Peter Hurlin

Summary

Affiliation: Shriners Hospital for Children
Country: USA

Publications

  1. 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. ..
  2. 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. ..
  3. 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. ..
  4. request reprint
    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. ..
  5. request reprint
    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. ..
  6. 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. ..
  7. 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. ..
  8. 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. ..

Locale

Detail Information

Publications8

  1. 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. ..
  2. 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. ..
  3. 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. ..
  4. request reprint
    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. ..
  5. request reprint
    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. ..
  6. 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. ..
  7. 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. ..
  8. 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. ..