نتایج جستجو برای: myc downstream

تعداد نتایج: 83881  

2016
Aleksandra Dakic Kyle DiVito Shuang Fang Frank Suprynowicz Anirudh Gaur Xin Li Nancy Palechor-Ceron Vera Simic Sujata Choudhury Songtao Yu Cynthia M. Simbulan-Rosenthal Dean Rosenthal Richard Schlegel Xuefeng Liu

The Myc/Max/Mad network plays a critical role in cell proliferation, differentiation and apoptosis and c-Myc is overexpressed in many cancers, including HPV-positive cervical cancer cell lines. Despite the tolerance of cervical cancer keratinocytes to high Myc expression, we found that the solitary transduction of the Myc gene into primary cervical and foreskin keratinocytes induced rapid cell ...

2009
Hyoung-gon Lee Qun Chen Julie A. Wolfram Sandy L. Richardson Anna Liner Sandra L. Siedlak Xiongwei Zhu Nicholas P. Ziats Hisashi Fujioka Dean W. Felsher Rudy J. Castellani Maria L. Valencik John A. McDonald Brian D. Hoit Edward J. Lesnefsky Mark A. Smith

While considerable evidence supports the causal relationship between increases in c-Myc (Myc) and cardiomyopathy as a part of a "fetal re-expression" pattern, the functional role of Myc in mechanisms of cardiomyopathy remains unclear. To address this, we developed a bitransgenic mouse that inducibly expresses Myc under the control of the cardiomyocyte-specific MHC promoter. In adult mice the in...

2005
Roy CY Choi Cecilia SS Wong Joseph Simon Eric A Barnard

The human P2Y1 sequence of 373 amino acids was terminated at position 354 (construct P2Y1-T1) or at position 334 (P2Y1-T2), covering almost all of the tail. These proteins were N-terminally tagged with the Myc epitope, giving Myc-P2Y1, Myc-P2Y1-T1 and MycP2Y1-T2, and expressed separately in 293 cells: reaction with fluorescent anti-Myc antibody showed in confocal microscopy that all three are t...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2010
Gregory S Yochum Colette M Sherrick Mary Macpartlin Richard H Goodman

Aberrant MYC gene expression by the Wnt/beta-catenin pathway is implicated in colorectal carcinogenesis. Wnt/beta-catenin signaling stimulates association of the beta-catenin coactivator complex with two Wnt responsive enhancers (WREs) located in close proximity to MYC gene boundaries. Each enhancer directly binds members of the TCF/Lef family of transcription factors that, in turn, recruit bet...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2012
Antje Menssen Per Hydbring Karsten Kapelle Jörg Vervoorts Joachim Diebold Bernhard Lüscher Lars-Gunnar Larsson Heiko Hermeking

Silent information regulator 1 (SIRT1) represents an NAD(+)-dependent deacetylase that inhibits proapoptotic factors including p53. Here we determined whether SIRT1 is downstream of the prototypic c-MYC oncogene, which is activated in the majority of tumors. Elevated expression of c-MYC in human colorectal cancer correlated with increased SIRT1 protein levels. Activation of a conditional c-MYC ...

2013
Maria B. Raeder Even Birkeland Jone Trovik Camilla Krakstad Shyemaa Shehata Steven Schumacher Travis I. Zack Antje Krohn Henrica MJ. Werner Susan E. Moody Elisabeth Wik Ingunn M. Stefansson Frederik Holst Anne M. Oyan Pablo Tamayo Jill P. Mesirov Karl H. Kalland Lars A. Akslen Ronald Simon Rameen Beroukhim Helga B. Salvesen

Chromosome 8q24 is the most commonly amplified region across multiple cancer types, and the typical length of the amplification suggests that it may target additional genes to MYC. To explore the roles of the genes most frequently included in 8q24 amplifications, we analyzed the relation between copy number alterations and gene expression in three sets of endometrial cancers (N = 252); and in g...

Journal: :Molecular and cellular biology 1999
M K Mateyak A J Obaya J M Sedivy

c-myc is a cellular proto-oncogene associated with a variety of human cancers and is strongly implicated in the control of cellular proliferation, programmed cell death, and differentiation. We have previously reported the first isolation of a c-myc-null cell line. Loss of c-Myc causes a profound growth defect manifested by the lengthening of both the G1 and G2 phases of the cell cycle. To gain...

Journal: :Cancer immunology research 2014
Suprawee Tepsuporn Jiazhi Hu Monica Gostissa Frederick W Alt

The Ataxia Telangiectasia-mutated (ATM) kinase senses DNA double-strand breaks (DSB) and facilitates their repair. In humans, ATM deficiency predisposes to B- and T-cell lymphomas, but in mice it leads only to thymic lymphomas. We tested the hypothesis that increased DSB frequency at a cellular oncogene could promote B-cell lymphoma by generating ATM-deficient mice with a V(D)J recombination ta...

Journal: :Cancer research 2000
K O Mitchell M S Ricci T Miyashita D T Dicker Z Jin J C Reed W S El-Deiry

The c-Myc oncoprotein is a transcription factor involved in cellular transformation as well as apoptotic cell death. We show here that over-expression of c-Myc delivered by an adenovirus vector up-regulates endogenous proapoptotic bax mRNA and protein expression in human cells. In contrast, the cytotoxic tumor necrosis factor-related apoptosis-inducing ligand induces cell death without up-regul...

Journal: :Molecular cancer research : MCR 2008
Konrad Huppi Natalia Volfovsky Timothy Runfola Tamara L Jones Mark Mackiewicz Scott E Martin J Frederic Mushinski Robert Stephens Natasha J Caplen

The PVT1 locus is identified as a cluster of T(2;8) and T(8;22) "variant" MYC-activating chromosomal translocation breakpoints extending 400 kb downstream of MYC in a subset (approximately 20%) of Burkitt's lymphoma (vBL). Recent reports that microRNAs (miRNA) may be associated with fragile sites and cancer-associated genomic regions prompted us to investigate whether the PVT1 region on chromos...

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