Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 1 and 29 bp deletion in exon 1 and 2 bp insertion in exon 1,
Antibiotic resistance:Puromycin 1µg/mL,
Disease:Adenocarcinoma
Product details:
We will provide viable cells that proliferate on revival.
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-DDB2, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
DDB2 also known as DNA damage-binding protein 2 plays a mechanical role in the nucleotide excision repair (NER) pathway. It is a part of the UV-damaged DNA-binding protein complex and assists in recognizing and cutting damaged DNA. The mass of DDB2 is approximately 48 kDa. The expression of DDB2 occurs broadly but it shows enhanced expression in tissues exposed to UV light like skin.
Biological function summary
Engagement in DNA repair mechanisms allows DDB2 to help maintain genomic stability. It forms a critical part of the DDB1-DDB2 complex which collaborates with other proteins in the initial damage recognition step of NER. This involvement ensures the repair of UV-induced damage and bulky DNA adducts preventing mutations that can cause harmful genetic alterations.
Pathways
The involvement of DDB2 is important within the nucleotide excision repair and transcription-coupled repair pathways. In these pathways DDB2 partners with proteins such as XPC and XPA facilitating the recognition and verification of DNA damage. These interactions ensure an accurate and efficient repair process protecting cells from potential genotoxic stress.
DDB2 has relevance to skin cancer and xeroderma pigmentosum. Among these mutations or dysregulation involving DDB2 can lead to skin cancer due to impaired DNA repair response to UV damage. It connects to p53 a protein that regulates the cell cycle and likewise contributes to cellular responses against DNA damage. In xeroderma pigmentosum defects in components of the NER pathway including DDB2 lead to extreme sensitivity to sunlight and subsequent skin abnormalities.
