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Mouse Monoclonal RAG-2 antibody [4D5] (STJ98352)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, ELISA
Recommended dilution: WB 1:500-1:2000; ELISA 1:10000
Recommended protocols: check protocols
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Check alternative names for the antibodyExpand
RAG2 antibody,|RAG 2 antibody|RAG-2 antibody|RAG2 antibody|RAG2_HUMAN antibody|Recombination activating gene 2 antibody|V(D)J recombination activating protein 2 antibody|V(D)J recombination-activating protein 2 antibody|Anti-RAG2 antibody (ab189835)
SCBT cat No: sc-517209|sc-7623|sc-5600|
RAG-2 Monoclonal Antibody
|Catalogue No.|| |
RAG-2 Monoclonal Antibody detects endogenous levels of RAG-2 protein.
Purified recombinant fragment of human RAG-2 (350-527aa) expressed in E Coli
|Recommended dilution|| |
WB 1:500-1:2000; ELISA 1:10000
RAG-2 Antibody was tube-contained. Ascitic fluid containing 0.03% sodium azide.
RAG-2 Antibody was purified using affinity purification.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
Vantibody, D antibody,J recombination-activating protein 2 antibody, RAG-2 antibody
|Protein names|| |
V, D ,J recombination-activating protein 2 , RAG-2
|Protein function|| |
Core component of the RAG complex, a multiprotein complex that mediates the DNA cleavage phase during V(D)J recombination. V(D)J recombination assembles a diverse repertoire of immunoglobulin and T-cell receptor genes in developing B and T-lymphocytes through rearrangement of different V (variable), in some cases D (diversity), and J (joining) gene segments. DNA cleavage by the RAG complex occurs in 2 steps: a first nick is introduced in the top strand immediately upstream of the heptamer, generating a 3′-hydroxyl group that can attack the phosphodiester bond on the opposite strand in a direct transesterification reaction, thereby creating 4 DNA ends: 2 hairpin coding ends and 2 blunt, 5′-phosphorylated ends. The chromatin structure plays an essential role in the V(D)J recombination reactions and the presence of histone H3 trimethylated at ‘Lys-4’ (H3K4me3) stimulates both the nicking and haipinning steps. The RAG complex also plays a role in pre-B cell allelic exclusion, a process leading to expression of a single immunoglobulin heavy chain allele to enforce clonality and monospecific recognition by the B-cell antigen receptor (BCR) expressed on individual B-lymphocytes. The introduction of DNA breaks by the RAG complex on one immunoglobulin allele induces ATM-dependent repositioning of the other allele to pericentromeric heterochromatin, preventing accessibility to the RAG complex and recombination of the second allele. In the RAG complex, RAG2 is not the catalytic component but is required for all known catalytic activities mediated by RAG1. It probably acts as a sensor of chromatin state that recruits the RAG complex to H3K4me3 (By similarity).
|Protein tissue specificity|| |
Cells of the B- and T-lymphocyte lineages.
|Involvement in disease|| |
Combined cellular and humoral immune defects with granulomas (CHIDG) [MIM:233650]: Immunodeficiency disease with granulomas in the skin, mucous membranes, and internal organs. Other characteristics include hypogammaglobulinemia, a diminished number of T and B-cells, and sparse thymic tissue on ultrasonography. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-negative/NK-cell-positive (T(-)B(-)NK(+) SCID) [MIM:601457]: A form of severe combined immunodeficiency (SCID), 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 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. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Omenn syndrome (OS) [MIM:603554]: Severe immunodeficiency characterized by the presence of activated, anergic, oligoclonal T-cells, hypereosinophilia, and high IgE levels. . Note: The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
The atypical PHD-type zinc finger recognizes and binds histone H3 trimethylated on ‘Lys-4’ (H3K4me3). The presence Tyr-445 instead of a carboxylate in classical PHD-type zinc fingers results in an enhanced binding to H3K4me3 in presence of dimethylated on ‘Arg-2’ (H3R2me2) rather than inhibited. The atypical PHD-type zinc finger also binds various phosphoinositides, such as phosphatidylinositol 3,4-bisphosphate binding (PtdIns(3,4)P2), phosphatidylinositol 3,5-bisphosphate binding (PtdIns(3,5)P2), phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) and phosphatidylinositol 3,4,5-trisphosphate binding (PtdIns(3,4,5)P3) (By similarity). / Belongs to the RAG2 family. / Contains 1 PHD-type zinc finger.
|Protein cellular localization|| |
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St John’s Laboratory Ltd.
|Product type|| |
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