A5028619599- Ubiquitin and proteasome pathways
- Cancer-related Molecular Pathways
- Autophagy in Disease and Therapy
- Cancer Research and Treatments
- Telomeres, Telomerase, and Senescence
- Protein Degradation and Inhibitors
- Endoplasmic Reticulum Stress and Disease
- CRISPR and Genetic Engineering
- PI3K/AKT/mTOR signaling in cancer
- Cancer, Hypoxia, and Metabolism
- Skin Protection and Aging
- Chromosomal and Genetic Variations
- Epigenetics and DNA Methylation
- Pluripotent Stem Cells Research
- RNA Interference and Gene Delivery
- Peptidase Inhibition and Analysis
- Retinal Development and Disorders
- Reliability and Agreement in Measurement
- HER2/EGFR in Cancer Research
- Statistical Methods in Epidemiology
- RNA regulation and disease
- Animal Genetics and Reproduction
- NF-κB Signaling Pathways
- Photoreceptor and optogenetics research
- Ocular Oncology and Treatments
Tribhuvan University Teaching Hospital
2024
Fate Therapeutics (United States)
2022
University of California, San Diego
2017-2021
Yonsei University
2010-2017
Sungkyunkwan University
2010
Seoul National University
2010
Augusta University
2004
Non-homologous end joining (NHEJ), and to a lesser extent, the error-free pathway known as homology-directed repair (HDR) are cellular mechanisms for recovery from double-strand DNA breaks (DSB) induced by RNA-guided programmable nuclease CRISPR/Cas. Since NHEJ is equivalent using duck tape stick two pieces of metals together, outcome this mechanism prone error. Any out-of-frame mutations or premature stop codons resulting extremely handy loss-of-function studies. Substitution mutation on...
Telomerase is a reverse transcriptase that consists of the telomerase RNA component (TERC) and catalytic subunit (TERT) specializes in elongation telomere ends. New evidence suggests beyond classical maintenance, TERT also possesses length-independent functions are executed via interaction with other binding proteins. One such reported TERT-interacting proteins mTOR, master nutrient sensor upregulated several cancers; however, physiological implications TERT-mTOR normal cellular processes as...
The molecular mechanism of memory formation remains a mystery. Here, we show that TERT, the catalytic subunit telomerase, gene knockout (Tert-/-) causes extremely poor ability in spatial formation. Knockdown TERT dentate gyrus adult hippocampus impairs processes, while overexpression facilitates it. We find plays critical role neural development including dendritic and neuritogenesis hippocampal newborn neurons. A monosynaptic pseudotyped rabies virus retrograde tracing method shows is...
Historically, the ubiquitin-proteasome system (UPS) and autophagy pathways were believed to be independent; however, recent data indicate that these engage in crosstalk. To date, players mediating this crosstalk have been elusive. Here, we show experimentally EI24 (EI24, associated transmembrane protein), a key component of basal macroautophagy/autophagy, degrades 14 physiologically important E3 ligases with RING (really interesting new gene) domain, whereas 5 other not degraded. Based on...
// Jung-Min Choi 1,* , Sushil Devkota Young Hoon Sung 1 and Han-Woong Lee 1,2 Department of Biochemistry, College Life Science Biotechnology, Yonsei University, Seoul 120-749, Korea, 2 Laboratory Animal Research Center, Korea * denotes equal contribution Correspondence: Lee, email: Keywords : EI24, EMT, Tumor progression, NF-κB Received September 26, 2013 Accepted November 16, Published 17, Abstract metastasis is a multistep process that requires the concerted activity discrete biological...
Abstract The role of telomerase reverse transcriptase (TERT) has been extensively investigated in the contexts aging and cancer. Interestingly, Tert −/− mice exhibit additional but unexpected aggressive depressive behaviors, implying potential involvement TERT function mood control. Our conditional rescue experiments revealed that behaviors originate from deficiency two distinct brain structures. Reactivation hippocampus was sufficient to normalize not mice. Conversely, re-expression medial...
