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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 23 Nov 2016.

RAD50 homolog

Rad50
The protein encoded by this gene is highly similar to Saccharomyces cerevisiae Rad50, a protein involved in DNA double-strand break repair. This protein forms a complex with MRE11 and NBS1. The protein complex binds to DNA and displays numerous enzymatic activities that are required for nonhomologous joining of DNA ends. This protein, cooperating with its partners, is important for DNA double-strand break repair, cell cycle checkpoint activation, telomere maintenance, and meiotic recombination. Knockout studies of the mouse homolog suggest this gene is essential for cell growth and viability. Mutations in this gene are the cause of Nijmegen breakage syndrome-like disorder.[provided by RefSeq, Apr 2010] (from NCBI)
Top mentioned proteins: Mre11, NBS1, CAN, Atm, Rad51
Papers on Rad50
Yeast MRX deletions have short chronological life span and more triacylglycerols.
New
Srinivasan et al., Mysore, India. In Fems Yeast Res, Feb 2016
Among these, RAD50, MRE11 and XRS2 form a complex, MRX that is involved in homologous recombination that showed an increase in the amount of TAG.
Multigene testing of moderate-risk genes: be mindful of the missense.
New
Tavtigian et al., Salt Lake City, United States. In J Med Genet, Feb 2016
METHODS: We evaluated rare missense substitutions identified from a mutation screen of ATM, CHEK2, MRE11A, RAD50, NBN, RAD51, RINT1, XRCC2 and BARD1 in 1297 cases of early-onset breast cancer and 1121 controls via scores from Align-Grantham Variation Grantham Deviation (GVGD), combined annotation dependent depletion (CADD), multivariate analysis of protein polymorphism (MAPP) and PolyPhen-2.
Chromatin perturbations during the DNA damage response in higher eukaryotes.
Review
New
Kastan et al., Pittsburgh, United States. In Dna Repair (amst), Dec 2015
The MRE11-RAD50-NBS1 (MRN) complex, which has a catalytic role in DNA repair, and the KAT5 (Tip60) acetyltransferase are required for maximal ATM kinase activation in cells exposed to low doses of ionizing radiation.
Prognostic Significance and Molecular Features of Colorectal Mucinous Adenocarcinomas: A Strobe-Compliant Study.
New
Sun et al., Chengdu, China. In Medicine (baltimore), Dec 2015
P = 0.013) and weak expression of RAD50 (HR 0.348, 95% CI, 0.106-1.192;
Heterozygous p.I171V mutation of the NBN gene as a risk factor for lung cancer development.
New
Nowak et al., Poznań, Poland. In Oncol Lett, Nov 2015
This protein is a member of the MRE1-RAD50-NBN nuclear complex, and is involved in numerous cell processes essential for maintaining genomic stability.
Viral and Cellular Genomes Activate Distinct DNA Damage Responses.
New
Impact
O'Shea et al., Los Angeles, United States. In Cell, Sep 2015
In response to cellular genome breaks, MRE11/RAD50/NBS1 (MRN) activates a global ATM DNA damage response (DDR) that prevents cellular replication.
DNA damage foci: Meaning and significance.
Review
New
Burdak-Rothkamm et al., United Kingdom. In Environ Mol Mutagen, Jul 2015
The discovery of DNA damage response proteins such as γH2AX, ATM, 53BP1, RAD51, and the MRE11/RAD50/NBS1 complex, that accumulate and/or are modified in the vicinity of a chromosomal DNA double-strand break to form microscopically visible, subnuclear foci, has revolutionized the detection of these lesions and has enabled studies of the cellular machinery that contributes to their repair.
High frequency of the SDK1:AMACR fusion transcript in Chinese prostate cancer.
Ren et al., Hangzhou, China. In Int J Clin Exp Med, 2014
Four high-frequency prostate cancer (CaP) specific fusion genes, SDK1:AMACR, RAD50:PDLIM4, CTAGE5:KHDRBS3 and USP9Y:TTTY15 have been reported in Chinese CaP samples through a transcriptome sequencing study.
Hsp90: A New Player in DNA Repair?
Review
di Masi et al., Roma, Italy. In Biomolecules, 2014
Multiple components of the DNA double strand breaks repair machinery, including BRCA1, BRCA2, CHK1, DNA-PKcs, FANCA, and the MRE11/RAD50/NBN complex, have been described to be client proteins of Hsp90, which acts as a regulator of the diverse DDR pathways.
