TNF-α Upregulates IKKε Expression via the Lin28B/let-7a Pathway to Induce Catecholamine Resistance in Adipocytes.

08:00 EDT 1st April 2019 | BioPortfolio

Summary of "TNF-α Upregulates IKKε Expression via the Lin28B/let-7a Pathway to Induce Catecholamine Resistance in Adipocytes."

Overexpression of inhibitor of nuclear factor kappa-B kinase subunit epsilon (IKKε) contributes to blunted catecholamine-induced lipolysis. Tumor necrosis factor α (TNF-α) upregulates adipose IKKε expression to inhibit stimulated lipolysis, which can be reversed by IKKε inhibitors. This study investigated adipose IKKε expression in children with and without obesity and potential involvement of the Lin28B/let-7a axis in posttranscriptional regulation of TNF-α-stimulated IKKε in adipocytes.


Journal Details

This article was published in the following journal.

Name: Obesity (Silver Spring, Md.)
ISSN: 1930-739X


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Medical and Biotech [MESH] Definitions

Cell surface proteins that bind catecholamines with high affinity and trigger intracellular changes which influence the behavior of cells. The catecholamine messengers epinephrine, norepinephrine, and dopamine are synthesized from tyrosine by a common biosynthetic pathway.

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A group of membrane transport proteins that transport biogenic amine derivatives of catechol across the PLASMA MEMBRANE. Catecholamine plasma membrane transporter proteins regulate neural transmission as well as catecholamine metabolism and recycling.

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