The optimal amount of antibody per ChIP assay should be empirically determined by the end-user depending upon the amount of chromatin used per reaction. We recommend testing 1-5 μg per ChIP assay.
The tumor suppressor protein p53 responds to diverse cellular stresses to regulate target genes that induce cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. Wildtype p53 protein is expressed at a low level in normal cells but often mutated and expressed at a high level in a variety of transformed cell lines, where it is believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing transcription activation, DNA-binding, and oligomerization domains. 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.
Immunogen
recombinant human wild type p531-5.
Application
Suitable for Chip and western blot.
Quality
ChIP Validation
Physical form
Supplied as a solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide as a preservative.
Storage and Stability
For continuous use, store at 2-8°C for up to one month. For extended storage, freeze at -20°C in working aliquots. Repeated freezing and thawing or storage in “frost-free” freezers is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilution samples should be discarded if not used within 12 hours.
Other Notes
View ChIP Validation Data for lot number: 032M4761
Legal Information
Imprint is a registered trademark of Sigma-Aldrich Co. LLC
Imprint is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
This product is for R&D use only, not for drug, household, or other uses. Please consult the Material Safety Data Sheet for information regarding hazards and safe handling practices.
As a component of the transcriptional repression complex 1 (PRC1), the ring finger protein RING1 participates in the epigenetic regulation in cancer. However, the contributions of RING1 to cancer etiology or development are unknown. In this study, we report that
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