염민규 교수

The 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>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>AIMP2 interacts with the DIX domain of DVL and modulate Wnt/β-catenin signaling in an Aimp2 gene dosage dependent manner</p>

<p>Analysis of polyposis and tumor initiation in Aimp2+/-:ApcMin/+ intestine</p>

<p>Aimp2+/- mice exhibit increased villi length, crypt depth, and colonic epithelial cell proliferation</p>