Application Note
*Optimal dilutions/concentrations should be determined by the researcher.
Application |
Recommended Dilution |
1:500-1:3000 |
1:100-1:1000 |
Not tested in other applications.
Calculated MW
Positive Control
293T (0.5 μM doxorubicin for 24 hr)
Predict Reactivity
Rhesus Monkey(>80% identity)
Form
Liquid
Buffer
PBS, 1% BSA, 20% Glycerol
Preservative
0.025% ProClin 300
Storage
Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.
Concentration
0.07 mg/ml (Please refer to the vial label for the specific concentration.)
Antigen Species
Human
Immunogen
Carrier-protein conjugated synthetic peptide surrounding phospho Ser46 of human p53. The exact sequence is proprietary.
Purification
Purified by antigen-affinity chromatography.
Conjugation
Unconjugated
RRID
AB_2886802
Note
For laboratory research use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Purchasers shall not, and agree not to enable third parties to, analyze, copy, reverse engineer or otherwise attempt to determine the structure or sequence of the product.
Synonyms
tumor protein p53 , BCC7 , BMFS5 , LFS1 , P53 , TRP53
Cellular Localization
Cytoplasm , Nucleus , Endoplasmic reticulum
Background
This gene encodes tumor protein p53, which responds to diverse cellular stresses to regulate target genes that induce cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. p53 protein is expressed at low level in normal cells and at a high level in a variety of transformed cell lines, where it's believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing transcription activation, DNA-binding, and oligomerization domains. It is postulated to bind to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity. Alterations of this gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome. Multiple p53 variants due to alternative promoters and multiple alternative splicing have been found. These variants encode distinct isoforms, which can regulate p53 transcriptional activity. [provided by RefSeq]
Database
Research Area