gopubmed logo
 
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 14 Mar 2013.

Protein kinase, DNA-activated, catalytic polypeptide

DNA-PKcs, DNA-dependent protein kinase catalytic subunit, P350, DNA-PK catalytic subunit
This gene encodes the catalytic subunit of the DNA-dependent protein kinase (DNA-PK). It functions with the Ku70/Ku80 heterodimer protein in DNA double strand break repair and recombination. The protein encoded is a member of the PI3/PI4-kinase family.[provided by RefSeq, Jul 2010] (from NCBI)
Papers using DNA-PKcs antibodies
Inhibition of radiation-induced EGFR nuclear import by C225 (Cetuximab) suppresses DNA-PK activity.
Supplier
Blagosklonny Mikhail V., In PLoS ONE, 2004
... mouse monoclonal, anti-Ku86 mouse monoclonal and anti-tubulin mouse monoclonal (Santa Cruz Biotechnology, Santa Cruz, CA); anti-DNA-PKcs Thr2609 phosphospecific rabbit polyclonal (Abcam, City, State); anti-RPA2 mouse ...
Papers on DNA-PKcs
Artemis-dependent DNA double-strand break formation at stalled replication forks.
New
Mizutani et al., Tokyo, Japan. In Cancer Sci, 06 Apr 2013
The kinase activity of the catalytic subunit of the DNA-dependent protein kinase (DNA-PKcs), a prerequisite for stimulation of the endonuclease activity of Artemis, is also required for DSB generation and subsequent ATM activation.
High LET Radiation Amplifies Centrosome Overduplication Through a Pathway of γ-Tubulin Monoubiquitination.
New
Komatsu et al., Kyoto, Japan. In Int J Radiat Oncol Biol Phys, 20 Mar 2013
To count centrosomes after IR exposure, human U2OS and mouse NIH3T3 cells were immunostained with antibodies of γ-tubulin and centrin 2. Similarly, Nbs1-, Brca1-, Ku70-, and DNA-PKcs-deficient mouse cells and their counterpart wild-type cells were used for measurement of centrosome overduplication.
Inhibition of DNA-dependent protein kinase catalytic subunit by small molecule inhibitor NU7026 sensitizes human leukemic K562 cells to benzene metabolite-induced apoptosis.
New
Bi et al., Wuhan, China. In J Huazhong Univ Sci Technolog Med Sci, 28 Feb 2013
We have previously reported that exposure of workers to benzene and to benzene metabolite hydroquinone in cultured cells induced DNA-dependent protein kinase catalytic subunit (DNA-PKcs) to mediate the cellular response to DNA double strand break (DSB) caused by DNA-damaging metabolites.
Host DNA damage response facilitates African swine fever virus infection.
New
Ferreira et al., Lisbon, Portugal. In Vet Microbiol, 23 Feb 2013
We evaluated protein levels during ASFV time-course infection, of several signalling cascade factors belonging to DDR pathways involved in double strand break repair - Ataxia Telangiectasia Mutated (ATM), ATM-Rad 3 related (ATR) and DNA dependent protein kinase catalytic subunit (DNA-PKcs).
New insights into the roles of ATM and DNA-PKcs in the cellular response to oxidative stress.
Review
New
Asaithamby et al., Dallas, United States. In Cancer Lett, Jan 2013
Attention is now focused on identifying the molecular contributions of the key DNA damage response kinases ataxia telangiectasia mutated (ATM), DNA-dependent protein kinase catalytic subunit (DNA-PKcs), and ATM- and Rad3-related (ATR) in the oxidative stress response.
Mutual regulation between DNA-PKcs and snail1 leads to increased genomic instability and aggressive tumor characteristics.
New
Lee et al., Seoul, South Korea. In Cell Death Dis, Dec 2012
Although the roles of DNA-dependent protein kinase catalytic subunits (DNA-PKcs) in the non-homologous end joining (NHEJ) of DNA repair are well-recognized, the biological mechanisms and regulators by DNA-PKcs besides DNA repair, have not been clearly described.
Regulation of DNA repair by S-nitrosylation.
Review
New
Liu et al., San Francisco, United States. In Biochim Biophys Acta, Jun 2012
CONCLUSIONS: Recent studies have identified a number of key DNA repair proteins as targets of S-nitrosylation, including O(6)-alkylguanine-DNA-alkyltransferase (AGT), 8-oxoguanine glycosylase, apurinic-apyrimidinic endonuclease 1, and DNA-dependent protein kinase catalytic subunit.
Essential role for DNA-PK-mediated phosphorylation of NR4A nuclear orphan receptors in DNA double-strand break repair.
GeneRIF
Perlmann et al., Stockholm, Sweden. In Genes Dev, 2011
NR4A functions directly at DNA repair sites by a process that requires phosphorylation by DNA-PK
