Results 31 to 40 of about 20,867,404 (313)
Overexpression of c-Myc and cell immortalization alters c-Myc phosphorylation [PDF]
Oncogene, 1997 Using an extensive series of deletion and site-specific mutation constructs, we have identified five new phosphorylation sites in c-Myc in the N-terminal transactivation domain and near the C-terminal DNA binding/heterodimerization domain. We have also found that Thr-58 phosphorylation is regulated by specific cellular events.
B, Lutterbach, S R, Hann
openaire +2 more sources
Global regulation of nucleotide biosynthetic genes by c-Myc. [PDF]
PLoS ONE, 2008 The c-Myc transcription factor is a master regulator and integrates cell proliferation, cell growth and metabolism through activating thousands of target genes.
Yen-Chun Liu +8 more
doaj +1 more source
Apoptotic signaling by c-MYC [PDF]
Oncogene, 2008 c-MYC has a pivotal function in growth control, differentiation and apoptosis, and its abnormal expression is associated with many tumors. Overexpression of c-MYC sensitizes cells to apoptosis by a variety of stimuli. The decision of a cell to undergo apoptosis and how this apoptotic response is regulated by c-MYC depends on the specific cell type and ...
B, Hoffman, D A, Liebermann
openaire +2 more sources
Runx transcription factors repress human and murine c-Myc expression in a DNA-binding and C-terminally dependent manner. [PDF]
PLoS ONE, 2013 The transcription factors Runx1 and c-Myc have individually been shown to regulate important gene targets as well as to collaborate in oncogenesis. However, it is unknown whether there is a regulatory relationship between the two genes. In this study, we
Paejonette T Jacobs +6 more
doaj +1 more source
Oncogenesis, 2020 Hepatocellular carcinoma (HCC) is a highly heterogeneous, multigene-driven malignant tumor. Long chain acyl-CoA synthetase 4 (ACSL4), an enzyme has pivotal roles in arachidonic acid (AA) metabolism.
Jun-Ru Chen +13 more
semanticscholar +1 more source
Integration of genome and chromatin structure with gene expression profiles to predict c-MYC recognition site binding and function. [PDF]
PLoS Computational Biology, 2007 The MYC genes encode nuclear sequence specific-binding DNA-binding proteins that are pleiotropic regulators of cellular function, and the c-MYC proto-oncogene is deregulated and/or mutated in most human cancers. Experimental studies of MYC binding to the
Yili Chen +5 more
doaj +1 more source
Sequential and coordinated actions of c-Myc and N-Myc control appendicular skeletal development. [PDF]
PLoS ONE, 2011 BACKGROUND: During limb development, chondrocytes and osteoblasts emerge from condensations of limb bud mesenchyme. These cells then proliferate and differentiate in separate but adjacent compartments and function cooperatively to promote bone growth ...
Zi-Qiang Zhou +5 more
doaj +1 more source
Myc interacts with Max and Miz1 to repress C/EBPδ promoter activity and gene expression
Molecular Cancer, 2010 Background "Loss of function" alterations in CCAAT/Enhancer Binding Proteinδ (C/EBPδ) have been reported in a number of human cancers including breast, prostate and cervical cancer, hepatocellular carcinoma and acute myeloid leukemia.
Yu Xueyan +3 more
doaj +1 more source
c-Myc and Cancer Metabolism [PDF]
Clinical Cancer Research, 2012 Abstract The processes of cellular growth regulation and cellular metabolism are closely interrelated. The c-Myc oncogene is a “master regulator” which controls many aspects of both of these processes. The metabolic changes which occur in transformed cells, many of which are driven by c-Myc overexpression, are necessary to support the ...
Donald M, Miller +4 more
openaire +2 more sources
c-MYC Copy-Number Gain Is an Independent Prognostic Factor in Patients with Colorectal Cancer. [PDF]
PLoS ONE, 2015 The aim of this study was to determine the incidence and clinicopathological significance of c-MYC gene copy-number (GCN) gain in patients with primary colorectal cancer (CRC).The c-MYC GCN was investigated in 367 consecutive CRC patients (cohort 1) by ...
Kyu Sang Lee +7 more
doaj +1 more source