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

RAD18 Rad18p

RAD18, Smc6
The protein encoded by this gene is highly similar to S. cerevisiae DNA damage repair protein Rad18. Yeast Rad18 functions through its interaction with Rad6, which is an ubiquitin-conjugating enzyme required for post-replication repair of damaged DNA. Similar to its yeast counterpart, this protein is able to interact with the human homolog of yeast Rad6 protein through a conserved ring-finger motif. Mutation of this motif results in defective replication of UV-damaged DNA and hypersensitivity to multiple mutagens. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Ubiquitin, PCNA, CAN, POLYMERASE, RAD52
Papers on RAD18
The p53-p21-DREAM-CDE/CHR pathway regulates G2/M cell cycle genes.
Engeland et al., Leipzig, Germany. In Nucleic Acids Res, Feb 2016
The target gene list was verified by detailed analysis of p53-dependent repression of the cell cycle genes B-MYB (MYBL2), BUB1, CCNA2, CCNB1, CHEK2, MELK, POLD1, RAD18 and RAD54L.
Genomic Copy Number Variations Characterize the Prognosis of Both P16-Positive and P16-Negative Oropharyngeal Squamous Cell Carcinoma After Curative Resection.
Jung et al., Seoul, South Korea. In Medicine (baltimore), Dec 2015
Loss of a locus containing FGF18 led to a worse, but gain of region including CDK10 and RAD18 led to better overall survival (OS) in all OSCC patients.
RAD18, WRNIP1 and ATMIN promote ATM signalling in response to replication stress.
Behrens et al., Pavia, Italy. In Oncogene, Dec 2015
ATMIN, WRNIP1 and RAD18, the E3 ligase responsible for PCNA monoubiquitination, are specifically required for ATM signalling and 53BP1 focus formation induced by replication stress, not ionising radiation.
FANCD2 and REV1 cooperate in the protection of nascent DNA strands in response to replication stress.
Guo et al., Beijing, China. In Nucleic Acids Res, Oct 2015
We found that REV1 is targeted to laser-induced DNA damage stripes in a manner dependent on its ubiquitin-binding motifs, on RAD18, and on monoubiquitinated FANCD2 (FANCD2-mUb) that associates with REV1.
RAD18 Is a Maternal Limiting Factor Silencing the UV-Dependent DNA Damage Checkpoint in Xenopus Embryos.
Maiorano et al., Montpellier, France. In Dev Cell, Sep 2015
Here we identify the RAD18 ubiquitin ligase as one such factor in Xenopus.
DNA repair. Proteomics reveals dynamic assembly of repair complexes during bypass of DNA cross-links.
Mann et al., Martinsried, Germany. In Science, Jun 2015
Among numerous prospective DNA repair factors, we identified SLF1 and SLF2, which form a complex with RAD18 and together define a pathway that suppresses genome instability by recruiting the SMC5/6 cohesion complex to DNA lesions.
Functional Role of NBS1 in Radiation Damage Response and Translesion DNA Synthesis.
Komatsu et al., Kyoto, Japan. In Biomolecules, 2014
In addition to DSB response, we showed that NBS1 initiates Polη-dependent translesion DNA synthesis by recruiting RAD18 through its binding at the NBS1 C-terminus after UV exposure, and it also functions after the generation of interstrand crosslink DNA damage.
Tolerating DNA damage during eukaryotic chromosome replication.
Tercero et al., Madrid, Spain. In Exp Cell Res, 2014
In eukaryotes, the evolutionarily conserved RAD6/RAD18 pathway of DNA damage tolerance overcomes unrepaired DNA lesions that interfere with the progression of replication forks, helping to ensure the completion of chromosome replication and the maintenance of genome stability in every cell cycle.
Regulation and roles of Cdc7 kinase under replication stress.
