uPAR: a versatile signalling orchestrator
By F. Blasi, Peter Carmeliet. Nature reviews. Molecular cell biology, 2002
1,285 citations recorded by the source corpus.
Subfields: Cancer Research, Hematology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/c9d1e1caa0dc04e26952eafa6f514589bf20bcb7
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
- Rakesh K. Jain
- Peter Carmeliet
- J. Campisi
- C. Esmon
- E. Koivunen
- Robert B. West
- M. Björklund
- Howard Y. Chang
In Hematology
In Molecular Biology
- Rakesh K. Jain
- Peter Carmeliet
- J. Campisi
- Patrick O. Brown
- P. Desprez
- Jean-Philippe Coppé
- Howard Y. Chang
- David Botstein
Citations in the corpus
- Molecular mechanisms and clinical applications of angiogenesis (2011, background): “For instance, loss of the inhibitor PAI-1 prevents vessel branching because excessive ECM breakdown leaves no matrix support for the sprou”
- Gene Expression Signature of Fibroblast Serum Response Predicts Human Cancer Progression: Similarities between Tumors and Wounds (2004, background): “PLAUR, also known as urokinase-type plasminogen activator receptor, is a well- characterized receptor for matrix-degrading proteases that has been implicated in tumor cell invasion (Blasi and Carmeliet 2002; Sidenius and Blasi 2003).”
- Reduction of macrophage infiltration and chemoattractant gene expression changes in white adipose tissue of morbidly obese subjects after surgery-induced weight loss. (2005, background): “Several chemokines, such as MCP-1 and CSF-3, but in addition other hitherto undefined factors, may be involved in macrophage recruitment into scWAT (5,31,43,44).”
- Integrin signalling during tumour progression (2004, background): “Plasmin, in turn, degrades ECM components both directly and through the activation of MMP”
- Gelatinase-mediated migration and invasion of cancer cells. (2005, background): “This has been well established with the uPA/uPAR system (Blasi and Carmeliet, 2002) and evidence is accumulating that the MMPs function similarily (Cao et al.”
- Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “Another family of proteases involved in carcinogenesis and present in the SASP are serine proteases and regulators of the plasminogen activation pathway: urokinase- or tissue-type plasminogen activators (uPA or tPA), the uPA receptor (uPAR), and inhibitors of these serine proteases (PAI-1 and -2) [6”
- Inflammation and coagulation (2010, background): “In addition, u-PAR exhibits protease-independent properties, involving transmembrane signal transduction after binding to various ligands, such as vitronectin and macrophage 1 antigen, which leads to cytokine and growth factor production (108).”
- The interactions between inflammation and coagulation (2005, background): “…plasminogen activator (u-PA) and its receptor (u-PAR) are involved in these processes. u-PAR is involved in leucocyte adhesion to either the vessel wall or extracellular matrix. u-PAR binding to Mac-1 or vitronectin leads to increased cytokine and growth factor production (Blasi & Carmeliet, 2002).”
- Basic and therapeutic aspects of angiogenesis. (2011, neutral): “Control of these proteinases is essential for sprouting, given that excessive degradation of the extracellular matrix, as occurs in plasminogen activator inhibitor 1 (PAI1) deficiency, leaves too little matrix support for the branch to sprout (Blasi and Carmeliet, 2002).”
- Regulation of cell signalling by uPAR (2010, background): “Early work in this field is discussed in previous publication”
- Molecular mechanisms of glioma invasiveness: the role of proteases (2003, neutral): “cgi?/&Q=CAV1%20or%20cav2%20or%20cav3&ORG=Hs">caveolin and G-protein-coupled receptor”