Anti-BRCA2 Antibody
Purified Mouse Monoclonal Antibody (Mab)
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Application ![]()
| WB, E |
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Primary Accession | P51587 |
Reactivity | Human |
Predicted | Human |
Host | Mouse |
Clonality | monoclonal |
Isotype | IgG1,κ |
Clone Names | 1847CT631.23.58 |
Calculated MW | 384230 Da |
Gene ID | 675 |
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Other Names | Breast cancer type 2 susceptibility protein, Fanconi anemia group D1 protein, BRCA2, FACD, FANCD1 |
Target/Specificity | This antibody is generated from a mouse immunized with a recombinant protein from human. |
Dilution | WB~~1:2000 E~~Use at an assay dependent concentration. |
Format | Purified monoclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein G column, followed by dialysis against PBS. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | Anti-BRCA2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | BRCA2 (HGNC:1101) |
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Synonyms | FACD, FANCD1 |
Function | Involved in double-strand break repair and/or homologous recombination. Binds RAD51 and potentiates recombinational DNA repair by promoting assembly of RAD51 onto single-stranded DNA (ssDNA). Acts by targeting RAD51 to ssDNA over double-stranded DNA, enabling RAD51 to displace replication protein-A (RPA) from ssDNA and stabilizing RAD51- ssDNA filaments by blocking ATP hydrolysis. Part of a PALB2-scaffolded HR complex containing RAD51C and which is thought to play a role in DNA repair by HR. May participate in S phase checkpoint activation. Binds selectively to ssDNA, and to ssDNA in tailed duplexes and replication fork structures. May play a role in the extension step after strand invasion at replication-dependent DNA double-strand breaks; together with PALB2 is involved in both POLH localization at collapsed replication forks and DNA polymerization activity. In concert with NPM1, regulates centrosome duplication. Interacts with the TREX-2 complex (transcription and export complex 2) subunits PCID2 and SEM1, and is required to prevent R-loop-associated DNA damage and thus transcription-associated genomic instability. Silencing of BRCA2 promotes R-loop accumulation at actively transcribed genes in replicating and non-replicating cells, suggesting that BRCA2 mediates the control of R-loop associated genomic instability, independently of its known role in homologous recombination (PubMed:24896180). |
Cellular Location | Nucleus. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Note=Colocalizes with ERCC5/XPG to nuclear foci following DNA replication stress |
Tissue Location | Highest levels of expression in breast and thymus, with slightly lower levels in lung, ovary and spleen |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Involved in double-strand break repair and/or homologous recombination. Binds RAD51 and potentiates recombinational DNA repair by promoting assembly of RAD51 onto single-stranded DNA (ssDNA). Acts by targeting RAD51 to ssDNA over double-stranded DNA, enabling RAD51 to displace replication protein-A (RPA) from ssDNA and stabilizing RAD51-ssDNA filaments by blocking ATP hydrolysis. Part of a PALB2-scaffolded HR complex containing RAD51C and which is thought to play a role in DNA repair by HR. May participate in S phase checkpoint activation. Binds selectively to ssDNA, and to ssDNA in tailed duplexes and replication fork structures. May play a role in the extension step after strand invasion at replication-dependent DNA double-strand breaks; together with PALB2 is involved in both POLH localization at collapsed replication forks and DNA polymerization activity. In concert with NPM1, regulates centrosome duplication. Interacts with the TREX-2 complex (transcription and export complex 2) subunits PCID2 and DSS1, and is required to prevent R-loop- associated DNA damage and thus transcription-associated genomic instability. Silencing of BRCA2 promotes R-loop accumulation at actively transcribed genes in replicating and non-replicating cells, suggesting that BRCA2 mediates the control of R-loop associated genomic instability, independently of its known role in homologous recombination (PubMed:24896180).
REFERENCES
Wooster R.,et al.Nature 378:789-792(1995).
Tavtigian S.V.,et al.Nat. Genet. 12:333-337(1996).
Dunham A.,et al.Nature 428:522-528(2004).
Ozcelik H.,et al.Nat. Genet. 16:17-18(1997).
Hussain S.,et al.Hum. Mol. Genet. 13:1241-1248(2004).

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