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Data suggest that stimulation of Artemis nuclease/DCLRE1C activity by XRCC4 (zeige XRCC4 Proteine)-DNA ligase IV (zeige LIG4 Proteine) hetero-complex and efficiency of blunt-end ligation are determined by structural configurations at the DNA ends. (XRCC4 (zeige XRCC4 Proteine) = 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 (zeige NCF1 Proteine) 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 (zeige PRKDC Proteine)
uncovered a nuclease, Artemis, as a PTIP (zeige PAXIP1 Proteine)-binding protein
the 5'-exonuclease (zeige EXO1 Proteine) is intrinsic to ARTEMIS, making it relevant to the role of ARTEMIS in nonhomologous DNA end joining
DNA ligase IV (zeige LIG4 Proteine) and Artemis act cooperatively to promote nonhomologous end-joining
2 siblings are described with combined immunodeficiency (CID (zeige CENPA Proteine)) and immunodysregulation caused by compound heterozygous Artemis mutations.
Artemis levels significantly influence radiation toxicity in human cells
ATM (zeige ATM Proteine) phosphorylates DNA-PKcs (zeige PRKDC Proteine) to recruit Artemis and promote end-processing.
we present T(-)B(-)NK(+) severe combined immunodeficiency (SCID (zeige PRKDC Proteine)) phenotype after spontaneously occurring modification of Artemis gene in mice.
deficient mice have a phenotype similar to that of DNA-PKcs (zeige PRKDC Proteine)-deficient mice-including severe combined immunodeficiency (zeige PRKDC Proteine) 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 (zeige TP53 Proteine)-deficient mouse tumors lacked der(12 (zeige SLC29A2 Proteine))t(12;15) translocations and c-myc (zeige MYC Proteine) 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 (zeige PRKDC Proteine) 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 (zeige PRKDC Proteine), we suggest that these patients may be at risk for both lymphoid and non-lymphoid cancers.
DNA-PKcs (zeige PRKDC Proteine) and Artemis open AAV inverted terminal repeat (ITR (zeige GPR180 Proteine)) hairpin loops in a tissue-dependent manner.
both DNA-PKcs (zeige PRKDC Proteine) and, unexpectedly, Artemis are necessary for joining a subset of activation-induced cytidine deaminase (zeige AICDA Proteine) (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