Abcam, ab263795, Human PTGS2 (COX2 / Cyclooxygenase 2) knockout HeLa cell lysate

Size: 1Kit
PTGS2 KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon2.
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 insertion in exon2.,
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-PTGS2, 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.
Cyclooxygenase 2 also known as COX2 is an enzyme involved in the conversion of arachidonic acid to prostaglandins which are lipid compounds with hormone-like effects. It has alternative names including prostaglandin-endoperoxide synthase 2. The molecular weight of COX2 is approximately 72 kDa. This enzyme is expressed in various tissues including the brain kidneys and areas of inflammation. COX2 expression increases during inflammatory responses and is induced by pro-inflammatory cytokines.
Biological function summary
COX2 plays a significant role in the inflammatory response and is part of the complex process of synthesizing prostaglandins. These compounds mediate inflammation and pain making COX2 an important target for understanding these processes. COX2 is not ubiquitously expressed but rather is induced in activated macrophages and other cells during inflammatory conditions. Its function is also important for normal physiological processes like ovulation and implantation.
Pathways
COX2 is essential in the prostaglandin biosynthesis pathway connecting it to the arachidonic acid metabolism pathway. Cyclooxygenase 2 works with phospholipase A2 which releases arachidonic acid from the phospholipid membrane. COX2 then converts this acid to prostaglandin H2 a precursor for other prostaglandins. COX1 the other isoform of cyclooxygenase is closely related to COX2 and while they have different expression patterns they share some functional similarities in these pathways.
COX2 is connected to inflammatory conditions like arthritis and cancer. Its expression often increases in various cancer types contributing to tumor growth and metastasis by promoting angiogenesis and suppressing immune responses. The enzyme is also linked to rheumatoid arthritis where its overexpression exacerbates inflammation. COX2 inhibitors like ketorolac tromethamine or naproxen structure mitigate symptoms by decreasing prostaglandin synthesis. These inhibitors also interact with COX1 but selective inhibition of COX2 targets inflammation more effectively with fewer gastric side effects associated with COX1 inhibition.