DCLRE1C sirna

DCLRE1C siRNA (Rat)

Cat. Num. AAA828892

• Gene Names: Dclre1c; Snm1l
• Reactivity: Rat
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: DCLRE1C; DCLRE1C siRNA (Rat); SNM1L; Protein artemis; DNA cross-link repair 1C protein; SNM1-like protein; DCLRE1C sirna

• Host: Synthetic
• Reactivity: Rat
• Specificity: DCLRE1C siRNA (Rat) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
• Purity/Purification: > 97%
• Form/Format: Lyophilized powder
• Sequence Length: 698

• Applicable Applications for DCLRE1C sirna: RNA Interference (RNAi)
• Quality Control: Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
• Directions for Use: We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
• Components: We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of rat DCLRE1C gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
• Preparation and Storage: Shipped at 4 degree C. Store at -20 degree C for one year.

Related Product Information for DCLRE1C sirna

siRNA to inhibit DCLRE1C expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 162135927
• NCBI GeneID: 259171
• NCBI Accession #: NP_671486.2
• NCBI GenBank Nucleotide #: NM_147145.2
• UniProt Accession #: Q5XIX3; Q8K4H7
• Molecular Weight: 78,189 Da
• NCBI Official Full Name: protein artemis
• NCBI Official Synonym Full Names: DNA cross-link repair 1C
• NCBI Official Symbol: Dclre1c
• NCBI Official Synonym Symbols: Snm1l
• NCBI Protein Information: protein artemis
• UniProt Protein Name: Protein artemis
• Protein Family: Protein artemis
• UniProt Gene Name: Dclre1c
• UniProt Synonym Gene Names: Snm1l
• UniProt Entry Name: DCR1C_RAT

NCBI Description

mouse homolog plays a role in non-homologous end joining DNA repair during VDJ recombination [RGD, Feb 2006]

Uniprot Description

Artemis: Required for V(D)J recombination, the process by which exons encoding the antigen-binding domains of immunoglobulins and T-cell receptor proteins are assembled from individual V, (D), and J gene segments. V(D)J recombination is initiated by the lymphoid specific RAG endonuclease complex, which generates site specific DNA double strand breaks (DSBs). These DSBs present two types of DNA end structures: hairpin sealed coding ends and phosphorylated blunt signal ends. These ends are independently repaired by the non homologous end joining (NHEJ) pathway to form coding and signal joints respectively. This protein exhibits single-strand specific 5'-3' exonuclease activity in isolation and acquires endonucleolytic activity on 5' and 3' hairpins and overhangs when in a complex with PRKDC. The latter activity is required specifically for the resolution of closed hairpins prior to the formation of the coding joint. May also be required for the repair of complex DSBs induced by ionizing radiation, which require substantial end-processing prior to religation by NHEJ. Defects in DCLRE1C are a cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell- negative/NK-cell-positive with sensitivity to ionizing radiation (RSSCID). SCID refers to a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients with SCID present in infancy with recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T- cell development. Individuals affected by RS-SCID show defects in the DNA repair machinery necessary for coding joint formation and the completion of V(D)J recombination. A subset of cells from such patients show increased radiosensitivity. Defects in DCLRE1C are the cause of severe combined immunodeficiency Athabaskan type (SCIDA). SCIDA is a variety of RS-SCID caused by a founder mutation in Athabascan- speaking native Americans, being inherited as an autosomal recessive trait with an estimated gene frequency of 2.1% in the Navajo population. Affected individuals exhibit clinical symptoms and defects in DNA repair comparable to those seen in RS-SCID. Defects in DCLRE1C are a cause of Omenn syndrome (OS). OS is characterized by severe combined immunodeficiency associated with erythrodermia, hepatosplenomegaly, lymphadenopathy and alopecia. Affected individuals have elevated T-lymphocyte counts with a restricted T- cell receptor (TCR) repertoire. They also generally lack B- lymphocytes, but have normal natural killer (NK) cell function (T+ B- NK+). Belongs to the DNA repair metallo-beta-lactamase (DRMBL) family. 4 isoforms of the human protein are produced by alternative splicing.

Protein type: EC 3.1.-.-; DNA repair, damage; Deoxyribonuclease

Cellular Component: nucleus

Molecular Function: 5'-3' exonuclease activity; single-stranded DNA specific endodeoxyribonuclease activity

Biological Process: V(D)J recombination; B cell differentiation; double-strand break repair; response to ionizing radiation; chromosome organization and biogenesis; DNA catabolic process, endonucleolytic; telomere maintenance; DNA recombination