| ATM phosphorylates DNA-PKcs to recruit Artemis and promote end-processing. | Differential phosphorylation of DNA-PKcs regulates the interplay between end-processing and end-ligation during nonhomologous end-joining.
Jiang W, Crowe JL, Liu X, Nakajima S, Wang Y, Li C, Lee BJ, Dubois RL, Liu C, Yu X, Lan L, Zha S., Free PMC Article | 06/20/2015 |
| we present T(-)B(-)NK(+) severe combined immunodeficiency (SCID) phenotype after spontaneously occurring modification of Artemis gene in mice. | Novel spontaneous deletion of artemis exons 10 and 11 in mice leads to T- and B-cell deficiency.
Barthels C, Puchałka J, Racek T, Klein C, Brocker T., Free PMC Article | 06/21/2014 |
| Loss of Artemis leads to reduced immunoglobulin class switch recombination. | Reduced immunoglobulin class switch recombination in the absence of Artemis.
Rivera-Munoz P, Soulas-Sprauel P, Le Guyader G, Abramowski V, Bruneau S, Fischer A, Pâques F, de Villartay JP. | 01/21/2010 |
| These data suggest that Artemis might be the nuclease responsible for nucleotide loss from signal ends during the repair process. | Distinct effects of DNA-PKcs and Artemis inactivation on signal joint formation in vivo.
Touvrey C, Couedel C, Soulas P, Couderc R, Jasin M, de Villartay JP, Marche PN, Jouvin-Marche E, Candéias SM. | 01/21/2010 |
| both DNA-PKcs and, unexpectedly, Artemis are necessary for joining a subset of activation-induced cytidine deaminase (AID)-dependent DNA double-strand breaks | DNA-PKcs and Artemis function in the end-joining phase of immunoglobulin heavy chain class switch recombination.
Franco S, Murphy MM, Li G, Borjeson T, Boboila C, Alt FW., Free PMC Article | 01/21/2010 |
| DNA-PKcs and Artemis open AAV inverted terminal repeat (ITR) hairpin loops in a tissue-dependent manner. | The role of DNA-PKcs and artemis in opening viral DNA hairpin termini in various tissues in mice.
Inagaki K, Ma C, Storm TA, Kay MA, Nakai H., Free PMC Article | 01/21/2010 |
| Since Art deficient mice represent a model for radiation-sensitive severe combined immunodeficiency, we suggest that these patients may be at risk for both lymphoid and non-lymphoid cancers. | The nonhomologous end joining factor Artemis suppresses multi-tissue tumor formation and prevents loss of heterozygosity.
Woo Y, Wright SM, Maas SA, Alley TL, Caddle LB, Kamdar S, Affourtit J, Foreman O, Akeson EC, Shaffer D, Bronson RT, Morse HC 3rd, Roopenian D, Mills KD. | 01/21/2010 |
| DNA-PK has Artemis-independent functions in class switch recombination and normal development | Artemis-independent functions of DNA-dependent protein kinase in Ig heavy chain class switch recombination and development.
Rooney S, Alt FW, Sekiguchi J, Manis JP., Free PMC Article | 01/21/2010 |
| V(D)J and DNA repair defects seen in this Artemis-deficient mouse model are direct evidence that defective Artemis is the pathologic mechanism for the immunodeficiency phenotype of SCID in Athabascan-speaking Native Americans. | Targeted disruption of the Artemis murine counterpart results in SCID and defective V(D)J recombination that is partially corrected with bone marrow transplantation.
Li L, Salido E, Zhou Y, Bhattacharyya S, Yannone SM, Dunn E, Meneses J, Feeney AJ, Cowan MJ. | 01/21/2010 |
| Artemis/p53-deficient mouse tumors lacked der(12)t(12;15) translocations and c-myc amplification. | Artemis and p53 cooperate to suppress oncogenic N-myc amplification in progenitor B cells.
Rooney S, Sekiguchi J, Whitlow S, Eckersdorff M, Manis JP, Lee C, Ferguson DO, Alt FW., Free PMC Article | 01/21/2010 |
| deficient mice have a phenotype similar to that of DNA-PKcs-deficient mice-including severe combined immunodeficiency associated with defects in opening and joining V(D)J coding hairpin ends and increased cellular ionizing radiation sensitivity (artemis) | Leaky Scid phenotype associated with defective V(D)J coding end processing in Artemis-deficient mice.
Rooney S, Sekiguchi J, Zhu C, Cheng HL, Manis J, Whitlow S, DeVido J, Foy D, Chaudhuri J, Lombard D, Alt FW. | 01/21/2010 |
| Data show that Artemis appears to be required for a subset of nonhomologous DNA end joining reactions that require end processing [Artemis]. | Defective DNA repair and increased genomic instability in Artemis-deficient murine cells.
Rooney S, Alt FW, Lombard D, Whitlow S, Eckersdorff M, Fleming J, Fugmann S, Ferguson DO, Schatz DG, Sekiguchi J., Free PMC Article | 01/21/2010 |