P. Hurlin

发表

The Mad protein family links transcriptional repression to cell differentiation.

R. Eisenman, Carol D. Laherty, C. Grandori, 1998, Cold Spring Harbor symposia on quantitative biology.

Suppression of FGFR3- and MYC-dependent oncogenesis by tubacin: association with HDAC6-dependent and independent activities

P. Hurlin, S. Ota, Zi-Qiang Zhou, 2017, Oncotarget.

Mnt, a novel Max-interacting protein is coexpressed with Myc in proliferating cells and mediates repression at Myc binding sites.

R. Eisenman, C. Quéva, P. Hurlin, 1997, Genes & development.

Progression of human papillomavirus type 18-immortalized human keratinocytes to a malignant phenotype.

J. McDougall, P. Hurlin, P. Kaur, 1991, Proceedings of the National Academy of Sciences of the United States of America.

Mga, a dual‐specificity transcription factor that interacts with Max and contains a T‐domain DNA‐binding motif

N. Jenkins, R. Eisenman, E. Steingrímsson, 1999, The EMBO journal.

Malignant transformation of human fibroblasts by oncogene transfection or carcinogen treatment.

P. Hurlin, J. Mccormick, D. Wilson, 1990, Progress in clinical and biological research.

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas.

Wei Zhao, Brady Bernard, Andrea Ventura, 2018, Cell systems.

MYC needs MNT

P. Hurlin, Jason M. Link, 2013, Cell cycle.

Activities of N-Myc in the developing limb link control of skeletal size with digit separation

P. Hurlin, D. Keene, S. Ota, 2007, Development.

Mga, a dual‐specificity transcription factor that interacts with Max and contains a T‐domain DNA‐binding motif

N. Copeland, N. Jenkins, R. Eisenman, 2013 .

Morphological transformation, focus formation, and anchorage independence induced in diploid human fibroblasts by expression of a transfected H-ras oncogene.

P. Hurlin, J. Mccormick, V. Maher, 1987, Cancer research.

A dominant repression domain in Tbx3 mediates transcriptional repression and cell immortalization: relevance to mutations in Tbx3 that cause ulnar-mammary syndrome.

P. Hurlin, S. Ota, C. Campbell, 2001, Human molecular genetics.

Mnt transcriptional repressor is functionally regulated during cell cycle progression

M. Henriksson, P. Hurlin, N. Popov, 2005, Oncogene.

Mad3 and Mad4: novel Max-interacting transcriptional repressors that suppress c-myc dependent transformation and are expressed during neural and epidermal differentiation.

N. Copeland, N. Jenkins, R. Eisenman, 1996, The EMBO journal.

A critical role for Mnt in Myc-driven T-cell proliferation and oncogenesis

Colin J. Daniel, R. Sears, P. Hurlin, 2012, Proceedings of the National Academy of Sciences.

Characteristics of an infinite life span diploid human fibroblast cell strain and a near-diploid strain arising from a clone of cells expressing a transfected v-myc oncogene.

P. Hurlin, J. Mccormick, V. Maher, 1991, Experimental cell research.

HDAC6 deficiency or inhibition blocks FGFR3 accumulation and improves bone growth in a model of achondroplasia.

P. Hurlin, S. Ota, Zi-Qiang Zhou, 2016, Human molecular genetics.

Mnt: a novel Max-interacting protein and Myc antagonist.

R. Eisenman, C. Quéva, P. Hurlin, 1997, Current topics in microbiology and immunology.

Functions of myc:max in the control of cell proliferation and tumorigenesis.

P. Hurlin, S. Dezfouli, Shala Dezfouli, 2004, International review of cytology.

Evidence of Mnt-Myc Antagonism Revealed by Mnt Gene Deletion

A. Wynshaw-Boris, P. Hurlin, S. Ota, 2004, Cell cycle.

Analysis of the max‐binding protein MNT in human medulloblastomas

J. Tonn, R. Eisenman, A. Sommer, 1999, International journal of cancer.

Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis

A. Wynshaw-Boris, P. Hurlin, S. Ota, 2003, The EMBO journal.

A repressor protein, Mnt, is a novel negative regulator of vascular smooth muscle cell hypertrophy by angiotensin II and neointimal hyperplasia by arterial injury.

P. Hurlin, S. Eguchi, A. Takaguri, 2013, Atherosclerosis.

The Max transcription factor network: involvement of Mad in differentiation and an approach to identification of target genes.

R. Eisenman, C. Grandori, D. Ayer, 1994, Cold Spring Harbor symposia on quantitative biology.

The activities of MYC, MNT and the MAX-interactome in lymphocyte proliferation and oncogenesis.

P. Hurlin, Jason M. Link, 2015, Biochimica et biophysica acta.

Malignant transformation of human fibroblasts caused by expression of a transfected T24 HRAS oncogene.

P. Hurlin, J. Mccormick, V. Maher, 1989, Proceedings of the National Academy of Sciences of the United States of America.

MNT and Emerging Concepts of MNT-MYC Antagonism

P. Hurlin, Guang Yang, 2017, Genes.

Tbx3 impinges on the p53 pathway to suppress apoptosis, facilitate cell transformation and block myogenic differentiation

P. Hurlin, S. Ota, Peter J Hurlin, 2002, Oncogene.

Control of vertebrate development by MYC.

P. Hurlin, 2013, Cold Spring Harbor perspectives in medicine.

The MAX-interacting transcription factor network.

