Genomes and Genes
Affiliation: Shriners Hospital for Children
- Yang G, Hurlin P. MNT and Emerging Concepts of MNT-MYC Antagonism. Genes (Basel). 2017;8: pubmed publisher..In this review, we discuss the current understanding of MNT, its regulation and how, as a MYC antagonist, it functions both as a tumor suppressor and facilitator of MYC-driven proliferation and oncogenesis. ..
- Hurlin P, Steingrimsson E, Copeland N, Jenkins N, Eisenman R. Mga, a dual-specificity transcription factor that interacts with Max and contains a T-domain DNA-binding motif. EMBO J. 1999;18:7019-28 pubmed..Our results suggest that Mga functions as a dual-specificity transcription factor that regulates the expression of both Max-network and T-box family target genes. ..
- Hurlin P, Zhou Z, Toyo oka K, Ota S, Walker W, Hirotsune S, et al. Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis. EMBO J. 2003;22:4584-96 pubmed..These results demonstrate a unique negative regulatory role for Mnt in governing key Myc functions associated with cell proliferation and tumorigenesis. ..
- Hurlin P, Zhou Z, Toyo oka K, Ota S, Walker W, Hirotsune S, et al. Evidence of mnt-myc antagonism revealed by mnt gene deletion. Cell Cycle. 2004;3:97-9 pubmed..The repressor with similar DNA binding specificity raised the possibility that Mnt may serve a general role as a Myc antagonist. ..
- Hurlin P, Huang J. The MAX-interacting transcription factor network. Semin Cancer Biol. 2006;16:265-74 pubmed..Here we review the activities of MAX, its interaction partners, and recent results showing that tissues lacking the MAX-interacting protein MNT are predisposed to tumor formation. ..
- Link J, Hurlin P. The activities of MYC, MNT and the MAX-interactome in lymphocyte proliferation and oncogenesis. Biochim Biophys Acta. 2015;1849:554-62 pubmed publisher..Here we review the activities of MYC, MNT and other MAX interacting proteins in the setting of T and B cell activation and oncogenesis. This article is part of a Special Issue entitled: Myc proteins in cell biology and pathology. ..
- Zhou Z, Ota S, Deng C, Akiyama H, Hurlin P. Mutant activated FGFR3 impairs endochondral bone growth by preventing SOX9 downregulation in differentiating chondrocytes. Hum Mol Genet. 2015;24:1764-73 pubmed publisher..These findings suggest that a proliferation-independent and SOX9-dependent differentiation block is a key driving mechanism responsible for poor endochondral bone growth in achondroplasia disorders caused by mutations in FGFR3. ..
- Ota S, Zhou Z, Romero M, Yang G, Hurlin P. HDAC6 deficiency or inhibition blocks FGFR3 accumulation and improves bone growth in a model of achondroplasia. Hum Mol Genet. 2016;25:4227-4243 pubmed publisher..These findings further define the mechanisms that control FGFR3 accumulation and contribute to skeletal pathology caused by mutations in FGFR3. ..