Damon B. Bowe, Ph.D.
Affiliations: | 2006 | University of Alabama, Birmingham, Birmingham, AL, United States |
Area:
Molecular Biology, Toxicology, Cell BiologyGoogle:
"Damon Bowe"
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Publications
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| Wu J, Bowe DB, Sadlonova A, et al. (2014) O-GlcNAc transferase is critical for transducin-like enhancer of split (TLE)-mediated repression of canonical Wnt signaling. The Journal of Biological Chemistry. 289: 12168-76 |
| Huang P, Ho SR, Wang K, et al. (2011) Muscle-specific overexpression of NCOATGK, splice variant of O-GlcNAcase, induces skeletal muscle atrophy. American Journal of Physiology. Cell Physiology. 300: C456-65 |
| Sadlonova A, Bowe DB, Novak Z, et al. (2009) Identification of molecular distinctions between normal breast-associated fibroblasts and breast cancer-associated fibroblasts. Cancer Microenvironment : Official Journal of the International Cancer Microenvironment Society. 2: 9-21 |
| Sadlonova A, Mukherjee S, Bowe DB, et al. (2007) Human breast fibroblasts inhibit growth of the MCF10AT xenograft model of proliferative breast disease. The American Journal of Pathology. 170: 1064-76 |
| Bowe DB, Sadlonova A, Toleman CA, et al. (2006) O-GlcNAc integrates the proteasome and transcriptome to regulate nuclear hormone receptors. Molecular and Cellular Biology. 26: 8539-50 |
| Whisenhunt TR, Yang X, Bowe DB, et al. (2006) Disrupting the enzyme complex regulating O-GlcNAcylation blocks signaling and development. Glycobiology. 16: 551-63 |
| Sadlonova A, Novak Z, Johnson MR, et al. (2005) Breast fibroblasts modulate epithelial cell proliferation in three-dimensional in vitro co-culture. Breast Cancer Research : Bcr. 7: R46-59 |
| Zhang F, Su K, Yang X, et al. (2003) O-GlcNAc modification is an endogenous inhibitor of the proteasome. Cell. 115: 715-25 |