SHP-77 In Vitro S-glutathionylation Assay (Oxidative Stress)
CAT#: ITS-0123-YF2484
Target Cell Organism: Human
Target Cell Name: SHP-77
Assay Type: Oxidative Stress Assays
Assay Overview
This assay is to provide SHP-77-based In Vitro S-glutathionylation Assay (Oxidative Stress) to accelerate our client's oncology projects. The assay will be customized according to the specific requirements. Please contact our scientists to discuss more details.
Target Cell Name
SHP-77
Target Cell Organism
Human
Target Cell Background
SHP-77 epithelial cells are derived from a non-encapsulated primary lung tumor from the apical portion of the upper lobe of the left lung of a 54-year-old, White male in 1977. SHP-77 cells can serve as an in vitro target in 51Cr and 111 in release cytotoxicity assays as well as in vivo nude mice assays for evaluating immune reactivity of cells and serum from lung cancer patients. The cells can be used to evaluate the immune status of patients with SCLC who are treated with radiation or chemotherapy.
Related Diseases
Lung Cancer
Research Area
Oncology
Assay Name
In Vitro S-glutathionylation Assay (Oxidative Stress)
Assay Description
S-nitrosylation (attachment of NO to thiol side chains of the amino acid cysteine) and S-glutathionylation (attachment of GSH to thiol side chains of the amino acid cysteine) are two post-translational modification processes reported to increase with oxidative stress.
Assay Type
Oxidative Stress Assays
Assay Type Details
Disturbance between the production of reactive oxygen species (ROS), free radicals and antioxidant mechanisms is defined as the oxidative stress, or more precisely, it is an imbalance between the oxidant and antioxidant state in cells. This imbalance can cause harmful effects to cells and biomolecules, which ultimately causes adverse effects in the whole organism. Oxidative imbalance can target important proteinsand lipids in cells, which can increase the risk of developing a cancer. On the other hand, increased ROS production in cancer cells by certain cancer drugs can also arrest cancer cell cycle and cause senescence and apoptosis through oxidative stress.