Abstract Retinoblastoma (Rb) and p53 genes are mutated or inactivated in most human cancers mutually regulate each other. Recently, we reported that expression of diverse was altered Rb-deficient mouse embryonic fibroblasts (MEF). In this study, found Pierce1, a novel transcript upregulated MEFs, is transcriptional target p53. Although Pierce1 promoter did not respond to the ectopic E2F1, it strongly activated by via 2 cis-elements. Consistently, induced genotoxic stresses activate but...
The deficiency of retinoblastoma (Rb) gene deregulates E2F transcription factors and thus induces target genes directly or p53 indirectly via mouse p19Arf (or p14ARF in humans), an gene. Here, we identified that etoposide-induced 2.4 mRNA (Ei24)/p53-induced 8 (Pig8), a involved apoptosis autophagy, was up-regulated Rb−/− embryonic fibroblasts (MEFs). Ei24 promoter activated by E2F1 multiple E2F-responsive elements, independently the previously reported p53-responsive element. Chromatin...
Abstract KRAS-mutant non-small cell lung cancer (NSCLC) is a major subtype that leads to many cancer-related deaths worldwide. Although numerous studies on type NSCLC have been conducted, new oncogenic or tumor suppressive genes need be detected because large proportion of patients does not respond currently used therapeutics. Here, we show the tumor-promoting function cycle-related protein, PIERCE1, in NSCLC. Mechanistically, PIERCE1 depletion inhibits growth and AKT phosphorylation (pAKT)...
CRISPR-based active genetic elements, or gene-drives, copied via homology-directed repair (HDR) in the germline, are transmitted to progeny at super-Mendelian frequencies. Active elements also can generate widespread somatic mutations, but basis for such phenotypes remains uncertain. It is generally assumed that mutations generated by non-homologous end-joining (NHEJ), predominant double stranded break pathway cells. Here, we develop CopyCatcher systems Drosophila detect and quantify gene...
The His723Arg (H723R) mutation in SLC26A4, encoding pendrin, is the most prevalent East Asia, resulting DFNB4, an autosomal recessive type of genetic hearing loss. Although main pathological mechanism H723R was identified as a protein-folding defect there still no curative treatment for associated Here, we show that H723R-pendrin expression and activity are rescued by activation chaperonin DNAJC14. In vitro, DNAJC14 activated via Japanese encephalitis virus (JEV) inoculation,...
The rapid development of engineered nucleases such as zinc finger (ZFNs), transcription activator-like effector (TALENs), and the clustered regulated interspaced short palindromic repeats (CRISPR)/CRISPR-associated endonuclease 9 (Cas9) system has ushered in era 'renaissance precision genome engineering' with profound potential to generate mouse models human diseases. However, accumulating experience, some drawbacks that we must seriously consider have appeared along recent advances...
genes determine positional codes along the head-to-tail axis. Here, we replaced entire
Supplementary Figures 1-6 from Pierce1, a Novel p53 Target Gene Contributing to the Ultraviolet-Induced DNA Damage Response
Supplementary Figure Legends 1-6 from Pierce1, a Novel p53 Target Gene Contributing to the Ultraviolet-Induced DNA Damage Response
Supplementary Figures 1-6 from Pierce1, a Novel p53 Target Gene Contributing to the Ultraviolet-Induced DNA Damage Response
Supplementary Figure Legends 1-6 from Pierce1, a Novel p53 Target Gene Contributing to the Ultraviolet-Induced DNA Damage Response
<div>Abstract<p><i>Retinoblastoma (Rb)</i> and <i>p53</i> genes are mutated or inactivated in most human cancers mutually regulate each other. Recently, we reported that expression of diverse was altered <i>Rb</i>-deficient mouse embryonic fibroblasts (MEF). In this study, found <i>Pierce1</i>, a novel transcript upregulated MEFs, is transcriptional target p53. Although Pierce1 promoter did not respond to the ectopic E2F1, it...