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BRCA2 Polyclonal Antibody

     
  • 14 - BRCA2 Polyclonal Antibody AP68703
    Immunohistochemical analysis of paraffin-embedded Human brain. Antibody was diluted at 1:100(4°,overnight). High-pressure and temperature Tris-EDTA,pH8.0 was used for antigen retrieval. Negetive contrl (right) obtaned from antibody was pre-absorbed by immunogen peptide.
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
IHC-P
Primary Accession P51587
Reactivity Human, Rat
Host Rabbit
Clonality Polyclonal
Calculated MW 384230 Da
Additional Information
Gene ID 675
Other Names BRCA2; FACD; FANCD1; Breast cancer type 2 susceptibility protein; Fanconi anemia group D1 protein
Dilution IHC-P~~Immunohistochemistry: 1/100 - 1/300. ELISA: 1/20000. Not yet tested in other applications.
Format Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.09% (W/V) sodium azide.
Storage Conditions-20℃
Protein Information
Name BRCA2 (HGNC:1101)
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
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

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 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).

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