for ADAM10 and ADAM17 in ectodomain shedding of six EGFR ligands (2004, methodology): “Genotyping was performed by Southern blot as described previously (Weskamp et al., 2002; Horiuchi et al., 2003; Kurisaki et al., 2003).”
• The ADAM metalloproteinases (2008, background): “Mice deficient in ADAM-15 show no overt phenotype, though tumour neovascularisation and growth was reduced (Horiuchi et al., 2003).”
• Antitumor and anti-angiogenic activity of the recombinant human disintegrin domain of A disintegrin and metalloproteinase 15. (2015, unknown): “In addition, the tumor sizes in the ADAM15 -/- mice were significantly smaller than those in the wild-type mice (15).”
• An Adam15 amplification loop promotes vascular endothelial growth factor‐induced ocular neovascularization (2008, background): “Despite expression of ADAM15 in developing vasculature, brain, and bone, Adam15 / mice are viable and appear normal, indicating that ADAM15 is not required for vascular development (9).”
• Deficits in spatial learning and motor coordination in ADAM11-deficient mice (2006, background): “In contrast, the functions of ADAM8, ADAM9, ADAM12 and ADAM15 are not essential for embryogenesis, suggesting a possible functional redundancy with other protease [ 7- 10 ].”
• ADAM‐15: a metalloprotease that mediates inflammation (2008, methodology): “(17) using HUVECs treated with vascular endothelial growth factor (VEGF) or basic fibroblast growth factor (bFGF), which are two potent angiogenic factors, for 3 and 9 h did not indicate that these two growth factors are involved in the regulation of ADAM-15 in endothelial cells and, therefore, in i”