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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

MAD3 Mad3p

Mad3, Mad3p
This gene encodes a member of the Myc superfamily of basic helix-loop-helix leucine zipper transcriptional regulators. The encoded protein forms a heterodimer with the cofactor MAX which binds specific E-box DNA motifs in the promoters of target genes and regulates their transcription. Disruption of the MAX-MXD3 complex is associated with uncontrolled cell proliferation and tumorigenesis. Transcript variants of this gene encoding different isoforms have been described.[provided by RefSeq, Dec 2008] (from NCBI)
Top mentioned proteins: Bub1, Bub3, Smad1, Mad2, CAN
Papers on Mad3
Three BUB1 and BUBR1/MAD3-related spindle assembly checkpoint proteins are required for accurate mitosis in Arabidopsis.
Favery et al., Antibes, France. In New Phytol, 2015
Early in mitosis, BUB3.1 and BUBR1/MAD3.1 localise to the mitotic spindle, where MAP65-3 organises spindle MTs.
Dot1L mediated histone H3 lysine79 methylation is essential to meiosis progression in mouse oocytes.
Liu et al., Nanjing, China. In Neuro Endocrinol Lett, 2013
In Dot1L deficient, accompanying with BubR1 (MAD3/Bub1b) remains on the chromosome, the mouse oocytes was blocked in metaphase of meiosis I.
Construction of protein phosphorylation networks by data mining, text mining and ontology integration: analysis of the spindle checkpoint.
Wu et al., Newark, United States. In Database (oxford), 2012
The phosphorylation networks we construct, centered on the human checkpoint kinase BUB1B (BubR1) and its yeast counterpart MAD3, offer a unique view of the spindle checkpoint that emphasizes biologically relevant phosphorylated forms, phosphorylation-state-specific PPIs and kinase-substrate relationships.
Kinase activity of fission yeast Mph1 is required for Mad2 and Mad3 to stably bind the anaphase promoting complex.
Hardwick et al., Edinburgh, United Kingdom. In Curr Biol, 2012
A kinase-dead allele of the fission yeast MPS1 homolog (Mph1) is checkpoint defective and levels of anaphase promoting complex-associated Mad2 and Mad3 are dramatically reduced in this mutant.
Mad2 and Mad3 cooperate to arrest budding yeast in mitosis.
Murray et al., Cambridge, United States. In Curr Biol, 2012
Mad3 is required for the stable binding of Mad2 to Cdc20 in vivo, which is sufficient to inhibit APC activity and is the most downstream event in spindle checkpoint activation.
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.
Effects of artesunate on cytokinesis and G₂/M cell cycle progression of tumour cells and budding yeast.
Efferth et al., Mainz, Germany. In Cancer Genomics Proteomics, 2010
The mitotic spindle checkpoint genes bub1, bub2, bub3, mad1, mad2 and mad3 were individually deleted and the sensitivity of these mutants towards artesunate was determined by monitoring the cell growth.
Mad3 negatively regulates B cell differentiation in the spleen by inducing Id2 expression.
Shachar et al., Israel. In Mol Biol Cell, 2010
Results demonstrate that high expression levels of Mad3 in immature B cells induce Id2 expression, which inhibits transcription of genes essential for B cell differentiation.
BubR1 is a spindle assembly checkpoint protein regulating meiotic cell cycle progression of mouse oocyte.
Sun et al., Beijing, China. In Cell Cycle, 2010
BubR1 (Bub1-related kinase or MAD3/Bub1b) is an essential component of the spindle assembly checkpoint (SAC) and plays an important role in kinetochore localization of other spindle checkpoint proteins in mitosis.
The synaptonemal complex protein, Zip1, promotes the segregation of nonexchange chromosomes at meiosis I.
Hoffmann et al., Brighton, United Kingdom. In Proc Natl Acad Sci U S A, 2010
A mutation in the MAD3 gene, which encodes a component of the spindle checkpoint, also increases the nondisjunction of NECs.
TGF-beta1-induced expression of human Mdm2 correlates with late-stage metastatic breast cancer.
Mayo et al., Dallas, United States. In J Clin Invest, 2010
In this study, we report that TGF-beta1-activated SMA- and MAD3 (Smad3/4) transcription factors specifically bound to the second promoter region of HDM2, leading to increased HDM2 protein expression and destabilization of p53 in human cancer cell lines.
Adenosine signaling mediates SUMO-1 modification of IkappaBalpha during hypoxia and reoxygenation.
Ibla et al., Boston, United States. In J Biol Chem, 2009
Adenosine signaling mediates SUMO-1 modification of IkappaBalpha during hypoxia and reoxygenation.
SPDL-1 functions as a kinetochore receptor for MDF-1 in Caenorhabditis elegans.
Kitagawa et al., Memphis, United States. In J Cell Biol, 2008
An RNA interference screen for synthetic genetic interactors with a conserved SAC gene, san-1/MAD3, identified spdl-1, a Caenorhabditis elegans homologue of Spindly.
The spindle checkpoint functions of Mad3 and Mad2 depend on a Mad3 KEN box-mediated interaction with Cdc20-anaphase-promoting complex (APC/C).
Hardwick et al., Edinburgh, United Kingdom. In J Biol Chem, 2008
the Mad3 KEN box is a critical mediator of Cdc20-APC/C inhibition, without which neither Mad3 nor Mad2 can associate with the APC/C or inhibit anaphase onset
Genetic analysis of the spindle checkpoint genes san-1, mdf-2, bub-3 and the CENP-F homologues hcp-1 and hcp-2 in Caenorhabditis elegans.
Padilla et al., Denton, United States. In Cell Div, 2007
To investigate the role san-1, the MAD3 homologue, has in Caenorhabditis elegans embryos we used RNA interference (RNAi) to identify genes synthetic lethal with the viable san-1(ok1580) deletion mutant.
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.
Lessons learned from Myc/Max/Mad knockout mice.
Schreiber-Agus et al., 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.
The roles of MAD1, MAD2 and MAD3 in meiotic progression and the segregation of nonexchange chromosomes.
Dawson et al., Boston, United States. In Nat Genet, 2005
These studies showed that the spindle checkpoint genes MAD1, MAD2 and MAD3 have different roles.
Suppression of spontaneous chromosomal rearrangements by S phase checkpoint functions in Saccharomyces cerevisiae.
Kolodner et al., 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.
Israël et al., 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.
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