Faculty

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Tin A Than, PhD, MD
Assistant Professor of Research Medicine
Medicine
HMR 612 Health Sciences Campus Los Angeles
+1 323 442 3175

Overview

Dr. Than's major areas of research interest include mitochondria biogensis, stress response and mitophagy in liver patho-physiology and developmental biology, and regulation of gene expression by reactive oxygen species and derivative DNA adducts in liver patho-physiology and developmental biology. His current research entails mitochondrial retrograde signaling and stress response, and mitochondrial biogenesis in liver diseases.

Dr. Than earned his medical degree from University of Yangon, Institute of Medicine. He then went on to earn his PhD in Free Radical Biology & Molecular Biology from Okayama University Graduate School of Medicine and Dentistry.

Publications

Antcin H Protects Against Acute Liver Injury Through Disruption of the Interaction of c-Jun-N-Terminal Kinase with Mitochondria. Antioxid Redox Signal. 2016 Oct 11. View in: PubMed

c-Jun N-terminal kinase mediates mouse liver injury through a novel Sab (SH3BP5)-dependent pathway leading to inactivation of intramitochondrial Src. Hepatology. 2016 Jun; 63(6):1987-2003. View in: PubMed

Targeting signal transduction pathways which regulate necrosis in acetaminophen hepatotoxicity. J Hepatol. 2015 Jul; 63(1):5-7. View in: PubMed

Sab (Sh3bp5) dependence of JNK mediated inhibition of mitochondrial respiration in palmitic acid induced hepatocyte lipotoxicity. J Hepatol. 2015 Jun; 62(6):1367-74. View in: PubMed

In vitro assays of mitochondrial function/dysfunction. Clin Pharmacol Ther. 2014 Dec; 96(6):665-8. View in: PubMed

JNK interaction with Sab mediates ER stress induced inhibition of mitochondrial respiration and cell death. Cell Death Dis. 2014; 5:e989. View in: PubMed

Regulation of drug-induced liver injury by signal transduction pathways: critical role of mitochondria. Trends Pharmacol Sci. 2013 Apr; 34(4):243-53. View in: PubMed

c-Jun N-terminal kinase (JNK)-dependent acute liver injury from acetaminophen or tumor necrosis factor (TNF) requires mitochondrial Sab protein expression in mice. J Biol Chem. 2011 Oct 7; 286(40):35071-8. View in: PubMed

Role of cAMP-responsive element-binding protein (CREB)-regulated transcription coactivator 3 (CRTC3) in the initiation of mitochondrial biogenesis and stress response in liver cells. J Biol Chem. 2011 Jun 24; 286(25):22047-54. View in: PubMed

Silencing glycogen synthase kinase-3beta inhibits acetaminophen hepatotoxicity and attenuates JNK activation and loss of glutamate cysteine ligase and myeloid cell leukemia sequence 1. J Biol Chem. 2010 Mar 12; 285(11):8244-55. View in: PubMed

Bevacizumab and chemotherapy for recurrent glioblastoma: a single-institution experience. Neurology. 2009 Apr 7; 72(14):1217-22. View in: PubMed

Taurine chloramine: a possible oxidant reservoir. Adv Exp Med Biol. 2009; 643:451-61. View in: PubMed

Effect of transgenic extrahepatic expression of betaine-homocysteine methyltransferase on alcohol or homocysteine-induced fatty liver. Alcohol Clin Exp Res. 2008 Jun; 32(6):1049-58. View in: PubMed

Endoplasmic reticulum stress and liver injury. Semin Liver Dis. 2007 Nov; 27(4):367-77. View in: PubMed

Physiological oxidants induce apoptosis and cell cycle arrest in a multidrug-resistant natural killer cell line, NK-YS. Leuk Lymphoma. 2003 Dec; 44(12):2109-16. View in: PubMed

Monochloramine inhibits the expression of E-selectin and intercellular adhesion molecule-1 induced by TNF-alpha through the suppression of NF-kappaB activation in human endothelial cells. Free Radic Res. 2002 Aug; 36(8):845-52. View in: PubMed

Monochloramine inhibits etoposide-induced apoptosis with an increase in DNA aberration. Free Radic Biol Med. 2001 Apr 15; 30(8):932-40. View in: PubMed

Monochloramine enhances Fas (APO-1/CD95)-induced apoptosis in Jurkat T cells. J Leukoc Biol. 2000 Jan; 67(1):46-52. View in: PubMed

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