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

REV7 Rev7p

The protein encoded by this gene is a component of the mitotic spindle assembly checkpoint that prevents the onset of anaphase until all chromosomes are properly aligned at the metaphase plate. The encoded protein, which is similar to MAD2L1, is capable of interacting with ADAM9, ADAM15, REV1, and REV3 proteins. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: REV3, POLYMERASE, Rev1, FUS, CAN
Papers using REV7 antibodies
Emerging roles of DNA tumor viruses in cell proliferation: new insights into genomic instability.
Abraham Edathara, In PLoS ONE, 2002
... The pJ69-4A strain was co-transfected with bait plasmid pBDT3C, carrying the human MAD2B coding sequence (AL031731), and the testis cDNA library using the Yeastmaker transformation kit (Clontech).
Papers on REV7
Targeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds.
Tarsounas et al., Roma, Italy. In Mol Cell, Jan 2016
PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7.
Rev7/Mad2B plays a critical role in the assembly of a functional mitotic spindle.
Xiao et al., Canada. In Cell Cycle, Jan 2016
Mad2, an anaphase-promoting complex/cyclosome-Cdc20 (APC/C(Cdc20)) inhibitor, has an additional homolog in mammals known as Mad2B, Mad2L2 or Rev7.
High expression of REV7 is an independent prognostic indicator in patients with diffuse large B-cell lymphoma treated with rituximab.
Murakumo et al., Sagamihara, Japan. In Int J Hematol, Dec 2015
REV7 is a multifunctional protein involved in DNA damage tolerance, cell-cycle regulation, gene expression, and carcinogenesis.
Visceral obesity stimulates anaphase bridge formation and spindle assembly checkpoint dysregulation in radioresistant oesophageal adenocarcinoma.
O'Sullivan et al., Dublin, Ireland. In Clin Transl Oncol, Nov 2015
Expression of two spindle assembly complex genes (MAD2L2, BUB1B) was assessed using qPCR, and validated in patient tumour specimens from viscerally obese (n = 46) and nonobese patients (n = 41).
REV7 counteracts DNA double-strand break resection and affects PARP inhibition.
Rottenberg et al., Amsterdam, Netherlands. In Nature, Jun 2015
Here we show that loss of REV7 (also known as MAD2L2) in mouse and human cell lines re-establishes CTIP-dependent end resection of DSBs in BRCA1-deficient cells, leading to HR restoration and PARP inhibitor resistance, which is reversed by ATM kinase inhibition.
MAD2L2 controls DNA repair at telomeres and DNA breaks by inhibiting 5' end resection.
Jacobs et al., Amsterdam, Netherlands. In Nature, Jun 2015
Here we identify MAD2L2 (also known as MAD2B or REV7) through functional genetic screening as a novel factor controlling DNA repair activities at mammalian telomeres.
Crystallization and X-ray diffraction analysis of the ternary complex of the C-terminal domain of human REV1 in complex with REV7 bound to a REV3 fragment involved in translesion DNA synthesis.
Hashimoto et al., Yokohama, Japan. In Acta Crystallogr Sect F Struct Biol Cryst Commun, 2012
ternary complex of the C-terminal domain of human REV1 in complex with REV7 bound to a REV3 fragment has been crystallized. The crystals belonged to space group P3(1)21, with unit-cell parameters a = b = 74.7, c = 124.5 A
Multifaceted recognition of vertebrate Rev1 by translesion polymerases ζ and κ.
Zhou et al., Durham, United States. In J Biol Chem, 2012
identification of the Rev7 binding surface of the Rev1 C-terminal domain
REV1 and polymerase ζ facilitate homologous recombination repair.
Canman et al., Ann Arbor, United States. In Nucleic Acids Res, 2012
The REV1/Polzeta complex maintains genomic stability by directly participating in DNA double-stranded break repair.
Lesion bypass by S. cerevisiae Pol ζ alone.
Kunkel et al., United States. In Dna Repair (amst), 2011
in addition to extending aberrant termini created by other DNA polymerases, Pol zeta has the potential to be the sole DNA polymerase involved in translesion synthesis
The mitotic arrest deficient protein MAD2B interacts with the clathrin light chain A during mitosis.
van Kessel et al., Nijmegen, Netherlands. In Plos One, 2009
Data show that MAD2B interacts with CLTA during the G2/M phase of the cell cycle and that depletion of MAD2B leads to a marked increase in the percentage of misaligned chromosomes and a redistribution of CLTA during mitosis.
DNA polymerase zeta (pol zeta) in higher eukaryotes.
Wood et al., Pittsburgh, United States. In Cell Res, 2008
Functions for REV3L and REV7(MAD2B) in higher eukaryotes have been suggested not only in translesion DNA synthesis but also in some forms of homologous recombination, repair of interstrand DNA crosslinks, somatic hypermutation of immunoglobulin genes and cell-cycle control.
A bacterial effector targets Mad2L2, an APC inhibitor, to modulate host cell cycling.
Sasakawa et al., Tokyo, Japan. In Cell, 2007
Here, we show that the Shigella effector IpaB, when delivered into epithelial cells, causes cell-cycle arrest by targeting Mad2L2, an anaphase-promoting complex/cyclosome (APC) inhibitor.
DNA polymerase zeta: new insight into eukaryotic mutagenesis and mammalian embryonic development.
Zhang et al., Hangzhou, China. In World J Gastroenterol, 2003
Human REV3 amino acid residues 1 776-2 195 provide a REV7 binding domain, and REV7 amino acid residues 1-211 provide a bind domain for REV1, REV3 and REV7 itself.
The property of DNA polymerase zeta: REV7 is a putative protein involved in translesion DNA synthesis and cell cycle control.
Murakumo, Nagoya, Japan. In Mutat Res, 2003
In yeast Saccharomyces cerevisiae (S. cerevisiae), DNA polymerase zeta, which consists of Rev3 and Rev7 proteins, and Rev1 are known to be involved in most damage-induced and spontaneous mutations.
Mutagenesis in eukaryotes dependent on DNA polymerase zeta and Rev1p.
Maher et al., Rochester, United States. In Philos Trans R Soc Lond B Biol Sci, 2001
Pol zeta, a non-processive enzyme that lacks a 3' to 5' exonuclease proofreading activity, is composed of Rev3p, the catalytic subunit, and a second subunit encoded by REV7.
Deoxycytidyl transferase activity of yeast REV1 protein.
Hinkle et al., Rochester, United States. In Nature, 1996
Mutagenesis induced by DNA damage in Saccharomyces cerevisiae requires the products of the REV1, REV3 and REV7 genes.
Thymine-thymine dimer bypass by yeast DNA polymerase zeta.
Hinkle et al., Rochester, United States. In Science, 1996
The REV3 and REV7 genes of the yeast Saccharomyces cerevisiae are required for DNA damage-induced mutagenesis.
DNA polymerase zeta and the control of DNA damage induced mutagenesis in eukaryotes.
Hinkle et al., Rochester, United States. In Cancer Surv, 1995
In budding yeast, Saccharomyces cerevisiae, a good model system with which to investigate this process, mutagenesis is associated with the RAD6 repair pathway and depends on the functions of the REV1, REV3 and REV7 genes.
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