The c-Myc proto-oncogene is an essential activator of cell proliferation and one of the genes most commonly deregulated in cancer. Although these activities of c-Myc are thought to result from its function as a transcription factor, the scientific literature contains hints that this is not the whole story. A new paper in Nature by Dominguez-Sola et al. reports the surprising observation that c-Myc promotes DNA replication via a nontranscriptional mechanism, and that c-Myc deregulation causes DNA damage predominately during S phase. These results identify c-Myc as a new DNA replication factor and suggest an alternative model for its role in cell growth and tumorigenesis
The cell culture environment (substrate, atmosphere, and medium) can have a significant influence on...
A major pathway for repair of DNA double-strand breaks is nonhomologous end-joining (NHEJ). In this ...
Clinical assessment of the response to antiangiogenic therapy has been cumbersome. A study in this i...
O2 deprivation (hypoxia) and cellular proliferation engage opposite cellular pathways, yet often coe...
Linker histones of the H1 family are among the most abundant components of chromatin. In this issue ...
In this issue of Cell, Grunewald et al. (2006) examine the role of hematopoietic cells in the format...
The complexity of genomic aberrations in most human tumors hampers delineation of the genes that dri...
Both cellular differentiation and stem cell maintenance must occur at the root apex in order to ensu...
The application of novel genetic/genomic technologies to the study of acute leukemia has frequently ...
The death receptor ligand TRAIL has shown remarkable promise as an anticancer agent. However, TRAIL ...
In this issue of Cell, Guenther et al. (2007) analyze the presence of chromatin marks and RNA polyme...
The posttranslational modification of proteins by methylglyoxal, a highly reactive compound derived ...
The use of integrating vectors for gene therapy - required for stable correction of gene expression ...
Although multiple members of the phosphatidylinositol-3-kinase pathway (PI3K) are targeted by germli...
In this Commentary we aim to provide an overview of some specific examples of cancer therapeutics, i...
The cell culture environment (substrate, atmosphere, and medium) can have a significant influence on...
A major pathway for repair of DNA double-strand breaks is nonhomologous end-joining (NHEJ). In this ...
Clinical assessment of the response to antiangiogenic therapy has been cumbersome. A study in this i...
O2 deprivation (hypoxia) and cellular proliferation engage opposite cellular pathways, yet often coe...
Linker histones of the H1 family are among the most abundant components of chromatin. In this issue ...
In this issue of Cell, Grunewald et al. (2006) examine the role of hematopoietic cells in the format...
The complexity of genomic aberrations in most human tumors hampers delineation of the genes that dri...
Both cellular differentiation and stem cell maintenance must occur at the root apex in order to ensu...
The application of novel genetic/genomic technologies to the study of acute leukemia has frequently ...
The death receptor ligand TRAIL has shown remarkable promise as an anticancer agent. However, TRAIL ...
In this issue of Cell, Guenther et al. (2007) analyze the presence of chromatin marks and RNA polyme...
The posttranslational modification of proteins by methylglyoxal, a highly reactive compound derived ...
The use of integrating vectors for gene therapy - required for stable correction of gene expression ...
Although multiple members of the phosphatidylinositol-3-kinase pathway (PI3K) are targeted by germli...
In this Commentary we aim to provide an overview of some specific examples of cancer therapeutics, i...
The cell culture environment (substrate, atmosphere, and medium) can have a significant influence on...
A major pathway for repair of DNA double-strand breaks is nonhomologous end-joining (NHEJ). In this ...
Clinical assessment of the response to antiangiogenic therapy has been cumbersome. A study in this i...