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MAX dimerization protein 4

This gene is a member of the MAD gene family . The MAD genes encode basic helix-loop-helix-leucine zipper proteins that heterodimerize with MAX protein, forming a transcriptional repression complex. The MAD proteins compete for MAX binding with MYC, which heterodimerizes with MAX forming a transcriptional activation complex. Studies in rodents suggest that the MAD genes are tumor suppressors and contribute to the regulation of cell growth in differentiating tissues. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: c-Myc, MAX, Smad1, Mad3, Mad2
Papers on Mad4
Clinicopathological significance of somatic RNF43 mutation and aberrant expression of ring finger protein 43 in intraductal papillary mucinous neoplasms of the pancreas.
Furukawa et al., Tokyo, Japan. In Mod Pathol, Feb 2015
Statistical analysis was used to evaluate the associations between RNF43 aberrations and molecular and clinicopathological features including GNAS mutations, KRAS mutations, loss of SMA and MAD4 homologue expression, tumor protein 53 overexpression, tumor grade, histological type, mural nodule detection, macroscopic type, stage, recurrence, and survival.
Antiviral effects of artesunate on JC polyomavirus replication in COS-7 cells.
Rinaldo et al., Tromsø, Norway. In Antimicrob Agents Chemother, 2014
The permissivity for JCPyV MAD-4 was first compared in four cell lines, and the monkey kidney cell line COS-7 was selected.
The human fetal glial cell line SVG p12 contains infectious BK polyomavirus.
Rinaldo et al., Tromsø, Norway. In J Virol, 2014
JCPyV (MAD-4) was found to infect apparently uninfected and BKPyV-infected SVG p12 cells.
cMyc/miR-125b-5p signalling determines sensitivity to bortezomib in preclinical model of cutaneous T-cell lymphomas.
Gniadecki et al., Copenhagen, Denmark. In Plos One, 2012
Bortezomib repressed cMyc and simultaneously induced miR-125b-5p that exerted a cytoprotective effect through the downmodulation of MAD4.
Comparison between two progesterone sources and two oestradiol formulations in a Heatsynch protocol for postpartum cycling dairy cows in pasture.
Cavestany et al., Utrecht, Netherlands. In J Vet Sci, 2012
To compare an injectable progesterone (MAD-4) with an intravaginal device (IPD), and natural O17 with synthetic oestradiol (OB) in a synchronisation protocol, 51 cows were divided into four groups.
Isoprenoid biosynthesis is required for miRNA function and affects membrane association of ARGONAUTE 1 in Arabidopsis.
Voinnet et al., Strasbourg, France. In Proc Natl Acad Sci U S A, 2012
Here, we isolate the genes defined by the previously described miRNA action deficient (mad) mutants, mad3 and mad4.
The transcription factor Mxd4 controls the proliferation of the first blood precursors at the onset of hematopoietic development in vitro.
Kouskoff et al., Manchester, United Kingdom. In Exp Hematol, 2011
during embryonic hematopoietic differentiation Mxd4 is an important player in the regulation of blood progenitor proliferation, and downregulation of its expression might be required for a proliferative burst preceding lineage specification.
OX40 engagement stabilizes Mxd4 and Mnt protein levels in antigen-stimulated T cells leading to an increase in cell survival.
Weinberg et al., Portland, United States. In Eur J Immunol, 2011
Mxd4 and Mnt upregulation following OX40 engagement most likely increases T-cell survival
Associations of a polymorphism in the ornithine decarboxylase gene with colorectal cancer survival.
Anton-Culver et al., Irvine, United States. In Clin Cancer Res, 2009
The E-box activator c-MYC and repressors MAD1 and MAD4 preferentially bind to ODC1 minor A-alleles, compared with major G-alleles, in cultured cells.
The MAX-interacting transcription factor network.
Huang et al., 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.
Coordinated regulation of c-Myc and Max in rat liver development.
Gruppuso et al., Providence, United States. In Am J Physiol Gastrointest Liver Physiol, 2006
In contrast, mad4 expression was decreased in the fetal liver compared with the adult liver.
c-Myc creates an activation loop by transcriptionally repressing its own functional inhibitor, hMad4, in young fibroblasts, a loop lost in replicatively senescent fibroblasts.
Wang et al., Montréal, Canada. In J Cell Biochem, 2006
replicative senescence-specific factors may block c-Myc inhibition of Miz-1 activation of hMad4 expression, and the continual presence of hMad4 protein may transcriptionally repress selected c-Myc target genes
Human liver specific transcriptional factor TCP10L binds to MAD4.
Yu et al., Shanghai, China. In J Biochem Mol Biol, 2004
Data suggest that the biological function of the interaction between T-complex protein 10-like and MAD4 may be to maintain the differentiation state in liver cells.
Kinetics of myc-max-mad gene expression during hepatocyte proliferation in vivo: Differential regulation of mad family and stress-mediated induction of c-myc.
Leon et al., Santander, Spain. In Mol Carcinog, 2004
Mad proteins (Mad1, Mxi1, Mad3, Mad4, Mnt/Rox) are biochemical and biological antagonists of c-Myc oncoprotein.
Mad4 is regulated by a transcriptional repressor complex that contains Miz-1 and c-Myc.
Wright et al., Leeds, United Kingdom. In Biochem J, 2003
regulation by a transcriptional repressor complex that contains Miz-1 and c-Myc
K-ras, p53, and DPC4 (MAD4) alterations in fine-needle aspirates of the pancreas: a molecular panel correlates with and supplements cytologic diagnosis.
Wilentz et al., Amsterdam, Netherlands. In Am J Clin Pathol, 2002
A molecular panel that includes the K-ras, p53, and DPC4 (MAD4) genes correlates with and can supplement traditional cytologic diagnosis of pancreatic fine-needle aspirates.
Novel expression patterns of the myc/max/mad transcription factor network in developing murine prostate gland.
Kretzner et al., United States. In J Urol, 2001
The expression patterns of the 3 myc genes c-, L- and N-myc, and the mad1, mxi1 and mad4 genes were studied in most detail with nonradioactive in situ and immunohistochemical analyses.
Tetracyclines inhibit activated B cell function.
Bottaro et al., Rochester, United States. In Int Immunol, 2001
Suppression of Ig secretion correlates with a decrease in levels of mRNA for the terminal B cell differentiation-associated genes Blimp-1 and mad-4, as well as to a reduction in expression of the plasma cell markers Syndecan-1 and J chain.
Reversal of Blimp-1-mediated apoptosis by A1, a member of the Bcl-2 family.
Schimpl et al., Würzburg, Germany. In Eur J Immunol, 1999
Concomitantly, they exhibit altered ratios of c-myc/mad4 mRNA levels, a reduction in the expression of the anti-apoptotic bcl-2 family member A1 and a distinct growth disadvantage, followed by cell death.
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