Min-Kyu Eom
Korea Advanced Institute of Science and Technology · 生化学・遺伝学・分子生物学
研究室紹介
Professor Min-Kyu Eom's research lab focuses on the molecular and cellular mechanisms governing epithelial stem cell dynamics and tissue homeostasis in the gastrointestinal tract, mammary gland, and intestinal tumorigenesis. The lab employs advanced genetic labeling, lineage tracing, and biophysical modeling to dissect the functional heterogeneity of stem cells and their roles in tissue regeneration and cancer. A central theme is the regulation of Wnt/β-catenin signaling by tumor suppressor-like proteins such as AIMP2, which modulate stem cell behavior and prevent polyposis and tumorigenesis. The lab also investigates transcriptional regulators like ID2 in mammary gland development, highlighting their roles in lineage commitment and branching morphogenesis.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15The gastric corpus epithelium is the thickest part of the gastrointestinal tract and is rapidly turned over. Several markers have been proposed for gastric corpus stem cells in both isthmus and base regions. However, the identity of isthmus stem cells (IsthSCs) and the interaction between distinct stem cell populations is still under debate. Here, based on unbiased genetic labeling and biophysical modeling, we show that corpus glands are compartmentalized into two independent zones, with slow-cy
Wnt/β-catenin (CTNNB1) signaling is crucial for the proliferation and maintenance of intestinal stem cells (ISC), but excessive activation leads to ISC expansion and eventually colorectal cancer. Thus, negative regulators are required to maintain optimal levels of Wnt/β-catenin signaling. Aminoacyl-tRNA synthetase-interacting multifunctional proteins (AIMP) function in protein synthesis, but have also been implicated in signaling cascades affecting angiogenesis, immunity, and apoptosis. In this
ABSTRACT Mammary glands develop through primary ductal elongation and side branching to maximize the spatial area. Although primary ducts are generated by bifurcation of terminal end buds, the mechanism through which side branching occurs is still largely unclear. Here, we show that inhibitor of DNA-binding 2 (ID2) drives side branch formation through the differentiation of K6+ bipotent progenitor cells (BPs) into CD61+ luminal progenitor cells (LPs). Id2-null mice had side-branching defects, al
<p>The role of AIMP2 in intestinal Wnt signaling is dependent on β-catenin destruction complex.</p>
<p>Supplemental Materials and Methods and Supplemental figure legends</p>
<p>Analysis of polyposis and tumor initiation in Aimp2+/-:ApcMin/+ intestine</p>
<p>Aimp2 gene dosage negatively correlates with organoid growth</p>
<p>The role of AIMP2 in intestinal Wnt signaling is dependent on β-catenin destruction complex.</p>
<p>AIMP2 interacts with the DIX domain of DVL and modulate Wnt/β-catenin signaling in an Aimp2 gene dosage dependent manner</p>
<p>Supplemental Materials and Methods and Supplemental figure legends</p>