Metalloprotease‐disintegrin ADAM8: Expression analysis and targeted deletion in mice

By Kristine Kelly, G. Hutchinson, D. Nebenius-Oosthuizen, Andrew J. H. Smith, J. Bartsch, K. Horiuchi, Andrea Rittger, K. Manova, Andrew J. P. Docherty, C. Blobel. 2005

128 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology and Allergy, Molecular Biology

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In Cancer Research

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

In Immunology and Allergy

1. S. Zhong
2. R. Khalil

In Molecular Biology

1. M. Handsley
2. D. Edwards
3. S. Zhong
4. R. Khalil
5. 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): “Although ADAM-8−/− mice develop and grow normally without a disease phenotype [63], ADAM-8 could contribute to cardiac inflammation as its levels are increased in the periinfarct myocardium following myocardial infarction, which is often associated with infiltration of inflammatory cells [64].”
• 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 ].”
• The ADAM metalloproteinases (2008, background): “Viable, fertile, no pathology (reduced CHL-1 shedding in brain) Kelly et al.”