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P J Hurlin

Explore the profile of P J Hurlin including associated specialties, affiliations and a list of published articles. Areas
Snapshot
Articles 19
Citations 631
Followers 0
Related Specialties
Molecular Biology
Oncology
Biotechnology
Top 10 Co-Authors
R N Eisenman
C Queva
D E Ayer
J J McCormick
V M Maher
K P Foley
D G Fry
E Steingrimsson
N G Copeland
P J Koskinen
Published In
EMBO J
Proc Natl Acad Sci U S A
Oncogene
Cold Spring Harb Symp Quant Biol
Cancer Res
Affiliations
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Recent Articles
1.
A dominant repression domain in Tbx3 mediates transcriptional repression and cell immortalization: relevance to mutations in Tbx3 that cause ulnar-mammary syndrome
Carlson H, Ota S, Campbell C, Hurlin P
Hum Mol Genet . 2001 Nov; 10(21):2403-13. PMID: 11689487
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 member of a family of...
2.
The interplay between Mad and Myc in proliferation and differentiation
Zhou Z, Hurlin P
Trends Cell Biol . 2001 Oct; 11(11):S10-4. PMID: 11684436
Members of the Myc family of transcription factors are key regulators of cell proliferation, and excessive levels of Myc lead to tumor formation. Mad family proteins are related to Myc,...
3.
Mga, a dual-specificity transcription factor that interacts with Max and contains a T-domain DNA-binding motif
Hurlin P, Steingrimsson E, Copeland N, Jenkins N, Eisenman R
EMBO J . 1999 Dec; 18(24):7019-28. PMID: 10601024
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 function of these proteins as transcription...
4.
Analysis of the Max-binding protein MNT in human medulloblastomas
Sommer A, Waha A, Tonn J, Sorensen N, Hurlin P, Eisenman R, et al.
Int J Cancer . 1999 Aug; 82(6):810-6. PMID: 10446446
Medulloblastomas (MBs) are the most frequent malignant brain tumors in children. The molecular pathogenesis of these tumors is still poorly understood. Microsatellite and restriction-fragment-length polymorphism studies have revealed allelic loss...
5.
The Mad protein family links transcriptional repression to cell differentiation
McArthur G, Laherty C, Queva C, Hurlin P, Loo L, James L, et al.
Cold Spring Harb Symp Quant Biol . 1999 Jun; 63:423-33. PMID: 10384307
No abstract available.
6.
Sequential expression of the MAD family of transcriptional repressors during differentiation and development
Queva C, Hurlin P, Foley K, Eisenman R
Oncogene . 1998 Mar; 16(8):967-77. PMID: 9519870
Members of the Myc proto-oncogene family encode transcription factors that function in multiple aspects of cell behavior, including proliferation, differentiation, transformation and apoptosis. Recent studies have shown that MYC activities...
7.
Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation
Foley K, McArthur G, Queva C, Hurlin P, Soriano P, Eisenman R
EMBO J . 1998 Mar; 17(3):774-85. PMID: 9451002
The switch from transcriptionally activating MYC-MAX to transcriptionally repressing MAD1-MAX protein heterodimers has been correlated with the initiation of terminal differentiation in many cell types. To investigate the function of...
8.
Mnt: a novel Max-interacting protein and Myc antagonist
Hurlin P, Queva C, Eisenman R
Curr Top Microbiol Immunol . 1997 Jan; 224:115-21. PMID: 9308234
We have identified a novel Max-binding protein, Mnt, which belongs to neither the Myc nor the Mad families (Hurlin et al. 1997). Mnt interacts with Max in vivo and functions...
9.
Mnt, a novel Max-interacting protein is coexpressed with Myc in proliferating cells and mediates repression at Myc binding sites
Hurlin P, Queva C, Eisenman R
Genes Dev . 1997 Jan; 11(1):44-58. PMID: 9000049
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 proteins. Myc:Max complexes activate...
10.
Mad3 and Mad4: novel Max-interacting transcriptional repressors that suppress c-myc dependent transformation and are expressed during neural and epidermal differentiation
Hurlin P, Queva C, Koskinen P, Steingrimsson E, Ayer D, Copeland N, et al.
EMBO J . 1996 Apr; 15(8):2030. PMID: 8617250
No abstract available.