The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Blocking - Blocking peptide for Anti-53BP1 antibody (ab87097)
Purity70 - 90% by HPLC.
- First try to dissolve a small amount of peptide in either water or buffer. The more charged residues on a peptide, the more soluble it is in aqueous solutions. - If the peptide doesn’t dissolve try an organic solvent e.g. DMSO, then dilute using water or buffer. - Consider that any solvent used must be compatible with your assay. If a peptide does not dissolve and you need to recover it, lyophilise to remove the solvent. - Gentle warming and sonication can effectively aid peptide solubilisation. If the solution is cloudy or has gelled the peptide may be in suspension rather than solubilised. - Peptides containing cysteine are easily oxidised, so should be prepared in solution just prior to use.
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Preparation and Storage
Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Information available upon request.
p53 binding protein 1
p53-binding protein 1
Tumor protein 53 binding protein 1
Tumor protein p53 binding protein 1
Tumor suppressor p53 binding protein 1
Tumor suppressor p53-binding protein 1
FunctionMay have a role in checkpoint signaling during mitosis. Enhances TP53-mediated transcriptional activation. Plays a role in the response to DNA damage.
Involvement in diseaseNote=A chromosomal aberration involving TP53BP1 is found in a form of myeloproliferative disorder chronic with eosinophilia. Translocation t(5;15)(q33;q22) with PDGFRB creating a TP53BP1-PDGFRB fusion protein.
Sequence similaritiesContains 2 BRCT domains.
Post-translational modificationsAsymmetrically dimethylated on Arg residues by PRMT1. Methylation is required for DNA binding. Phosphorylated at basal level in the absence of DNA damage. Hyper-phosphorylated in an ATM-dependent manner in response to DNA damage induced by ionizing radiation. Hyper-phosphorylated in an ATR-dependent manner in response to DNA damage induced by UV irradiation.
Cellular localizationNucleus. Chromosome > centromere > kinetochore. Associated with kinetochores. Both nuclear and cytoplasmic in some cells. Recruited to sites of DNA damage, such as double stand breaks. Methylation of histone H4 at 'Lys-20' is required for efficient localization to double strand breaks.