Rabbit Anti-DCLRE1C Recombinant Antibody (EG933) (CBMAB-EN1105-LY)

Name: Rabbit Anti-DCLRE1C Recombinant Antibody (EG933)
SKU: CBMAB-EN1105-LY
Rating: 5 (1 reviews)

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Published Data

Rabbit Anti-DCLRE1C Recombinant Antibody (EG933) (CBMAB-EN1105-LY) in IHC

The tissue expression of Artemis was evaluated by IHC in 46 cervix cancer patients receiving radical chemo-radiotherapy. Protein levels were scored for four categories: score-, score+, score++, and score+++. ...View More

Zhang, Q., Yang, L., Gao, H., Kuang, X., Xiao, H., Yang, C., ... & Li, M. (2023). APE1 promotes non-homologous end joining by initiating DNA double-strand break formation and decreasing ubiquitination of artemis following oxidative genotoxic stress. Journal of Translational Medicine, 21(1), 183. Distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Rabbit Anti-DCLRE1C Recombinant Antibody (EG933) (CBMAB-EN1105-LY) in Immunoblotting

(A, B) NHEJ protein-protein interactions are significantly decreased in the absence of RECQL4. DNA-PKcs (A) and Ku70 (B) were immunoprecipitated from U2OS wild-type (WT) or RECQL4 knockout (RQ4KO) cells that were treated with 10 Gy of IR and allowed to recover for 10 minutes. The samples were resolved via SDS-PAGE and interactions between DNA-PKcs and Ku70 with NHEJ factors (LIG4, XRCC4, XLF and/or Artemis) and RECQL4 were determined via immunoblotting. ...View More

Lu, H., Guan, J., Wang, S. Y., Li, G. M., Bohr, V. A., & Davis, A. J. (2022). DNA-PKcs-dependent phosphorylation of RECQL4 promotes NHEJ by stabilizing the NHEJ machinery at DNA double-strand breaks. Nucleic acids research, 50(10), 5635-5651. Distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Rabbit Anti-DCLRE1C Recombinant Antibody (EG933) (CBMAB-EN1105-LY) in Immunoblotting

Immunoblot validation of CRISPR-Cas9 generated knockout cell lines that were pre-validated by deep sequencing to bear all-allelic frame shift mutations (knockout (KO) A, B) or heterozygous mutations (−/+). Size marker bands are indicated in the first column; expected protein sizes are given in the last column. ...View More

Schmid-Burgk, J. L., Höning, K., Ebert, T. S., & Hornung, V. (2016). CRISPaint allows modular base-specific gene tagging using a ligase-4-dependent mechanism. Nature communications, 7(1), 12338. Distributed under Open Access license CC BY 4.0, without modification.

Datasheet

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Rabbit

Clone

EG933

Application

WB, IP

Immunogen

Synthetic peptide corresponding to residues surrounding Pro367 of human artemis protein.

Host Species

Rabbit

Specificity

Human, Monkey

Antibody Isotype

IgG

Clonality

Monoclonal Antibody

Application Notes

Application	Note
WB	1:1,000
IP	1:200

Formulations & Storage [For reference only, actual COA shall prevail!]

Format

Liquid

Buffer

100 µg/ml BSA, 50% glycerol

Preservative

0.02% sodium azide

Concentration

Batch dependent

More Infomation

Target

Full Name

DNA Cross-Link Repair 1C

Entrez Gene ID

64421

UniProt ID

Q96SD1

Function

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.