Unique and redundant functions of ATM and DNA-PKcs during V(D)J recombination.
Review
Sleckman et al., Saint Louis, United States. In Cell Cycle, 2011
The ataxia telangiectasia mutated (ATM) and the DNA-dependent protein kinase catalytic subunit (DNA-PKcs), two related kinases, both function in the repair of DNA breaks generated during antigen receptor gene assembly.
A DNA-dependent stress response involving DNA-PK occurs in hypoxic cells and contributes to cellular adaptation to hypoxia.
GeneRIF
Muller et al., Toulouse, France. In J Cell Sci, 2011
hypoxia initiates chromatin modification and consequently DNA-PK activation, which positively regulate cellular oxygen-sensing and oxygen-signalling pathways
Mechanistic rationale for inhibition of poly(ADP-ribose) polymerase in ETS gene fusion-positive prostate cancer.
Impact
Chinnaiyan et al., Ann Arbor, United States. In Cancer Cell, 2011
We investigate the mechanisms by which ETS fusions mediate their effects, and find that the product of the predominant ETS gene fusion, TMPRSS2:ERG, interacts in a DNA-independent manner with the enzyme poly (ADP-ribose) polymerase 1 (PARP1) and the catalytic subunit of DNA protein kinase (DNA-PKcs).
Recapitulation of premature ageing with iPSCs from Hutchinson-Gilford progeria syndrome.
Impact
Izpisua Belmonte et al., Los Angeles, United States. In Nature, 2011
Additionally, our studies identify DNA-dependent protein kinase catalytic subunit (DNAPKcs, also known as PRKDC) as a downstream target of progerin.
More forks on the road to replication stress recovery.
Review
Nickoloff et al., Fort Collins, United States. In J Mol Cell Biol, 2011
In recent years, several proteins involved in DSB repair by non-homologous end joining (NHEJ) have been implicated in the replication stress response, including DNA-PKcs, Ku, DNA Ligase IV-XRCC4, Artemis, XLF and Metnase.
Concordant and opposite roles of DNA-PK and the "facilitator of chromatin transcription" (FACT) in DNA repair, apoptosis and necrosis after cisplatin.
GeneRIF
Lazaro et al., Boston, United States. In Mol Cancer, 2010
DNA-PK and FACT both play roles in DNA repair. Therefore both are putative targets for therapeutic inhibition.
DNA-PK-dependent RPA2 hyperphosphorylation facilitates DNA repair and suppresses sister chromatid exchange.
GeneRIF
Myung et al., Bethesda, United States. In Plos One, 2010
RPA2 hyperphosphorylation by DNA-PK in response to DNA double-strand breaks blocks unscheduled homologous recombination and delays mitotic entry.
Gene expression associated with DNA-dependent protein kinase activity under normoxia, hypoxia, and reoxygenation.
GeneRIF
Hareyama et al., Sapporo, Japan. In J Radiat Res (tokyo), 2010
analysis of gene expression associated with DNA-dependent protein kinase activity under normoxia, hypoxia, and reoxygenation
The role of survivin for radiation oncology: moving beyond apoptosis inhibition.
Review
Rödel et al., Frankfurt am Main, Germany. In Curr Med Chem, 2010
These properties were linked to a nuclear import and physical interrelationship with members of the DNA-DSB repair machinery such as phospho-histone H2AX and DNA dependent Protein Kinase (DNA-PKcs).
Crystal structure of DNA-PKcs reveals a large open-ring cradle comprised of HEAT repeats.
Impact
GeneRIF
Blundell et al., Cambridge, United Kingdom. In Nature, 2010
crystal structure of human DNA-PKcs at 6.6 A resolution, in which the overall fold is clearly visible for the first time
DNA-PKcs-PIDDosome: a nuclear caspase-2-activating complex with role in G2/M checkpoint maintenance.
Impact
Du et al., Kansas City, United States. In Cell, 2009
This phosphorylation is carried out by the nuclear serine/threonine protein kinase DNA-PKcs and promoted by the p53-inducible death-domain-containing protein PIDD within a large nuclear protein complex consisting of DNA-PKcs, PIDD, and caspase-2, which we have named the DNA-PKcs-PIDDosome.
Tel2 regulates the stability of PI3K-related protein kinases.
Impact
de Lange et al., New York City, United States. In Cell, 2008
The effects of Tel2 deletion correlated with significantly reduced protein levels for the PI3K-related kinases ataxia telangiectasia mutated (ATM), ATM and Rad3 related (ATR), DNA-dependent protein kinase catalytic subunit ataxia (DNA-PKcs).
share on facebooktweetadd +1mail to friends