The Myc/Max/Mad network and the transcriptional control of cell behavior
C Grandori, SM Cowley, LP James… - Annual review of cell …, 2000 - annualreviews.org
▪ Abstract The Myc/Max/Mad network comprises a group of transcription factors whose
distinct interactions result in gene-specific transcriptional activation or repression. A great …
distinct interactions result in gene-specific transcriptional activation or repression. A great …
HIF and c-Myc: sibling rivals for control of cancer cell metabolism and proliferation
JD Gordan, CB Thompson, MC Simon - Cancer cell, 2007 - cell.com
O 2 deprivation (hypoxia) and cellular proliferation engage opposite cellular pathways, yet
often coexist during tumor growth. The ability of cells to grow during hypoxia results in part …
often coexist during tumor growth. The ability of cells to grow during hypoxia results in part …
Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis
N Santana-Codina, AA Roeth, Y Zhang, A Yang… - Nature …, 2018 - nature.com
Oncogenic KRAS is the key driver of pancreatic ductal adenocarcinoma (PDAC). We
previously described a role for KRAS in PDAC tumor maintenance through rewiring of …
previously described a role for KRAS in PDAC tumor maintenance through rewiring of …
Genomic targets of the human c-Myc protein
PC Fernandez, SR Frank, L Wang… - Genes & …, 2003 - genesdev.cshlp.org
The transcription factor Myc is induced by mitogenic signals and regulates downstream
cellular responses. If overexpressed, Myc promotes malignant transformation. Myc …
cellular responses. If overexpressed, Myc promotes malignant transformation. Myc …
c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function: a mechanism for oncogene-induced genetic instability
O Vafa, M Wade, S Kern, M Beeche, TK Pandita… - Molecular cell, 2002 - cell.com
Oncogene overexpression activates p53 by a mechanism posited to involve uncharacterized
hyperproliferative signals. We determined whether such signals produce metabolic …
hyperproliferative signals. We determined whether such signals produce metabolic …
X-ray structures of Myc-Max and Mad-Max recognizing DNA: molecular bases of regulation by proto-oncogenic transcription factors
X-ray structures of the basic/helix-loop-helix/leucine zipper (bHLHZ) domains of Myc-Max
and Mad-Max heterodimers bound to their common DNA target (Enhancer or E box …
and Mad-Max heterodimers bound to their common DNA target (Enhancer or E box …
The interplay between MYC and HIF in cancer
The interaction of MYC and hypoxia inducible factors (HIFs) under physiological, non-
tumorigenic conditions provides insights into normal homeostatic cellular responses to low …
tumorigenic conditions provides insights into normal homeostatic cellular responses to low …
Translocations involving c-myc and c-myc function
LM Boxer, CV Dang - Oncogene, 2001 - nature.com
Abstract c-MYC is the prototype for oncogene activation by chromosomal translocation. In
contrast to the tightly regulated expression of c-myc in normal cells, c-myc is frequently …
contrast to the tightly regulated expression of c-myc in normal cells, c-myc is frequently …
Repression of p15INK4b expression by Myc through association with Miz-1
P Staller, K Peukert, A Kiermaier, J Seoane, J Lukas… - Nature cell …, 2001 - nature.com
Deregulated expression of c-myc can induce cell proliferation in established cell lines and in
primary mouse embryonic fibroblasts (MEFs), through a combination of both transcriptional …
primary mouse embryonic fibroblasts (MEFs), through a combination of both transcriptional …
Low molecular weight inhibitors of Myc–Max interaction and function
X Yin, C Giap, JS Lazo, EV Prochownik - Oncogene, 2003 - nature.com
Abstract c-Myc is helix–loop–helix–leucine zipper (HLH–ZIP) oncoprotein that is frequently
deregulated in human cancers. In order to bind DNA, regulate target gene expression, and …
deregulated in human cancers. In order to bind DNA, regulate target gene expression, and …