The Myc/Max/Mad network and the transcriptional control of cell behavior.

By C. Grandori, S. Cowley, L. James, R. Eisenman. Annual Review of Cell and Developmental Biology, 2000

1,370 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/8e2b26d081c9ce9b4fb3aa75e933fb8da5359faa

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Citations in the corpus

Nucleotide Deficiency Promotes Genomic Instability in Early Stages of Cancer Development (2011, neutral): “In many cancers, c-myc is highly expressed at a later stage in development (Grandori et al., 2000).”
Genomic targets of the human c-Myc protein. (2003, background): “Sequence analysis of Myc-target sites reveals a preponderance of CpG islands The above data confirm that recognition of the E-box motif by Myc/Max is a primary determinant of target gene selectivity in vivo (Amati et al. 1992; Kretzner et al. 1992; Boyd and Farnham 1997; Frank et al. 2001; Zeller et”
MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “Elevated c-Myc expression is common in many cancers (Grandori et al., 2000).”
The interplay between MYC and HIF in cancer (2008, background): “MYC is a helix–loop–helix leucine zipper transcription factor that heterodimerizes with a partner protein, MYC-associated protein X ( MAX ), which is itself under tight regulation by a network of protein–protein interactions with MAX dimerization protein (MAD, also known as MXD1 ) and MAX interacto”
Malignant glioma: genetics and biology of a grave matter. (2001, background): “Mad proteins modulate cellular growth control and may participate in the induction and maintenance of the differentiated state (Grandori et al. 2000).”
The Rice Tapetum Degeneration Retardation Gene Is Required for Tapetum Degradation and Anther Development[W] (2006, background): “…and developmental processes (Murre et al., 1989; Goodrich et al., 1992; Ferre-D’Amare et al., 1994; Kawagoe and Murai, 1996; Abe et al., 1997; Ni et al., 1998; Fairchild et al., 2000; Grandori et al., 2000; Massari and Murre, 2000; Spelt et al., 2000; Heisler et al., 2001; Chinnusamy et al., 2003).”
Myc suppression of the p21Cip1 Cdk inhibitor influences the outcome of the p53 response to DNA damage (2002, background): “Myc is a transcription factor that promotes cell growth and proliferation, and, under certain conditions, apoptosi”
Transcription factors as targets for cancer therapy (2002, background): “cgi?l=4609">MYC , which is pervasively increased in cance”
The Arabidopsis Basic/Helix-Loop-Helix Transcription Factor Family Online version contains Web-only data. Article, publication date, and citation information can be found at www.plantcell.org/cgi/doi/10.1105/tpc.013839. (2003, background): “We also experimentally test the predicted DNA binding activity and heterodimerization potential of two related members of the family, PIF3 and PIF4 (Huq and Quail, 2002), that are involved in phytochrome signaling to test the hypothesis that heterodimeric interactions between the members of the fami”
c-Myc controls the balance between hematopoietic stem cell self-renewal and differentiation. (2004, background): “…in the BM, the effect of c-Myc loss on proliferation and survival of KLS-HSCs was determined. c-Myc is known to play an important role in the control of proliferation and survival of various cell GENES & DEVELOPMENT 2749 types (Grandori et al. 2000; Trumpp et al. 2001; Pelengaris et al. 2002a).”