Other search tools

About this data

The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.

If you have any questions or comments, please contact us.

Results: 1 to 3 of 3

Publication Record


Nkx2.2 is expressed in a subset of enteroendocrine cells with expanded lineage potential.
Gross S, Balderes D, Liu J, Asfaha S, Gu G, Wang TC, Sussel L
(2015) Am J Physiol Gastrointest Liver Physiol 309: G975-87
MeSH Terms: Animals, Basic Helix-Loop-Helix Transcription Factors, Biomarkers, Cell Differentiation, Cell Lineage, Cell Proliferation, Cells, Cultured, Enteroendocrine Cells, Genotype, Homeodomain Proteins, Intestinal Mucosa, Luminescent Proteins, Mice, Inbred C57BL, Mice, Transgenic, Nerve Tissue Proteins, Phenotype, Pluripotent Stem Cells, Polycomb Repressive Complex 1, Proto-Oncogene Proteins, Receptors, G-Protein-Coupled, Transcription Factors, Whole-Body Irradiation, Zebrafish Proteins
Show Abstract · Added February 3, 2017
There are two major stem cell populations in the intestinal crypt region that express either Bmi1 or Lgr5; however, it has been shown that other populations in the crypt can regain stemness. In this study, we demonstrate that the transcription factor NK2 homeobox 2 (Nkx2.2) is expressed in enteroendocrine cells located in the villus and crypt of the intestinal epithelium and is coexpressed with the stem cell markers Bmi1 and Lgr5 in a subset of crypt cells. To determine whether Nkx2.2-expressing enteroendocrine cells display cellular plasticity and stem cell potential, we performed genetic lineage tracing of the Nkx2.2-expressing population using Nkx2.2(Cre/+);R26RTomato mice. These studies demonstrated that Nkx2.2+ cells are able to give rise to all intestinal epithelial cell types in basal conditions. The proliferative capacity of Nkx2.2-expressing cells was also demonstrated in vitro using crypt organoid cultures. Injuring the intestine with irradiation, systemic inflammation, and colitis did not enhance the lineage potential of Nkx2.2-expressing cells. These findings demonstrate that a rare mature enteroendocrine cell subpopulation that is demarcated by Nkx2.2 expression display stem cell properties during normal intestinal epithelial homeostasis, but is not easily activated upon injury.
Copyright © 2015 the American Physiological Society.
1 Communities
0 Members
0 Resources
23 MeSH Terms
In vivo RNAi screen for BMI1 targets identifies TGF-β/BMP-ER stress pathways as key regulators of neural- and malignant glioma-stem cell homeostasis.
Gargiulo G, Cesaroni M, Serresi M, de Vries N, Hulsman D, Bruggeman SW, Lancini C, van Lohuizen M
(2013) Cancer Cell 23: 660-76
MeSH Terms: Activating Transcription Factor 3, Animals, Bone Morphogenetic Proteins, Cell Nucleus, Chromatin, Endoplasmic Reticulum Stress, Glioblastoma, Homeostasis, Humans, Mice, Neoplastic Stem Cells, Neural Stem Cells, Polycomb Repressive Complex 1, Proto-Oncogene Proteins, RNA Interference, Signal Transduction, Transforming Growth Factor beta
Show Abstract · Added July 31, 2013
In mouse and human neural progenitor and glioblastoma "stem-like" cells, we identified key targets of the Polycomb-group protein BMI1 by combining ChIP-seq with in vivo RNAi screening. We discovered that Bmi1 is important in the cellular response to the transforming growth factor-β/bone morphogenetic protein (TGF-β/BMP) and endoplasmic reticulum (ER) stress pathways, in part converging on the Atf3 transcriptional repressor. We show that Atf3 is a tumor-suppressor gene inactivated in human glioblastoma multiforme together with Cbx7 and a few other candidates. Acting downstream of the ER stress and BMP pathways, ATF3 binds to cell-type-specific accessible chromatin preloaded with AP1 and participates in the inhibition of critical oncogenic networks. Our data support the feasibility of combining ChIP-seq and RNAi screens in solid tumors and highlight multiple p16(INK4a)/p19(ARF)-independent functions for Bmi1 in development and cancer.
Copyright © 2013 Elsevier Inc. All rights reserved.
0 Communities
0 Members
0 Resources
17 MeSH Terms
Opposing roles for RelB and Bcl-3 in regulation of T-box expressed in T cells, GATA-3, and Th effector differentiation.
Corn RA, Hunter C, Liou HC, Siebenlist U, Boothby MR
(2005) J Immunol 175: 2102-10
MeSH Terms: Animals, B-Cell Lymphoma 3 Protein, Cell Differentiation, Cells, Cultured, DNA-Binding Proteins, GATA3 Transcription Factor, Humans, Interferon-gamma, Jurkat Cells, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Polycomb Repressive Complex 1, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-rel, T-Box Domain Proteins, T-Lymphocytes, Helper-Inducer, Th1 Cells, Th2 Cells, Transcription Factors
Show Abstract · Added December 10, 2013
CD4+ T cells with a block in the NF-kappaB signaling pathway exhibit decreases in Th1 responses and diminished nuclear levels of multiple transactivating NF-kappaB/Rel/IkappaB proteins. To determine the lineage-intrinsic contributions of these transactivators to Th differentiation, T cells from mice deficient in specific subunits were cultured in exogenous cytokines promoting either Th1 or Th2 differentiation. RelB-deficient cells exhibited dramatic defects in Th1 differentiation and IFN-gamma production, whereas no consistent defect in either Th1 or Th2 responses was observed with c-Rel-deficient cells. In sharp contrast, Bcl-3-null T cells displayed no defect in IFN-gamma production, but their Th2 differentiation and IL-4, IL-5, and IL-13 production were significantly impaired. The absence of RelB led to a dramatic decrease in the expression of T-box expressed in T cells and Stat4. In contrast, Bcl-3-deficient cells exhibited decreased GATA-3, consistent with evidence that Bcl-3 can transactivate a gata3 promoter. These data indicate that Bcl-3 and RelB exert distinct and opposing effects on the expression of subset-determining transcription factors, suggesting that the characteristics of Th cell responses may be regulated by titrating the stoichiometry of transactivating NF-kappaB/Rel/IkappaB complexes in the nuclei of developing helper effector cells.
0 Communities
1 Members
0 Resources
21 MeSH Terms