P. Hurlin, Jie Huang, 2006, Seminars in cancer biology.

Mnt-deficient mammary glands exhibit impaired involution and tumors with characteristics of myc overexpression.

C. Glass, R. Eisenman, M. Rosenfeld, 2006, Cancer research.

Of Myc and Mnt

P. Hurlin, C. Hooker, 2006, Journal of Cell Science.

N-Myc functions in transcription and development.

P. Hurlin, 2005, Birth defects research. Part C, Embryo today : reviews.

Loss of the Max-interacting protein Mnt in mice results in decreased viability, defective embryonic growth and craniofacial defects: relevance to Miller-Dieker syndrome.

R. Eisenman, M. Rosenfeld, A. Wynshaw-Boris, 2004, Human molecular genetics.

The interplay between Mad and Myc in proliferation and differentiation.

P. Hurlin, Z. Q. Zhou, Z. Zhou, 2001, Trends in cell biology.

Mad3 and Mad4: novel Max‐interacting transcriptional repressors that suppress c‐myc dependent transformation and are expressed during neural and epidermal differentiation.

N. Copeland, N. Jenkins, R. Eisenman, 1995, The EMBO journal.

Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation

R. Eisenman, Philippe Soriano, G. McArthur, 1998, The EMBO journal.

Mnt–Max to Myc–Max complex switching regulates cell cycle entry

A. Wynshaw-Boris, P. Hurlin, S. Ota, 2005, The Journal of cell biology.

expressed during neural and epidermal differentiation

N. Copeland, N. Jenkins, R. Eisenman, 2004 .

Differential Regulation of N-Myc and c-Myc Synthesis, Degradation, and Transcriptional Activity by the Ras/Mitogen-activated Protein Kinase Pathway*

P. Hurlin, Katannya Kapeli, 2011, The Journal of Biological Chemistry.

Mnt modulates Myc-driven lymphomagenesis

S. Cory, C. Vandenberg, P. Hurlin, 2017, Cell Death and Differentiation.

The transcriptional represser Mnt is a functional antagonist of the proto-oncoprotein Myc

S. Cory, C. Vandenberg, P. Hurlin, 2017 .

Disruption of a Sox9-β-catenin circuit by mutant Fgfr3 in thanatophoric dysplasia type II.

P. Hurlin, D. Keene, S. Ota, 2012, Human molecular genetics.

Cyclin-Dependent Kinase-9 Is a Therapeutic Target in MYC-Expressing Diffuse Large B-Cell Lymphoma

L. Drew, P. Hurlin, E. Gilbert, 2019, Molecular Cancer Therapeutics.

The role of senescence and prosurvival signaling in controlling the oncogenic activity of FGFR2 mutants associated with cancer and birth defects

P. Hurlin, S. Ota, Jason M. Link, 2009, Human molecular genetics.

Transformation of diploid human fibroblasts by transfection with the v-sis, PDGF2/c-sis, or T24 H-ras genes.

P. Hurlin, J. Mccormick, V. Maher, 1988, Mutation research.

Sequential and Coordinated Actions of c-Myc and N-Myc Control Appendicular Skeletal Development

H. Akiyama, P. Hurlin, D. Keene, 2011, PloS one.

Mutant activated FGFR3 impairs endochondral bone growth by preventing SOX9 downregulation in differentiating chondrocytes.

H. Akiyama, P. Hurlin, C. Deng, 2015, Human molecular genetics.

Sequential expression of the MAD family of transcriptional repressors during differentiation and development

R. Eisenman, K. Foley, C. Quéva, 1998, Oncogene.

Regulation of Myc and Mad during epidermal differentiation and HPV-associated tumorigenesis.

D. Hanahan, R. Eisenman, J. Arbeit, 1995, Oncogene.

The MNT transcription factor autoregulates its expression and supports proliferation in MYC-associated factor X (MAX)-deficient cells

I. Varela, R. Eisenman, J. León, 2020, The Journal of Biological Chemistry.

The MYC antagonist MNT autoregulates its expression and supports proliferation in MAX deficient cells

I. Varela, R. Eisenman, J. León, 2017, bioRxiv.

OX40 engagement stabilizes Mxd4 and Mnt protein levels in antigen‐stimulated T cells leading to an increase in cell survival

N. Vasilevsky, P. Hurlin, A. Weinberg, 2011, European journal of immunology.

Inflammatory Disease and Lymphomagenesis Caused by Deletion of the Myc Antagonist Mnt in T Cells

A. Wynshaw-Boris, P. Hurlin, Jie Huang, 2006, Molecular and Cellular Biology.

A novel role of MNT as a negative regulator of REL and the NF-κB pathway

A. von Kriegsheim, L. Espinosa, A. Bigas, 2020, bioRxiv.

Jie Huang , Anthony the Myc Antagonist Mnt in T Cells Lymphomagenesis Caused by Deletion of Inflammatory Disease and

A. Wynshaw-Boris, P. Hurlin, Jie Huang, 2005 .

Development of human gene reporter cell lines using rAAV mediated homologous recombination

D. Russell, P. Hurlin, S. Fernández, 2007, Biological Procedures Online.

The activities of MYC, MNT and the MAX-interactome in lymphocyte proliferation and oncogenesis.

P. Hurlin, Jason M. Link, 2015, Biochimica et biophysica acta.