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Data suggest that stimulation of Artemis nuclease/DCLRE1C activity by XRCC4 (show XRCC4 Proteins)-DNA ligase IV (show LIG4 Proteins) hetero-complex and efficiency of blunt-end ligation are determined by structural configurations at the DNA ends. (XRCC4 (show XRCC4 Proteins) = X-ray repair cross complementing 4)
An N-terminal fragment comprising the catalytic domain can interact both with itself and with a C-terminal fragment. Amino acid exchanges N456A+S457A+E458Q in the C terminus of full-length SCIDA resulted in unmasking of the N terminus and in increased SCIDA activity in cellular V(D)J recombination assays.
Data demonstrate that DCLRE1C mutations can cause a phenotype presenting as only antibody deficiency.
DCLRE1C and NCF1 (show NCF1 Proteins) mutations have been found by whole-genome sequencing to cause primary immunodeficiency in unrelated patients.
the nature and location of mutations correlate with the clinical phenotype of severe combined immunodeficiency (show PRKDC Proteins)
uncovered a nuclease, Artemis, as a PTIP (show PAXIP1 Proteins)-binding protein
the 5'-exonuclease (show EXO1 Proteins) is intrinsic to ARTEMIS, making it relevant to the role of ARTEMIS in nonhomologous DNA end joining
DNA ligase IV (show LIG4 Proteins) and Artemis act cooperatively to promote nonhomologous end-joining
2 siblings are described with combined immunodeficiency (CID (show CENPA Proteins)) and immunodysregulation caused by compound heterozygous Artemis mutations.
Artemis levels significantly influence radiation toxicity in human cells
ATM (show ATM Proteins) phosphorylates DNA-PKcs (show PRKDC Proteins) to recruit Artemis and promote end-processing.
we present T(-)B(-)NK(+) severe combined immunodeficiency (SCID (show PRKDC Proteins)) phenotype after spontaneously occurring modification of Artemis gene in mice.
deficient mice have a phenotype similar to that of DNA-PKcs (show PRKDC Proteins)-deficient mice-including severe combined immunodeficiency (show PRKDC Proteins) associated with defects in opening and joining V(D)J coding hairpin ends and increased cellular ionizing radiation sensitivity (artemis)
Data show that Artemis appears to be required for a subset of nonhomologous DNA end joining reactions that require end processing [Artemis].
Artemis/p53 (show TP53 Proteins)-deficient mouse tumors lacked der(12 (show SLC29A2 Proteins))t(12;15) translocations and c-myc (show MYC Proteins) amplification.
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 (show PRKDC Proteins) in Athabascan-speaking Native Americans.
DNA-PK has Artemis-independent functions in class switch recombination and normal development
Since Art deficient mice represent a model for radiation-sensitive severe combined immunodeficiency (show PRKDC Proteins), we suggest that these patients may be at risk for both lymphoid and non-lymphoid cancers.
DNA-PKcs (show PRKDC Proteins) and Artemis open AAV inverted terminal repeat (ITR (show GPR180 Proteins)) hairpin loops in a tissue-dependent manner.
both DNA-PKcs (show PRKDC Proteins) and, unexpectedly, Artemis are necessary for joining a subset of activation-induced cytidine deaminase (show AICDA Proteins) (AID)-dependent DNA double-strand breaks
This gene encodes a nuclear protein that is involved in V(D)J recombination and DNA repair. The protein has single-strand-specific 5'-3' exonuclease activity\; it also exhibits endonuclease activity on 5' and 3' overhangs and hairpins when complexed with protein kinase, DNA-activated, catalytic polypeptide. Mutations in this gene cause Athabascan-type severe combined immunodeficiency (SCIDA).
DNA cross-link repair 1C (PSO2 homolog, S. cerevisiae)
, artemis protein
, protein artemis
, DNA cross-link repair 1C
, protein artemis-like
, DNA cross-link repair 1C protein
, PSO2 homolog
, SNM1 homolog C
, SNM1-like protein
, severe combined immunodeficiency, type a (Athabascan)
, Artemis protein
, DNA cross-link repair 1A, PSO2 homolog