TTC39B deficiency stabilizes LXR reducing both atherosclerosis and steatohepatitis

Joanne Hsieh, Masahiro Koseki (), Matthew M. Molusky, Emi Yakushiji, Ikuyo Ichi, Marit Westerterp, Jahangir Iqbal, Robin B. Chan, Sandra Abramowicz, Liana Tascau, Shunichi Takiguchi, Shizuya Yamashita, Carrie L. Welch, Gilbert Di Paolo, M. Mahmood Hussain, Jay H. Lefkowitch, Daniel J. Rader and Alan R. Tall ()
Additional contact information
Joanne Hsieh: Columbia University
Masahiro Koseki: Columbia University
Matthew M. Molusky: Columbia University
Emi Yakushiji: Columbia University
Ikuyo Ichi: Faculty of Core Research, Ochanomizu University
Marit Westerterp: Columbia University
Jahangir Iqbal: State University of New York Health Science Center at Brooklyn (SUNY Downstate Medical Center)
Robin B. Chan: Columbia University
Sandra Abramowicz: Columbia University
Liana Tascau: Columbia University
Shunichi Takiguchi: Perelman School of Medicine, University of Pennsylvania
Shizuya Yamashita: Cardiovascular Medicine, Osaka University Graduate School of Medicine
Carrie L. Welch: Columbia University
Gilbert Di Paolo: Columbia University
M. Mahmood Hussain: State University of New York Health Science Center at Brooklyn (SUNY Downstate Medical Center)
Jay H. Lefkowitch: Columbia University
Daniel J. Rader: Perelman School of Medicine, University of Pennsylvania
Alan R. Tall: Columbia University

Nature, 2016, vol. 535, issue 7611, 303-307

Abstract: In mice, deficiency in the high-density lipoprotein gene T39 stabilizes liver X receptor (LXR), reducing both atherosclerosis and steatohepatitis, suggesting that T39 inhibition could be an effective strategy for reducing these diseases.

Date: 2016
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DOI: 10.1038/nature18628

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