The MAX-interacting transcription factor network.
Portland, United States. In Semin Cancer Biol, 2006
MAX serves as a cofactor for DNA binding by the various members of this network, which include the MYC family of oncoproteins and a group of putative MYC antagonists that include MNT, MXD1-4 (formerly MAD1, MXI1, MAD3 and MAD4) and MGA.
Lessons learned from Myc/Max/Mad knockout mice.
United States. In Curr Top Microbiol Immunol, 2005
Here we summarize the findings obtained from the myc/max/mad knockout mice generated to date, namely those in which the N-myc, c-myc, L-myc, mad1, mxi1, mad3, mnt, or max genes have been targeted.
Suppression of spontaneous chromosomal rearrangements by S phase checkpoint functions in Saccharomyces cerevisiae.
San Diego, United States. In Cell, 2001
Mutations in Saccharomyces cerevisiae RFC5, DPB11, MEC1, DDC2 MEC3, RAD53, CHK1, PDS1, and DUN1 increased the rate of genome rearrangements up to 200-fold whereas mutations in RAD9, RAD17, RAD24, BUB3, and MAD3 had little effect.
Activation of NF-kappa B by the Tax protein of HTLV-1.
Paris, France. In Immunobiology, 1995
It has been previously shown that Tax is able to induce nuclear translocation of NF-kappa B. The activity of the NF-kappa B transcription factor is normally controlled through cytoplasmic retention by either of two types of molecules: the inhibitor I kappa B alpha/MAD3 or the p105 and p100 precursors of the p50 and p52 DNA-binding subunits.