• BMB Reports
• /
• v.28 no.6
• /
• pp.523-526
• /
• 1995

Administering ${\delta}-aminolevulinic$ acid (ALA) to isolated pea (Pisum sativum L.) chloroplasts resulted in an increase of heme synthesis in the heme branch of the tetrapyrrole pathway. At 0.1 mM ALA, in the presence of 1 mM $FeSO_4$ heme synthesis was stimulated up to 7 fold of that in the absence of $FeSO_4$. N-Methylmesoporphyrin IX (NMMP), a powerful inhibitor of ferrochelatase, inhibited heme synthesis by 95% at one micromolar concentration. The addition of A TP to the chloroplasts caused not only heme synthesis, but Mg-protoporphyrin IX synthesis in the chlorophyll branch of the tetrapyrrole pathway. In the presence of NMMP, however, inhibition of Mg-protoporphyrin IX synthesis was not observed whereas heme synthesis was inhibited completely.

• BMB Reports
• /
• v.51 no.4
• /
• pp.194-199
• /
• 2018

Mesenchymal stem cells (MSCs) have shown great potential in treating bone deficiency. Human adipose-derived stem cells (HASCs) are multipotent progenitor cells with multi-lineage differentiation potential. Human amnion-derived mesenchymal stem cells (HAMSCs) are capable of promoting osteogenic differentiation of MSCs. In this study, we investigated the effect of HAMSCs on HASCs by a transwell co-culture system. HAMSCs promoted proliferation, osteogenic differentiation, angiogenic potential and adiponectin (APN) secretion of HASCs. Moreover, the positive effect of HAMSCs was significantly inhibited by U0126, a highly selective inhibitor of extracellular signaling-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) signaling pathway. These observations suggested that HAMSCs induced bone regeneration in HASCs via ERK1/2 MAPK signaling pathway.

• Molecules and Cells
• /
• v.38 no.8
• /
• pp.669-676
• /
• 2015

Genome instability, primarily caused by faulty DNA repair mechanisms, drives tumorigenesis. Therapeutic interventions that exploit deregulated DNA repair in cancer have made considerable progress by targeting tumor-specific alterations of DNA repair factors, which either induces synthetic lethality or augments the efficacy of conventional chemotherapy and radiotherapy. The study of Fanconianemia (FA), a rare inherited blood disorder and cancer predisposition syndrome, has been instrumental in understanding the extent to which DNA repair defects contribute to tumorigenesis. The FA pathway functions to resolve blocked replication forks in response to DNA interstrand cross-links (ICLs), and accumulating knowledge of its activation by the ubiquitin-mediated signaling pathway has provided promising therapeutic opportunities for cancer treatment. Here, we discuss recent advances in our understanding of FA pathway regulation and its potential application for designing tailored therapeutics that take advantage of deregulated DNA ICL repair in cancer.

• Molecules and Cells
• /
• v.37 no.3
• /
• pp.196-201
• /
• 2014

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by the vascular remodeling of the pulmonary arterioles, including formation of plexiform and concentric lesions comprised of proliferative vascular cells. Clinically, PAH leads to increased pulmonary arterial pressure and subsequent right ventricular failure. Existing therapies have improved the outcome but mortality still remains exceedingly high. There is emerging evidence that the seven-transmembrane G-protein coupled receptor APJ and its cognate endogenous ligand apelin are important in the maintenance of pulmonary vascular homeostasis through the targeting of critical mediators, such as Kr$\ddot{u}$ppel-like factor 2 (KLF2), endothelial nitric oxide synthase (eNOS), and microRNAs (miRNAs). Disruption of this pathway plays a major part in the pathogenesis of PAH. Given its role in the maintenance of pulmonary vascular homeostasis, the apelin-APJ pathway is a potential target for PAH therapy. This review highlights the current state in the understanding of the apelin-APJ axis related to PAH and discusses the therapeutic potential of this signaling pathway as a novel paradigm of PAH therapy.

• BMB Reports
• /
• v.54 no.6
• /
• pp.285-294
• /
• 2021

The lymphatic vasculature plays important role in regulating fluid homeostasis, intestinal lipid absorption, and immune surveillance in humans. Malfunction of lymphatic vasculature leads to several human diseases. Understanding the fundamental mechanism in lymphatic vascular development not only expand our knowledge, but also provide a new therapeutic insight. Recently, Hippo-YAP/TAZ signaling pathway, a key mechanism of organ size and tissue homeostasis, has emerged as a critical player that regulate lymphatic specification, sprouting, and maturation. In this review, we discuss the mechanistic regulation and pathophysiological significant of Hippo pathway in lymphatic vascular development.

• Korean Journal of Radiology
• /
• v.23 no.6
• /
• pp.649-663
• /
• 2022

The role of magnetic resonance imaging (MRI) in diplopia is to diagnose various diseases that occur along the neural pathway governing eye movement. However, the lesions are frequently small and subtle and are therefore difficult to detect on MRI. This article presents representative cases of diseases that cause diplopia. The purpose of this article was to 1) describe the anatomy of the neural pathway governing eye movement, 2) recommend optimal MRI targets and protocols for the diagnosis of diseases causing diplopia, 3) correlate MRI findings with misalignment of the eyes (i.e., strabismus), and 4) help familiarize the reader with the imaging diagnosis of diplopia.

• Quality Improvement in Health Care
• /
• v.6 no.1_2
• /
• pp.6-11
• /
• 1999

• Quality Improvement in Health Care
• /
• v.6 no.1_2
• /
• pp.12-17
• /
• 1999

• Quality Improvement in Health Care
• /
• v.6 no.1_2
• /
• pp.32-36
• /
• 1999

• 대한동의생리학회:학술대회논문집
• /
• 2005.07a
• /
• pp.21-21
• /
• 2005