The spectrum of genetic mutations in breast cancer.
Review
Al Tamimi et al., Karāchi, Pakistan. In Asian Pac J Cancer Prev, 2014
However, the great majority of breast cancer cases are not related to a mutated gene of high penetrance, but to genes of low penetrance such as CHEK2, CDH1, NBS1, RAD50, BRIP1 and PALB2, which are frequently mutated in the general population.
Along the Axis between Type 1 and Type 2 Immunity; Principles Conserved in Evolution from Fish to Mammals.
Review
Dijkstra et al., Greifswald, Germany. In Biology (basel), 2014
Furthermore, the present study is the first to identify a canonical TH2 cytokine locus in a bony fish, namely spotted gar, in the sense that it includes RAD50 and bona fide genes of both IL-4/13 and IL-3/ IL-5/GM-CSF families.
A genome-wide association study identifies CDHR3 as a susceptibility locus for early childhood asthma with severe exacerbations.
Impact
Bisgaard et al., Copenhagen, Denmark. In Nat Genet, 2014
Four of these, GSDMB, IL33, RAD50 and IL1RL1, were previously reported as asthma susceptibility loci, but the effect sizes for these loci in our cohort were considerably larger than in the previous genome-wide association studies of asthma.
A structural basis for the assembly and functions of a viral polymer that inactivates multiple tumor suppressors.
Impact
O'Shea et al., Los Angeles, United States. In Cell, 2012
E4-ORF3 forms a nuclear polymer and simultaneously inactivates p53, PML, TRIM24, and MRE11/RAD50/NBS1 (MRN) tumor suppressors.
Adenovirus regulates sumoylation of Mre11-Rad50-Nbs1 components through a paralog-specific mechanism.
GeneRIF
Hearing et al., Stony Brook, United States. In J Virol, 2012
Adenovirus 5 regulates sumoylation of Mre11-Rad50-Nbs1 components through a paralog-specific mechanism.
Misregulation of Rad50 expression in melanoma cells.
GeneRIF
Cheung et al., Little Rock, United States. In J Cutan Pathol, 2012
The staining features of Rad50, a component of an essential DNA double-strand break repair complex, are clearly increased in melanoma cells with regards to both staining intensity and the number of positive melanoma cells
Human Ku70/80 protein blocks exonuclease 1-mediated DNA resection in the presence of human Mre11 or Mre11/Rad50 protein complex.
GeneRIF
Chen et al., Dallas, United States. In J Biol Chem, 2012
Human Ku70/80 protein blocks exonuclease 1-mediated DNA resection in the presence of human Mre11 or Mre11/Rad50 protein complex.
Variants in activators and downstream targets of ATM, radiation exposure, and contralateral breast cancer risk in the WECARE study.
GeneRIF
Bernstein et al., New York City, United States. In Hum Mutat, 2012
Carriers of the RAD50 haplotype may be susceptible to the DNA-damaging effects of radiation therapy associated with radiation-induced breast cancer.
Correct end use during end joining of multiple chromosomal double strand breaks is influenced by repair protein RAD50, DNA-dependent protein kinase DNA-PKcs, and transcription context.
GeneRIF
Stark et al., Duarte, United States. In J Biol Chem, 2012
RAD50, DNA-PKcs kinase activity, and transcription context are each important to limit incorrect end use during EJ repair of multiple DSBs, but each has distinct roles during repair events requiring end processing
The MRE11 complex: starting from the ends.
Review
Impact
Petrini et al., Barcelona, Spain. In Nat Rev Mol Cell Biol, 2011
The MRE11 complex, composed of the meiotic recombination 11 (MRE11), RAD50 and Nijmegen breakage syndrome 1 (NBS1; also known as nibrin) proteins is central to the DDR, and recent insights into its structure and function have been gained from in vitro structural analysis and studies of animal models in which the DDR response is deficient.
Multiple roles for MRE11 at uncapped telomeres.
Impact
Chang et al., Houston, United States. In Nature, 2009
The mammalian MRE11-RAD50-NBS1 (MRN; NBS1 is also known as NBN) complex interacts with ATM to sense chromosomal double-strand breaks and coordinate global DNA damage responses.
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