Abcam, ab265536, Human TDP2 knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
TDP2 KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, 2 bp deletion in exon 1 and Insertion of the selection cassette in exon 1. To order both knockout and wild-type control cells: select 2 x 1000000Cells/vial. To order only knockout cells: select 1000000Cells/vial.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 2 bp deletion in exon 1 and Insertion of the selection cassette in exon 1,
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-TDP2, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
TDP2 also known as Tyrosyl-DNA phosphodiesterase 2 functions mechanically by repairing DNA through removing topoisomerase II-DNA adducts. It has a mass of approximately 53 kDa. TDP2 shows expression in various tissues with notable levels in brain and muscle. The enzyme exhibits phosphodiesterase activity which is essential for resolving stalled topoisomerase-2-mediated breaks during the repair process.
Biological function summary
TDP2 plays an important role in DNA repair mechanisms. It participates in excising 5'-phosphotyrosyl moieties linked to DNAn important for maintaining genomic stability. TDP2 does not work as a part of a large protein complex but its activity supports several cellular processes by ensuring proper DNA repair. It facilitates the release of covalent protein-DNA complexes therefore aiding cell survival and function.
Pathways
TDP2 contributes to the DNA damage response and repair pathways. It acts in concert with proteins like XRCC1 and PARP1 to ensure repair of DNA strand breaks. Additionally TDP2 is involved in the non-homologous end joining (NHEJ) pathway an important mechanism for repairing double-strand breaks. Its function complements topoisomerase-related activities maintaining genomic integrity during cell division.
TDP2 has been connected to neurodegenerative diseases and certain cancers. Mutations or dysfunctions in TDP2 can lead to spinocerebellar ataxia and intellectual disability as the enzyme's role in DNA repair is compromised. In cancer disruptions in TDP2 activity can influence cancer progression with interactions involving proteins like ATM playing a role in oncogenesis. Understanding these relationships highlights potential therapeutic targets for treatment strategies.