Bartek et al., Olomouc, Czech Republic. In Cell Cycle, 2013
In this review, we first highlight the recent findings on a novel pathway that regulates the stability of the human Cdc7-ASK/Dbf4 complex under replication stress, its interplay with ATR-Chk1 signaling, and significance in the RAD18-dependent DNA damage bypass pathway.
Two replication fork maintenance pathways fuse inverted repeats to rearrange chromosomes.
Hasty et al., San Antonio, United States. In Nature, 2013
EF-PRR bypasses DNA incongruities that impede replication by ubiquitinating PCNA (proliferating cell nuclear antigen) using the RAD6-RAD18 and UBC13-MMS2-RAD5 ubiquitin ligase complexes.
Tandem protein interaction modules organize the ubiquitin-dependent response to DNA double-strand breaks.
Durocher et al., Toronto, Canada. In Mol Cell, 2012
RNF168, its paralog RNF169, RAD18, and the BRCA1-interacting RAP80 protein accumulate at DNA double strand break sites through the use of bipartite modules composed of ubiquitin binding sites.
Requirement of Rad18 protein for replication through DNA lesions in mouse and human cells.
Prakash et al., Galveston, United States. In Proc Natl Acad Sci U S A, 2012
The Rad6-Rad18 enzyme plays an essential role in promoting replication through DNA lesions by translesion synthesis in mammalian cells.
c-Jun N-terminal kinase-mediated Rad18 phosphorylation facilitates Polη recruitment to stalled replication forks.
Vaziri et al., Galway, Ireland. In Mol Biol Cell, 2012
Ser409, located within the pol-eta binding domain of Rad18, is phosphorylated by c-jun kinase in response to dna damage, promoting the interaction between Rad18 and pol-eta.
[RAD18 gene product of yeast Saccharomyces cerevisiae controls mutagenesis induced by hydrogen peroxide].
Korolev et al., In Genetika, 2012
In this study we showed that DNA damage induced by hydrogen peroxide at the same mutagen doses causes significantly more mutations and lethal events in the rad18 mutant cells compared to control wild-type cells
Rad18 is a transcriptional target of E2F3.
Martinez et al., Jackson, United States. In Cell Cycle, 2012
E2F3 controls the ubiquitination of PCNA through the transcriptional regulation of Rad18.
Ubiquitylation of the 9-1-1 checkpoint clamp is independent of rad6-rad18 and DNA damage.
Ulrich et al., London, United Kingdom. In Cell, 2010
Rad17, a subunit of the PCNA-like 9-1-1 checkpoint clamp is ubiquitylated; however, in contrast to previous results, modification of Rad17 is found to be independent of DNA damage, the Rad6-Rad18 complex.
RAD18 transmits DNA damage signalling to elicit homologous recombination repair.
Chen et al., New Haven, United States. In Nat Cell Biol, 2009
Data indicate RAD18 as a key factor that orchestrates HRR through surveillance of the DNA damage signal.
RAD6-RAD18-RAD5-pathway-dependent tolerance to chronic low-dose ultraviolet light.
Iwasaki et al., Suita, Japan. In Nature, 2009
key role for the RAD6-RAD18-RAD5 error-free postreplication repair (RAD6 error-free PRR) pathway in promoting cell growth and survival, in response to chronic low-dose ultraviolet light
The unnamed complex: what do we know about Smc5-Smc6?
Aragón et al., London, United Kingdom. In Chromosome Res, 2008
The structural maintenance of chromosome (SMC) proteins constitute the cores of three protein complexes involved in chromosome metabolism; cohesin, condensin and the Smc5-Smc6 complex.
Regulation of DNA double-strand break repair pathway choice.
Nickoloff et al., Albuquerque, United States. In Cell Res, 2008
While most DSB repair proteins appear to function exclusively in NHEJ or HR, a number of proteins influence both pathways, including the MRE11/RAD50/NBS1(XRS2) complex, BRCA1, histone H2AX, PARP-1, RAD18, DNA-dependent protein kinase catalytic subunit (DNA-PKcs), and ATM.
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