Peter Hurlin

Summary

Affiliation: Shriners Hospital for Children
Country: USA

Publications

  1. pmc Mnt-Max to Myc-Max complex switching regulates cell cycle entry
    William Walker
    Shriners Hospitals for Children, Portland, OR 97201, USA
    J Cell Biol 169:405-13. 2005
  2. pmc Sequential and coordinated actions of c-Myc and N-Myc control appendicular skeletal development
    Zi Qiang Zhou
    Shriners Hospitals for Children Portland, Portland, Oregon, United States of America
    PLoS ONE 6:e18795. 2011
  3. pmc The role of senescence and prosurvival signaling in controlling the oncogenic activity of FGFR2 mutants associated with cancer and birth defects
    Sara Ota
    Shriners Hospitals for Children, Oregon Health and Science University, 3101 SW Sam Jackson Park Road, Portland, OR 97201 3095, USA
    Hum Mol Genet 18:2609-21. 2009
  4. pmc MYC needs MNT
    Jason M Link
    Shriners Hospitals for Children Portland Portland, OR USA
    Cell Cycle 12:385-6. 2013
  5. ncbi request reprint The interplay between Mad and Myc in proliferation and differentiation
    Z Q Zhou
    Shriners Hospitals for Children, Department of Cell and Developmental Biology, Oregon Health Sciences University, 3101 Sam Jackson Park Road, Portland, OR 97201, USA
    Trends Cell Biol 11:S10-4. 2001
  6. pmc Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis
    Peter J Hurlin
    Shriners Hospitals for Children, Department of Cell and Developmental Biology, Oregon Health Sciences University, Portland, OR, USA
    EMBO J 22:4584-96. 2003
  7. ncbi request reprint Evidence of mnt-myc antagonism revealed by mnt gene deletion
    Peter J Hurlin
    Shriners Hospital for Children, Department of Cell and Developmental Biology, Oregon Health Sciences University, Portland, Oregon USA
    Cell Cycle 3:97-9. 2004
  8. ncbi request reprint The MAX-interacting transcription factor network
    Peter J Hurlin
    Shriners Hospitals for Children and Department of Cell and Developmental Biology, Oregon Health and Science University, Portland, OR 97201, USA
    Semin Cancer Biol 16:265-74. 2006
  9. pmc Mga, a dual-specificity transcription factor that interacts with Max and contains a T-domain DNA-binding motif
    P J Hurlin
    Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, Seattle, WA 98109 1024, USA
    EMBO J 18:7019-28. 1999
  10. ncbi request reprint N-Myc functions in transcription and development
    Peter J Hurlin
    Shriners Hospitals for Children and the Department of Cell and Developmental Biology, Oregon Health Sciences University, Portland, Oregon 97201, USA
    Birth Defects Res C Embryo Today 75:340-52. 2005

