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抗Human DCLRE1C 抗体:
抗Rat (Rattus) DCLRE1C 抗体:
抗Mouse (Murine) DCLRE1C 抗体:
Human Polyclonal DCLRE1C Primary Antibody for IHC - ABIN965976
Moshous, Callebaut, de Chasseval, Corneo, Cavazzana-Calvo, Le Deist, Tezcan, Sanal, Bertrand, Philippe, Fischer, de Villartay: Artemis, a novel DNA double-strand break repair/V(D)J recombination protein, is mutated in human severe combined immune deficiency. in Cell 2001
Show all 7 Pubmed References
Human Polyclonal DCLRE1C Primary Antibody for IHC - ABIN965977
Ma, Pannicke, Schwarz, Lieber: Hairpin opening and overhang processing by an Artemis/DNA-dependent protein kinase complex in nonhomologous end joining and V(D)J recombination. in Cell 2002
Show all 7 Pubmed References
Human Polyclonal DCLRE1C Primary Antibody for WB - ABIN151340
Davies, Pettijohn, Fike, Wang, Nahas, Tunuguntla, Hu, Gatti, McCurdy: Defective DNA double-strand break repair in pediatric systemic lupus erythematosus. in Arthritis and rheumatism 2012
Data suggest that stimulation of Artemis nuclease/DCLRE1C activity by XRCC4 (显示 XRCC4 抗体)-DNA ligase IV (显示 LIG4 抗体) hetero-complex and efficiency of blunt-end ligation are determined by structural configurations at the DNA ends. (XRCC4 (显示 XRCC4 抗体) = 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 (显示 NCF1 抗体) 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 (显示 PRKDC 抗体)
uncovered a nuclease, Artemis, as a PTIP (显示 PAXIP1 抗体)-binding protein
the 5'-exonuclease (显示 EXO1 抗体) is intrinsic to ARTEMIS, making it relevant to the role of ARTEMIS in nonhomologous DNA end joining
DNA ligase IV (显示 LIG4 抗体) and Artemis act cooperatively to promote nonhomologous end-joining
2 siblings are described with combined immunodeficiency (CID (显示 CENPA 抗体)) and immunodysregulation caused by compound heterozygous Artemis mutations.
Artemis levels significantly influence radiation toxicity in human cells
ATM (显示 ATM 抗体) phosphorylates DNA-PKcs (显示 PRKDC 抗体) to recruit Artemis and promote end-processing.
we present T(-)B(-)NK(+) severe combined immunodeficiency (SCID (显示 PRKDC 抗体)) phenotype after spontaneously occurring modification of Artemis gene in mice.
deficient mice have a phenotype similar to that of DNA-PKcs (显示 PRKDC 抗体)-deficient mice-including severe combined immunodeficiency (显示 PRKDC 抗体) 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 (显示 TP53 抗体)-deficient mouse tumors lacked der(12 (显示 SLC29A2 抗体))t(12;15) translocations and c-myc (显示 MYC 抗体) 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 (显示 PRKDC 抗体) 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 (显示 PRKDC 抗体), we suggest that these patients may be at risk for both lymphoid and non-lymphoid cancers.
DNA-PKcs (显示 PRKDC 抗体) and Artemis open AAV inverted terminal repeat (ITR (显示 GPR180 抗体)) hairpin loops in a tissue-dependent manner.
both DNA-PKcs (显示 PRKDC 抗体) and, unexpectedly, Artemis are necessary for joining a subset of activation-induced cytidine deaminase (显示 AICDA 抗体) (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