ADAMs: key components in EGFR signalling and development

By C. Blobel. 2005

1,114 citations recorded by the source corpus.

Subfields: 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 Molecular Biology

1. R. Khalil
2. S. Zhong
3. S. Takeda
4. J. Guan
5. M. Handsley
6. Carlos Fernandez-Patron
7. P. Dempsey
8. S. Apte

In Oncology

1. S. Zhong
2. M. Handsley
3. Carlos Fernandez-Patron
4. J. Guan
5. P. Dempsey
6. S. Apte
7. D. Edwards
8. Pu Zhang

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 is also related to vessel formation, and has been shown to induce the expression of vascular endothelial growth factor (VEGF), VEGFR1 and VEGFR2, which are closely related to angiogenesis [79].”
• The ADAM metalloproteinases (2008, background): “In part this may involve ligand solubilisation to allow diffusion and action in a paracrine fashion, but by analogy with the ephrin-A5/EphA3 signalling scenario discussed earlier (Janes et al., 2005) it is possible that ADAM-17-mediated cleavage of the TGFa/EGFR complex may be necessary to elicit EG”
• ADAMs family and relatives in cardiovascular physiology and pathology. (2016, background): “As such, ADAMs are important mediators of cell signaling that determine cell fate, differentiation, proliferation and growth [10,11].”
• The Lack of ADAM17 Activity during Embryonic Development Causes Hemorrhage and Impairs Vessel Formation (2010, positive): “ADAM17, also referred to as Tumor necrosis factor Alpha Converting Enzyme (TACE, CD156b) [1], is the most studied member of this family and participates in the shedding of more than 40 different substrates [2–4].”
• Deletion of Cdc42 Enhances ADAM17-Mediated Vascular Endothelial Growth Factor Receptor 2 Shedding and Impairs Vascular Endothelial Cell Survival and Vasculogenesis (2013, background): “The ADAM family of proteases cleaves the ectodomains of growth factors and their receptors (42, 43).”
• ADAMs as mediators of EGF receptor transactivation by G protein-coupled receptors. (2006, background): “However, no evidence of pathological or developmental defects was observed in ADAM8 / , ADAM9 / , and ADAM33 / mice (9, 46).”
• ADAM15 regulates endothelial permeability and neutrophil migration via Src/ERK1/2 signalling. (2010, background): “ADAMs (a disintegrin and metalloprotease) are a family of type I transmembrane glycoproteins that have been implicated in inflammation, angiogenesis, and cancer growth and metastasis.(11,12)”
• The ErbB/HER family of protein-tyrosine kinases and cancer. (2014, background): “The ErbB/HER ligands generally act over short distances rom their sites of generation [28].”
• Targeting proteases: successes, failures and future prospects (2006, background): “, ectodomain shedding (that is, release of extracellular domains of integral membrane proteins from the cell surface by members of the ADAM (a disintegrin and metalloproteinase) famil”
• ADAM and ADAMTS gene expression in native and wound healing human lens epithelial cells (2010, background): “Several ADAM/ ADAMTS enzymes have roles in cell differentiation and cell guidance mechanisms during development [2,3].”