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Dna pk

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DNA-PK is a serine/threonine protein kinase that plays a critical role in DNA double-strand break repair and V(D)J recombination. It is a key component of the non-homologous end joining (NHEJ) pathway, which is one of the primary mechanisms for repairing DNA double-strand breaks in mammalian cells.

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Lab products found in correlation

Ve 82139, by Axon Medchem (2 mentions) Ku5593351, by Bio-Techne (2 mentions) Nu702653, by Bio-Techne (2 mentions) Lipofectamine 2000, by Thermo Fisher Scientific (1 mentions) Mg132, by Merck Group (1 mentions) Blasticidin, by Thermo Fisher Scientific (1 mentions) Nu7026, by Bio-Techne (1 mentions) Ku55933, by Bio-Techne (1 mentions)

Spelling variants of this product

DNA-PK inhibitor (2 citations) DNA-PK inhibitor NU7441 (2 citations)

3 protocols using dna pk

1

Standardized Mouse Embryonic Fibroblast Culture

Cited 2 times
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All MEFs used in this study were derived in house from day e13.5 embryos and grown in standard culture conditions as described21 (link). MEFs tested negative for mycoplasma contamination and genotypes were confirmed by PCR14 (link) and Western blot (Fig. 1c and Supplementary Fig. 1). Primary MEFs were immortalized by transfection with pBsSVD2005 (SV40 large T antigen expression vector). Adeno-Cre at a MOI of 500 was used. MEFs were grown for 3 days post-infection and split once prior to plating for experiments. Kinase inhibitors were used as follows: ATM, KU5593351 (link),52 (link) (10μM or 20 μM for 1-2 hrs as indicated, Tocris Biosciences); DNA-PK, NU702653 (link),54 (link) (20μM for 2 hrs, Tocris Biosciences); ATR, VE-82139 (10μM for 2 hrs, Axon Medchem).
Hartlerode A.J., Morgan M.J., Wu Y., Buis J, & Ferguson D.O. (2015). Recruitment and activation of the ATM kinase in the absence of DNA damage sensors. Nature structural & molecular biology, 22(9), 736-743.
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2

Standardized Mouse Embryonic Fibroblast Culture

Cited 2 times
Check if the same lab product or an alternative is used in the 5 most similar protocols
All MEFs used in this study were derived in house from day e13.5 embryos and grown in standard culture conditions as described21 (link). MEFs tested negative for mycoplasma contamination and genotypes were confirmed by PCR14 (link) and Western blot (Fig. 1c and Supplementary Fig. 1). Primary MEFs were immortalized by transfection with pBsSVD2005 (SV40 large T antigen expression vector). Adeno-Cre at a MOI of 500 was used. MEFs were grown for 3 days post-infection and split once prior to plating for experiments. Kinase inhibitors were used as follows: ATM, KU5593351 (link),52 (link) (10μM or 20 μM for 1-2 hrs as indicated, Tocris Biosciences); DNA-PK, NU702653 (link),54 (link) (20μM for 2 hrs, Tocris Biosciences); ATR, VE-82139 (10μM for 2 hrs, Axon Medchem).
Hartlerode A.J., Morgan M.J., Wu Y., Buis J, & Ferguson D.O. (2015). Recruitment and activation of the ATM kinase in the absence of DNA damage sensors. Nature structural & molecular biology, 22(9), 736-743.
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3

Immortalized MEFs Expressing Mutant MRE11

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MEFs were isolated from day e13.5 embryos and grown in standard culture conditions as described38 . Primary MEFs were immortalized by transfection with pBsSVD2005 (SV40 large T antigen expression vector). To create cDNA clones, cells were transfected (Lipofectamine 2000, Life Technologies) with mutant MRE11-expressing constructs10 and clones were isolated and grown under blasticidin (Life Technologies) selection. Adeno-Cre (University of Michigan Vector Core) at an MOI of 500 was used. MEFs were grown 3 days post-infection and split once prior to plating for experiments. Kinase inhibitors were used as follows: ATM, KU55933 (10 μM for 1 hr, Tocris Biosciences); DNA-PK, NU7026 (20 μM for 2 hrs, Tocris Biosciences). Proteasome inhibition was carried out for 8 hrs in 20 µM MG-132 (Sigma). Where IR treatment is indicated, cells were exposed to a 137Cs source.
Hartlerode A.J., Regal J.A, & Ferguson D.O. (2018). Reversible mislocalization of a disease-associated MRE11 splice variant product. Scientific Reports, 8, 10121.
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