Abcam, ab258890, Human GSTM4 knockout HeLa cell lysate

Size: 1Kit
GSTM4 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon1.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon1.,
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-GSTM4, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
The enzyme GSTM4 also known as Glutathione S-transferase mu 4 plays a significant role in detoxification processes within the cell. It has a molecular weight of approximately 26 kilodaltons. GSTM4 is part of the mu class of Glutathione S-transferases and is expressed widely in many tissues with notable expression in the liver brain and heart. The enzyme facilitates the conjugation of the reduced form of glutathione to electrophilic compounds aiding in the detoxification of endogenous and xenobiotic substances.
Biological function summary
GSTM4 functions as a detoxification enzyme that protects cells from oxidative stress and damage from harmful compounds. It operates as part of a complex system of enzymes collectively known for their role in phase II metabolism which is important for clearing toxins from the body. By contributing to the neutralization of reactive oxygen species GSTM4 helps maintain cell health and prevent damage to cellular components like DNA proteins and lipids which could otherwise lead to cell dysfunction or death.
Pathways
GSTM4's activity integrates into pathways such as glutathione metabolism and the xenobiotic detoxification pathway. These pathways utilize GSTM4 and other proteins including the glutathione itself to neutralize toxic compounds and mitigate cellular stress. Other related proteins in these pathways include various isoforms of Glutathione S-transferases highlighting a cooperative network essential for effective detoxification processes inside the body.
Research links GSTM4 to susceptibility to cancer and neurodegenerative diseases. It is implicated in the risk of certain cancers particularly those related to oxidative stress and damage where its detoxification capability may be challenged. Furthermore GSTM4 interacts with proteins such as p53 a critical protein in regulating the cell cycle and apoptosis demonstrating its potential influence on cancer development. In neurodegenerative diseases the relationship between GSTM4 and oxidative damage highlights its significance in the context of diseases like Alzheimer's where increased oxidative stress plays a role in disease pathology.