Abcam, ab265440, Human VIMP (SELS) knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
SELENOS KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, Homozygous: 1 bp insertion 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, Homozygous: 1 bp insertion 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-SELENOS, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Zygosity-Homozygous, 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.
Selenoprotein S (SELS) also known as VIMP has a significant role in promoting the degradation of misfolded proteins in the endoplasmic reticulum (ER). It is part of the selenoprotein family incorporating selenium in the form of selenocysteine. The protein has a molecular mass of approximately 22 kDa. SELS localizes to the membrane of the ER and is expressed broadly across various tissues showing higher levels in liver and muscle.
Biological function summary
SELS participates actively in the regulation of ER stress response and inflammation. It functions as an important component of the ER-associated degradation (ERAD) pathway mediating the extraction and degradation of faulty proteins. This activity stems from its ability to interact with ubiquitin ligase complexes aiding in protein quality control. Its role is integral for maintaining cellular homeostasis and preventing accumulation of protein aggregates.
Pathways
SELS engages profoundly with the oxidative stress and inflammatory pathways. It modulates the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling pathway which influences inflammation and immune responses. SELS also interfaces with other proteins like p97/VCP and Derlin-1 which assist in the ERAD process demonstrating its connectivity within cellular stress response pathways.
SELS has connections to metabolic syndrome and inflammatory diseases. Altered expression levels of SELS are linked to the development of type 2 diabetes and obesity by influencing inflammatory mechanisms. SELS interacts with inflammatory cytokines like tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) highlighting its relevance in modulating immune responses linked to these conditions.