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

PJ Hurlin, C Queva, PJ Koskinen… - The EMBO …, 1995 - embopress.org
The basic helix‐loop‐helix‐leucine zipper (bHLHZip) protein Max associates with members
of the Myc family, as well as with the related proteins Mad (Mad1) and Mxi1. Whereas both …

[HTML][HTML] Pan-cancer alterations of the MYC oncogene and its proximal network across the cancer genome atlas

…, X Zhang, A Ventura, Y Liu, DE Ayer, PJ Hurlin… - Cell systems, 2018 - cell.com
Although the MYC oncogene has been implicated in cancer, a systematic assessment of
alterations of MYC, related transcription factors, and co-regulatory proteins, forming the …

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

PJ Hurlin, C Queva, RN Eisenman - Genes & development, 1997 - genesdev.cshlp.org
The small constitutively expressed bHLHZip protein Max is known to form sequence-specific
DNA binding heterodimers with members of both the Myc and Mad families of bHLHZip …

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

PJ Hurlin, E Steingrìmsson, NG Copeland… - The EMBO …, 1999 - embopress.org
The basic‐helix‐loop‐helix‐leucine zipper (bHLHZip) proteins Myc, Mad and Mnt are part of
a transcription activation/repression system involved in the regulation of cell proliferation. …

The MAX-interacting transcription factor network

PJ Hurlin, J Huang - Seminars in cancer biology, 2006 - Elsevier
The small bHLHZip protein MAX functions at the center of a transcription factor network that
governs many aspects of cell behavior, including cell proliferation and tumorigenesis. MAX …

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

PJ Hurlin, P Kaur, PP Smith… - Proceedings of the …, 1991 - National Acad Sciences
We have developed a model system for progression of human epithelial cells to malignancy,
using a human papillomavirus type 18 (HPV-18)-immortalized human keratinocyte cell line. …

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

…, S Ota, CE Campbell, PJ Hurlin - Human molecular …, 2001 - academic.oup.com
Mutations in Tbx3 are responsible for ulnar-mammary syndrome (UMS), an autosomal
dominant disorder affecting limb, tooth, hair, apocrine gland and genital development. Tbx3 is a …

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

H Carlson, S Ota, Y Song, Y Chen, PJ Hurlin - Oncogene, 2002 - nature.com
Tbx3 is a member of the T-box family of transcription factors. Mutations in Tbx3 cause ulnar-mammary
syndrome, an autosomal dominant disorder characterized by upper limb defects, …

[HTML][HTML] Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis

PJ Hurlin, ZQ Zhou, K Toyo‐oka, S Ota… - The EMBO …, 2003 - embopress.org
Mnt is a Max‐interacting transcriptional repressor that has been hypothesized to function as
a Myc antagonist. To investigate Mnt function we deleted the Mnt gene in mice. Since mice …

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

C Quéva, PJ Hurlin, KP Foley, RN Eisenman - Oncogene, 1998 - nature.com
Members of the Myc proto-oncogene family encode transcription factors that function in
multiple aspects of cell behavior, including proliferation, differentiation, transformation and …