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|Title:||The role of ELKS isoforms in leptin and NF-κB signaling.||Authors:||Woo, Yissue.||Keywords:||DRNTU::Science::Biological sciences::Molecular biology
|Issue Date:||2012||Abstract:||Obesity had been linked to a state of constant low-grade systemic inflammation, and a series of metabolic disorders, like insulin insensitivity and leptin resistance. The origin of the state of low-grade inflammation was tied to various adipocyte-secreted adipokines, including leptin and TNF-α. One of the pathways of TNF-α signaling leads to the activation of IKKβ/NF-κB signaling, of which the protein, ELKS, was suspected to be involved. ELKS was hypothesized to be recruited in proximity to the leptin receptor, upon consistent induction by low doses of TNF-α, and affect the signaling pathway of the leptin receptor. ELKS was found to contribute to the inhibition of POMC promoter activity, the downstream target of leptin signaling, but did not affect the phosphorylation of STAT3, the secondary messenger of leptin receptor. ELKS’ interaction with IKKβ was confirmed, affirming the hypothesis of ELKS being co-recruited along with IKKβ. ELKS’ interaction with STAT3 was also observed, suggesting the role of physical interaction in the inhibition of STAT3 downstream activities. Although the observations reported might not be sufficiently conclusive, this study should receive further investigation to better illustrate ELKS’ role in leptin resistance, in the environment of low-grade inflammation.||URI:||http://hdl.handle.net/10356/49383||Rights:||Nanyang Technological University||Fulltext Permission:||restricted||Fulltext Availability:||With Fulltext|
|Appears in Collections:||SBS Student Reports (FYP/IA/PA/PI)|
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