Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon 1 and Insertion of the selection cassette in exon 1.,
Disease:Adenocarcinoma
Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-RRM2B, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
P53R2 also known as RRM2B is a ribonucleotide reductase subunit with a molecular mass of 41 kDa. This protein is primarily expressed in the cytoplasm and mitochondria of various cell types including liver and kidney tissues. Mechanically p53R2 functions by reducing ribonucleotides into deoxyribonucleotides which are necessary for DNA synthesis and repair. This process is important for maintaining genomic stability especially under conditions of cellular stress or damage.
Biological function summary
P53R2 plays a role in the synthesis of deoxyribonucleotide triphosphates (dNTPs) for DNA repair. It forms part of a ribonucleotide reductase complex working with other subunits to ensure cells have sufficient dNTP pools for DNA replication and repair. The presence of p53R2 is integral for DNA damage response pathways where it gets activated to supply dNTPs during periods when the p53 tumor suppressor pathway senses DNA damage and activates DNA repair processes.
Pathways
P53R2 is involved in DNA damage response and cell cycle regulation. It interacts with the tumor suppressor protein p53 especially during instances of genotoxic stress facilitating DNA repair and cell cycle arrest to prevent propagation of damaged DNA. Additionally p53R2 relates to proteins such as p21 which are components of the p53 pathway influencing cell cycle arrest and allowing time for DNA repair before cell division resumes.
Researchers link p53R2 to cancer and mitochondrial depletion syndrome. In cancer mutations or dysregulated expression of p53R2 can impair DNA repair leading to genomic instability and tumorigenesis. The protein associates with p53 in these processes and its dysfunction may contribute to cancer progression. Furthermore mutations in p53R2 have implications in mitochondrial depletion syndrome where reduced functionality can affect mitochondrial DNA maintenance and cellular energy metabolism.
