Dataset Information


Adam17-Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling (macrophage)

ABSTRACT: Gene expression analysis in tissues of Adam17 hypomorphic and wildtype control C57BL/6 mice. Overall design: Gene expression level in primary macrophages of Adam17 hypomorphic (n = 8) and wildtype control C57BL/6 mice (n = 8).

INSTRUMENT(S): Illumina MouseRef-8 v2.0 expression beadchip

SUBMITTER: Bernd Henrik Northoff  

PROVIDER: GSE79999 | GEO | 2017-01-30



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Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.

Nicolaou Alexandros A   Zhao Zhen Z   Northoff Bernd H BH   Sass Kristina K   Herbst Andreas A   Kohlmaier Alexander A   Chalaris Athena A   Wolfrum Christian C   Weber Christian C   Steffens Sabine S   Rose-John Stefan S   Teupser Daniel D   Holdt Lesca M LM  

Arteriosclerosis, thrombosis, and vascular biology 20161222 2

<h4>Objective</h4>ADAM17 (a disintegrin and metalloproteinase 17) is a sheddase releasing different types of membrane-bound proteins, including adhesion molecules, cytokines, and their receptors as well as inflammatory mediators. Because these substrates modulate important mechanisms of atherosclerosis, we hypothesized that ADAM17 might be involved in the pathogenesis of this frequent disease.<h4>Approach and results</h4>Because Adam17-knockout mice are not viable, we studied the effect of Adam1  ...[more]

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