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Open Access Green as soon as Postprint is submitted to ZB.
A macrophage NBR1-MEKK3 complex triggers JNK-mediated adipose tissue inflammation in obesity.
Cell Metab. 20, 499-511 (2014)
The c-Jun NH(2)-terminal kinase (JNK) is a critical determinant of obesity-associated inflammation and glucose intolerance. The upstream mechanisms controlling this pathway are still unknown. Here we report that the levels of the PB1 domain-containing adaptor NBR1 correlated with the expression of proinflammatory molecules in adipose tissue from human patients with metabolic syndrome, suggesting that NBR1 plays a key role in adipose-tissue inflammation. We also show that NBR1 inactivation in the myeloid compartment impairs the function, M1 polarization, and chemotactic activity of macrophages; prevents inflammation of adipose tissue; and improves glucose tolerance in obese mice. Furthermore, we demonstrate that an interaction between the PB1 domains of NBR1 and the mitogen-activated kinase kinase 3 (MEKK3) enables the formation of a signaling complex required for the activation of JNK. Together, these discoveries identify an NBR1-MEKK3 complex as a key regulator of JNK signaling and adipose tissue inflammation in obesity.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Induced Insulin-resistance; Diet-induced Obesity; In-vivo; Glucose-intolerance; Signaling Adapter; Skeletal-muscle; Activation; Sensitivity; Cells; P62
ISSN (print) / ISBN
1550-4131
e-ISSN
1932-7420
Journal
Cell Metabolism
Quellenangaben
Volume: 20,
Issue: 3,
Pages: 499-511
Publisher
Elsevier
Publishing Place
Cambridge
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Obesity (IDO)