alexa Critical Roles Of The Histone Methyltransferase MLL4 In Metabolic Syndrome
ISSN: 2376-0419

Journal of Pharmaceutical Care & Health Systems
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10TH Asia-Pacific Pharma Congress
May 08-10, 2017 Singapore

Seunghee Lee
Seoul National University, South Korea
Posters & Accepted Abstracts: J Pharma Care Health Sys
DOI: 10.4172/2376-0419-C1-021
Abstract
The pathophysiologic continuum of non-alcoholic fatty liver disease begins with steatosis. Despite recent advances in our understanding of the gene regulatory program directing steatosis, how it is orchestrated at the chromatin level is unclear. PPARγ2 is a hepatic steatotic transcription factor induced by overnutrition. Here, we report that the histone H3 lysine 4 methyltransferase MLL4/ KMT2D directs overnutrition-induced murine steatosis via its coactivator function for PPARγ2. We demonstrate that overnutrition facilitates the recruitment of MLL4 to steatotic target genes of PPARγ2 and their transactivation via H3 lysine 4 methylation because PPARγ2 phosphorylated by overnutrition-activated ABL1 kinase shows enhanced interaction with MLL4. We further show that Pparg2 (encoding PPARγ2) is also a hepatic target gene of ABL1-PPARγ2-MLL4. Consistently, inhibition of ABL1 improves the fatty liver condition of mice with overnutrition by suppressing the pro-steatotic action of MLL4. Our results uncover a murine hepatic steatosis regulatory axis consisting of ABL1-PPARγ2-MLL4, which may serve as a target of anti-steatosis drug development.
Biography

Seunghee Lee is working as a Professor at Seoul National University in South Korea.

Email: [email protected]

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