Research Grants

Collaborators

Detail Information

Publications22

  1. pmc Mnt-Max to Myc-Max complex switching regulates cell cycle entry
    William Walker
    Shriners Hospitals for Children, Portland, OR 97201, USA
    J Cell Biol 169:405-13. 2005
    ..These results demonstrate that Mnt-Myc antagonism plays a fundamental role in regulating cell cycle entry and proliferation...
  2. pmc Sequential and coordinated actions of c-Myc and N-Myc control appendicular skeletal development
    Zi Qiang Zhou
    Shriners Hospitals for Children Portland, Portland, Oregon, United States of America
    PLoS ONE 6:e18795. 2011
    ..The aim of this study was to gain insight into these processes by examining the roles of c-Myc and N-Myc in morphogenesis of the limb skeleton...
  3. pmc The role of senescence and prosurvival signaling in controlling the oncogenic activity of FGFR2 mutants associated with cancer and birth defects
    Sara Ota
    Shriners Hospitals for Children, Oregon Health and Science University, 3101 SW Sam Jackson Park Road, Portland, OR 97201 3095, USA
    Hum Mol Genet 18:2609-21. 2009
    ..Our results also raise the possibility that cancers originating through a combination of constitutive FGFR activation and deregulated Myc expression may be particularly sensitive to small molecule inhibitors of FGF receptors...
  4. pmc MYC needs MNT
    Jason M Link
    Shriners Hospitals for Children Portland Portland, OR USA
    Cell Cycle 12:385-6. 2013
    ..Comment on: Link JM, et al. Proc Natl Acad Sci USA 2012; 109:19685-90...
  5. ncbi request reprint The interplay between Mad and Myc in proliferation and differentiation
    Z Q Zhou
    Shriners Hospitals for Children, Department of Cell and Developmental Biology, Oregon Health Sciences University, 3101 Sam Jackson Park Road, Portland, OR 97201, USA
    Trends Cell Biol 11:S10-4. 2001
    ..Here, we examine current models of Mad function and the relationship between Mad and Myc in cell proliferation, differentiation and tumorigenesis...
  6. pmc Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis
    Peter J Hurlin
    Shriners Hospitals for Children, Department of Cell and Developmental Biology, Oregon Health Sciences University, Portland, OR, USA
    EMBO J 22:4584-96. 2003
    ..These results demonstrate a unique negative regulatory role for Mnt in governing key Myc functions associated with cell proliferation and tumorigenesis...
  7. ncbi request reprint Evidence of mnt-myc antagonism revealed by mnt gene deletion
    Peter J Hurlin
    Shriners Hospital for Children, Department of Cell and Developmental Biology, Oregon Health Sciences University, Portland, Oregon USA
    Cell Cycle 3:97-9. 2004
    ..The repressor with similar DNA binding specificity raised the possibility that Mnt may serve a general role as a Myc antagonist...
  8. ncbi request reprint The MAX-interacting transcription factor network
    Peter J Hurlin
    Shriners Hospitals for Children and Department of Cell and Developmental Biology, Oregon Health and Science University, Portland, OR 97201, USA
    Semin Cancer Biol 16:265-74. 2006
    ..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...
  9. pmc Mga, a dual-specificity transcription factor that interacts with Max and contains a T-domain DNA-binding motif
    P J Hurlin
    Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, Seattle, WA 98109 1024, USA
    EMBO J 18:7019-28. 1999
    ..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...
  10. ncbi request reprint N-Myc functions in transcription and development
    Peter J Hurlin
    Shriners Hospitals for Children and the Department of Cell and Developmental Biology, Oregon Health Sciences University, Portland, Oregon 97201, USA
    Birth Defects Res C Embryo Today 75:340-52. 2005
    ..In this review I summarize our understanding of the transcriptional activities of Myc family proteins and the roles of N-myc in morphogenesis, particularly as they relate to cellular proliferation and apoptosis...
  11. ncbi request reprint Mnt, a novel Max-interacting protein is coexpressed with Myc in proliferating cells and mediates repression at Myc binding sites
    P J Hurlin
    Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98104, USA
    Genes Dev 11:44-58. 1997
    ..We propose that Mnt:Max:Sin3 complexes normally function to restrict Myc:Max activities associated with cell proliferation...
  12. ncbi request reprint Sequential expression of the MAD family of transcriptional repressors during differentiation and development
    C Queva
    Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109 1024, USA
    Oncogene 16:967-77. 1998
    ..Taken together, our data suggest that the different members of the MAD protein family exert their functions at distinct steps during the transition between proliferation and differentiation...
  13. pmc Mad3 and Mad4: novel Max-interacting transcriptional repressors that suppress c-myc dependent transformation and are expressed during neural and epidermal differentiation
    P J Hurlin
    Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98104, USA
    EMBO J 14:5646-59. 1995
    ....
  14. ncbi request reprint A dominant repression domain in Tbx3 mediates transcriptional repression and cell immortalization: relevance to mutations in Tbx3 that cause ulnar-mammary syndrome
    H Carlson
    Shriners Hospitals for Children and Department of Cell and Developmental Biology, Oregon Health Sciences University, 3101 Sam Jackson Park Road, Portland, OR 97201, USA
    Hum Mol Genet 10:2403-13. 2001
    ..Our results identify critical functional domains within the Tbx3 protein and facilitate interpretation of the functional consequences of present and future UMS mutations...
  15. pmc Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation
    K P Foley
    Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North Mailstop A2 025, P O Box 19024, Seattle, WA 98109 1024, USA
    EMBO J 17:774-85. 1998
    ....
  16. ncbi request reprint Mnt transcriptional repressor is functionally regulated during cell cycle progression
    Nikita Popov
    Microbiology and Tumor Biology Center, Karolinska Institutet, Box 280, SE 171 77 Stockholm, Sweden
    Oncogene 24:8326-37. 2005
    ..Our data suggest a model in which phosphorylation of Mnt at cell cycle entry results in disruption of Mnt-mSin3-HDAC1 interaction, which allows induction of Myc target genes by release of Mnt-mediated transcriptional repression...
  17. pmc Inflammatory disease and lymphomagenesis caused by deletion of the Myc antagonist Mnt in T cells
    Shala Dezfouli
    Shriners Hospital for Children, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA
    Mol Cell Biol 26:2080-92. 2006
    ..These results strengthen the argument that Mnt functions as a tumor suppressor and reveal a critical and surprising role for Mnt in the regulation of T-cell development and in T-cell-dependent immune homeostasis...
  18. ncbi request reprint Functions of myc:max in the control of cell proliferation and tumorigenesis
    Peter J Hurlin
    Portland Shriners Hospitals for Children and Department of Cell and Developmental Biology Oregon Health Sciences University, Portland, Oregon 97201, USA
    Int Rev Cytol 238:183-226. 2004
    ..In this review, we examine the complex activities of Myc family proteins and how their actions might be regulated in the context of a network of bHLHZip proteins...
  19. ncbi request reprint Activities of N-Myc in the developing limb link control of skeletal size with digit separation
    Sara Ota
    Shriners Hospitals for Children Portland, OR 97239, USA
    Development 134:1583-92. 2007
    ..Our results provide new insight into mechanisms that control limb development and suggest that defects in the formation of N-Myc-dependent interdigital tissue may be a root cause of common syndromic forms of syndactyly...
  20. ncbi request reprint Tbx3 impinges on the p53 pathway to suppress apoptosis, facilitate cell transformation and block myogenic differentiation
    Hanqian Carlson
    Shriners Hospitals for Children, Oregon Health Sciences University, 3101 Sam Jackson Park Road, Portland, OR 97201, USA
    Oncogene 21:3827-35. 2002
    ..Our results support the idea that deregulation and/or excessive levels of Tbx3 may have oncogenic potential in vivo...
  21. ncbi request reprint Of Myc and Mnt
    C William Hooker
    Shriners Hospitals for Children and Department of Cell and Developmental Biology, Oregon Health and Science University, 3101 SW Sam Jackson Park Rd, Portland, OR 97239, USA
    J Cell Sci 119:208-16. 2006
    ..The interplay between these proteins is postulated to fine-tune Myc activity for cell-cycle entry and exit, proliferation rate and apoptosis...

Research Grants2

  1. FUNCTION OF A DUAL SPECIFICITY TRANSCRIPTION FACTOR
    Peter Hurlin; Fiscal Year: 2003
    ..Finally, gene targeting in the mouse will be used to study the biological activities of Mga and the individual roles of its bHLHZip domain and T-domain. ..
  2. Myc Antagonism and Tumor Suppression by Mnt
    Peter Hurlin; Fiscal Year: 2008
    ..abstract_text> ..