Biological Process

Adaptive immune response Source: UniProtKB-KW
B cell differentiation Source: Ensembl
Double-strand break repair via nonhomologous end joining Source: GO_Central
Interstrand cross-link repair Source: GO_Central
Protection from non-homologous end joining at telomere Source: GO_Central
Response to ionizing radiation Source: Ensembl
V(D)J recombination Source: Ensembl

Cellular Location

Nucleus

Involvement in disease

Severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-negative/NK-cell-positive with sensitivity to ionizing radiation (RSSCID):
A form of severe combined immunodeficiency, 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 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.
Severe combined immunodeficiency Athabaskan type (SCIDA):
A variety of SCID with sensitivity to ionizing radiation. A founder mutation has been detected in Athabascan-speaking native Americans, being inherited as an autosomal recessive trait. Affected individuals exhibit clinical symptoms and defects in DNA repair comparable to those seen in RS-SCID.
Omenn syndrome (OS):
Severe immunodeficiency characterized by the presence of activated, anergic, oligoclonal T-cells, hypereosinophilia, and high IgE levels.

PTM

Phosphorylation on undefined residues by PRKDC may stimulate endonucleolytic activity on 5' and 3' hairpins and overhangs. PRKDC must remain present, even after phosphorylation, for efficient hairpin opening. Also phosphorylated by ATM in response to ionizing radiation (IR) and by ATR in response to ultraviolet (UV) radiation.

Strubbe, S., De Bruyne, M., Pannicke, U., Beyls, E., Vandekerckhove, B., Leclercq, G., ... & Taghon, T. (2021). A Novel Non-Coding Variant in DCLRE1C Results in Deregulated Splicing and Induces SCID Through the Generation of a Truncated ARTEMIS Protein That Fails to Support V (D) J Recombination and DNA Damage Repair. Frontiers in immunology, 12, 2398.

Li, Y., Adur, M. K., Wang, W., Schultz, R. B., Hale, B., Wierson, W., ... & Ross, J. W. (2021). Effect of ARTEMIS (DCLRE1C) deficiency and microinjection timing on editing efficiency during somatic cell nuclear transfer and in vitro fertilization using the CRISPR/Cas9 system. Theriogenology, 170, 107-116.

Mou, W., Gao, L., He, J., Yin, J., Xu, B., & Gui, J. (2021). Compound heterozygous DCLRE1C mutations lead to clinically typical Severe Combined Immunodeficiency presenting with Graft Versus Host Disease. Immunogenetics, 73(6), 425-434.

Rajaei, A. A., RASHIDINEZHAD, A., Alebouyeh, M., & Shirkoohi, R. (2021). Examining of relative alternations in the expression of CHEK2, DCLRE1C and XRCC4 genes in patients with Gastritis.

Nahum, A., Somech, R., Shubinsky, G., Levy, J., & Broides, A. (2020). Unusual phenotype in patients with a hypomorphic mutation in the DCLRE1C gene: IgG hypergammaglobulinemia with IgA and IgE deficiency. Clinical Immunology, 213, 108366.

Choe, N., Brick, L., Kozenko, M., Chakraborty, P., Kernohan, K. D., Bulman, D., & Brager, R. (2020). Positive newborn screen: a case of a novel variant in DCLRE1C in a patient with SCID. LymphoSign Journal, 7(1), 46-48.

Sundin, M., Marits, P., Ramme, K., Kolios, A. G., & Nilsson, J. (2019). Severe combined immunodeficiency (SCID) presenting in childhood, with agammaglobulinemia, associated with novel compound heterozygous mutations in DCLRE1C. Clinical Immunology, 200, 16-18.

Wu, Z., Subramanian, N., Jacobsen, E. M., Laib Sampaio, K., van der Merwe, J., Hönig, M., & Mertens, T. (2019). NK cells from RAG-or DCLRE1C-deficient patients inhibit HCMV. Microorganisms, 7(11), 546.

Sundin, M., Uhlin, M., Gaballa, A., Ramme, K., Kolios, A. G., Marits, P., & Nilsson, J. (2018). Late presenting atypical severe combined immunodeficiency (SCID) associated with a novel missense mutation in DCLRE1C. Pediatric Allergy and Immunology, 29(1), 108-111.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

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For research use only. Not intended for any clinical use.

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