The disintegrin-like metalloproteinase ADAM10 is involved in constitutive cleavage of CX3CL1 (fractalkine) and regulates CX3CL1-mediated cell-cell adhesion.
By C. Hundhausen, D. Misztela, T. Berkhout, N. Broadway, P. Saftig, K. Reiss, D. Hartmann, F. Fahrenholz, R. Postina, V. Matthews and 3 more. Blood, 2003
741 citations recorded by the source corpus.
Subfields: Immunology, Immunology and Allergy, Oncology
View Paper: https://www.semanticscholar.org/paper/c1d7c4ad86862452b89c0ea7a4640343659fcdc0
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In Immunology
- R. Ransohoff
- Steffen Jung
- A. Cardona
- Dan R. Littman
- J. McGuire
- A. Manicone
- Berislav Zlokovic
- F. Geissmann
In Immunology and Allergy
In Oncology
Citations in the corpus
- Control of microglial neurotoxicity by the fractalkine receptor (2006, background): “In support of this concept, we found >300 pg of soluble CX3CL1 per milligram of aqueous extracts of the adult mouse brain (data not shown), and others have reported the presence in the CNS of ADAM10, the catalyst of constitutive CX3CL1 releas”
- Matrix metalloproteinases as modulators of inflammation. (2008, background): “Fractalkine can exist as a membrane-anchored adhesion molecule, and as a soluble form shed from the cell membrane by ADAM10 and ADAM 17 that functions as a chemoattractant [44,45].”
- The ADAM metalloproteinases (2008, background): “This compound was used to provide evidence that ADAM10 is involved in constitutive shedding of IL6R from cells, whereas PMA-stimulated shedding was inhibited by GW280264X, a mixed ADAM10/ADAM-17 inhibitor (Hundhausen et al., 2003; Ludwig et al., 2005).”