Community Academic Profiles - Faculty & Researchers

Bio

Honors & Awards

Medical Faculty Association?s Best Research Award, Third Place Winner, University of Miami (2019)
Stanford CVI Travel Award, Stanford Cardiovascular Institute (10/2019)
Wood-Whelan Research Fellowships, International Union of Biochemistry and Molecular Biology (IUBMB) (02/2017)
Predoctoral Fellowships, American Heart Association (AHA) (01/2016-12/2017)
Fellowships, Sangmyung University (03/1997-08/1997)

Professional Education

Doctor of Philosophy, University of Miami (2018)
Master of Arts, University of Kentucky (2011)
Master of Arts, SangMyung University (2002)
Bachelor of Arts, SangMyung University (2000)

Stanford Advisors

Thomas Quertermous, Postdoctoral Faculty Sponsor

Publications

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Mitochondrial MTG1 is necessary for proper human cardiomyocyte activity and zebrafish cardiac development. Comment to "Novel role of mitochondrial GTPases 1 in pathological cardiac hypertrophy" JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY Kim, H., Barrientos, A. 2019; 129: 1
View details for DOI 10.1016/j.yjmcc.2019.02.005

View details for Web of Science ID 000466833500001

View details for PubMedID 30763588
Human GTPBP10 is required for mitoribosome maturation NUCLEIC ACIDS RESEARCH Maiti, P., Kim, H., Tu, Y., Barrientos, A. 2018; 46 (21): 11423?37
Abstract

Most steps on the biogenesis of the mitochondrial ribosome (mitoribosome) occur near the mitochondrial DNA nucleoid, in RNA granules, which contain dedicated RNA metabolism and mitoribosome assembly factors. Here, analysis of the RNA granule proteome identified the presence of a set of small GTPases that belong to conserved families of ribosome assembly factors. We show that GTPBP10, a member of the conserved Obg family of P-loop small G proteins, is a mitochondrial protein and have used gene-editing technologies to create a HEK293T cell line KO for GTPBP10. The absence of GTPBP10 leads to attenuated mtLSU and mtSSU levels and the virtual absence of the 55S monosome, which entirely prevents mitochondrial protein synthesis. We show that a fraction of GTPBP10 cosediments with the large mitoribosome subunit and the monosome. GTPBP10 physically interacts with the 16S rRNA, but not with the 12S rRNA, and crosslinks with several mtLSU proteins. Additionally, GTPBP10 is indirectly required for efficient processing of the 12S-16S rRNA precursor transcript, which could explain the mtSSU accumulation defect. We propose that GTPBP10 primarily ensures proper mtLSU maturation and ultimately serves to coordinate mtSSU and mtLSU accumulation then providing a quality control check-point function during mtLSU assembly that minimizes premature subunit joining.

View details for DOI 10.1093/nar/gky938

View details for Web of Science ID 000456710000029

View details for PubMedID 30321378

View details for PubMedCentralID PMC6265488
MTG1 couples mitoribosome large subunit assembly with intersubunit bridge formation NUCLEIC ACIDS RESEARCH Kim, H., Barrientos, A. 2018; 46 (16): 8435?53
Abstract

Mammalian mitochondrial ribosomes (mitoribosomes) synthesize 13 proteins, essential components of the oxidative phosphorylation system. They are linked to mitochondrial disorders, often involving cardiomyopathy. Mitoribosome biogenesis is assisted by multiple cofactors whose specific functions remain largely uncharacterized. Here, we examined the role of human MTG1, a conserved ribosome assembly guanosine triphosphatase. MTG1-silencing in human cardiomyocytes and developing zebrafish revealed early cardiovascular lesions. A combination of gene-editing and biochemical approaches using HEK293T cells demonstrated that MTG1 binds to the large subunit (mtLSU) 16S ribosomal RNA to facilitate incorporation of late-assembly proteins. Furthermore, MTG1 interacts with mtLSU uL19 protein and mtSSU mS27, a putative guanosine triphosphate-exchange factor (GEF), to enable MTG1 release and the formation of the mB6 intersubunit bridge. In this way, MTG1 establishes a quality control checkpoint in mitoribosome assembly. In conclusion, MTG1 controls mitochondrial translation by coupling mtLSU assembly with intersubunit bridge formation using the intrinsic GEF activity acquired by the mtSSU through mS27, a unique occurrence in translational systems.

View details for DOI 10.1093/nar/gky672

View details for Web of Science ID 000450950500035

View details for PubMedID 30085276

View details for PubMedCentralID PMC6144824
Mitochondrial ribosomes in cancer SEMINARS IN CANCER BIOLOGY Kim, H., Maiti, P., Barrientos, A. 2017; 47: 67?81
Abstract

Mitochondria play fundamental roles in the regulation of life and death of eukaryotic cells. They mediate aerobic energy conversion through the oxidative phosphorylation (OXPHOS) system, and harbor and control the intrinsic pathway of apoptosis. As a descendant of a bacterial endosymbiont, mitochondria retain a vestige of their original genome (mtDNA), and its corresponding full gene expression machinery. Proteins encoded in the mtDNA, all components of the multimeric OXPHOS enzymes, are synthesized in specialized mitochondrial ribosomes (mitoribosomes). Mitoribosomes are therefore essential in the regulation of cellular respiration. Additionally, an increasing body of literature has been reporting an alternative role for several mitochondrial ribosomal proteins as apoptosis-inducing factors. No surprisingly, the expression of genes encoding for mitoribosomal proteins, mitoribosome assembly factors and mitochondrial translation factors is modified in numerous cancers, a trait that has been linked to tumorigenesis and metastasis. In this article, we will review the current knowledge regarding the dual function of mitoribosome components in protein synthesis and apoptosis and their association with cancer susceptibility and development. We will also highlight recent developments in targeting mitochondrial ribosomes for the treatment of cancer.

View details for DOI 10.1016/j.semcancer.2017.04.004

View details for Web of Science ID 000418223400008

View details for PubMedID 28445780

View details for PubMedCentralID PMC5662495
Methamphetamine-induced Occludin Endocytosis Is Mediated by the Arp2/3 Complex-regulated Actin Rearrangement JOURNAL OF BIOLOGICAL CHEMISTRY Park, M., Kim, H., Lim, B., Wylegala, A., Toborek, M. 2013; 288 (46): 33324?34
Abstract

Methamphetamine (METH) is a drug of abuse with neurotoxic and neuroinflammatory effects, which include disruption of the blood-brain barrier (BBB) and alterations of tight junction protein expression. This study focused on the actin cytoskeletal rearrangement as a modulator of METH-induced redistribution of tight junction protein occludin in brain endothelial cells. Exposure to METH resulted in a shift of occludin localization from plasma membranes to endosomes. These changes were accompanied by activation of the actin-related protein 2/3 (Arp2/3) complex, which stimulates actin polymerization by promoting actin nucleation. In addition, METH-induced coronin-1b phosphorylation diminishes the inhibitory effect of nonphosphorylated coronin-1b on actin nucleation. Blocking actin nucleation with CK-666, a specific inhibitor of the Arp2/3 complex, protected against METH-induced occludin internalization and increased transendothelial monocyte migration. Importantly, treatment with CK-666 attenuated a decrease in occludin levels in brain microvessels and BBB permeability of METH-injected mice. These findings indicate that actin cytoskeletal dynamics is detrimental to METH-induced BBB dysfunction by increasing internalization of occludin.

View details for DOI 10.1074/jbc.M113.483487

View details for Web of Science ID 000328841700047

View details for PubMedID 24081143

View details for PubMedCentralID PMC3829179
Cancer Prevention with Promising Natural Products: Mechanisms of Action and Molecular Targets ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY Pratheeshkumar, P., Sreekala, C., Zhang, Z., Budhraja, A., Ding, S., Son, Y., Wang, X., Hitron, A., Hyun-Jung, K., Wang, L., Lee, J., Shi, X. 2012; 12 (10): 1159?84
Abstract

Cancer is the second leading cause of death worldwide. There is greater need for more effective and less toxic therapeutic and preventive strategies. Natural products are becoming an important research area for novel and bioactive molecules for drug discovery. Phytochemicals and dietary compounds have been used for the treatment of cancer throughout history due to their safety, low toxicity, and general availability. Many active phytochemicals are in human clinical trials. Studies have indicated that daily consumption of dietary phytochemicals have cancer protective effects against carcinogens. They can inhibit, delay, or reverse carcinogenesis by inducing detoxifying and antioxidant enzymes systems, regulating inflammatory and proliferative signaling pathways, and inducing cell cycle arrest and apoptosis. Epidemiological studies have also revealed that high dietary intakes of fruits and vegetables reduce the risk of cancer. This review discusses potential natural cancer preventive compounds, their molecular targets, and their mechanisms of actions.

View details for DOI 10.2174/187152012803833035

View details for Web of Science ID 000311073800002

View details for PubMedID 22583402

View details for PubMedCentralID PMC4983770
Nucleotide divergence analysis of IGS region in Fusarium oxysporum and its formae speciales based on the sequence Mycobiology Kim, H., Min, B. 2004; 32 (3): 119-122
Variation of the Intergenetic Spacer (IGS) Region of Ribosomal DNA among Fusarium oxysporum formae species The Journal of Microbiology Kim, H., Choi, Y., Min, B. 2001; 39 (4): 265-272

Hyun-Jung Kim

Postdoctoral Research Fellow, Cardiovascular Medicine

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Hyun-Jung Kim

Postdoctoral Research Fellow, Cardiovascular Medicine

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