Description
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 2,
Antibiotic resistance:Puromycin 1µg/mL,
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-DDIT3, 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.
DDIT3 also known as CHOP (C/EBP homologous protein) is a transcription factor commonly expressed in cells under stress conditions such as endoplasmic reticulum stress. It has a molecular weight of approximately 29 kDa. As part of the system that manages cell stress responses DDIT3 expression can occur in various tissues but it is particularly notable in the context of cellular stress regulation. Researchers often use DDIT3 immunohistochemistry to study its presence and expression pattern in different tissues.
Biological function summary
DDIT3 plays a significant role in mediating cellular stress responses and promoting apoptosis when adaptive pathways fail. DDIT3 is not typically part of a multi-subunit complex but it acts in concert with other stress-related proteins to modulate gene expression. By inducing apoptosis DDIT3 helps remove severely damaged cells maintaining overall tissue health. However excessive DDIT3 activity under prolonged stress can lead to cell loss and tissue damage.
Pathways
DDIT3 is involved in the unfolded protein response (UPR) and endoplasmic reticulum stress pathways. It interacts with proteins such as ATF4 and PERK which are part of the mechanism that governs these pathways. DDIT3 induction contributes to the UPR pathway balancing the cell's fate between repair and apoptosis. This balance is important for cell survival under stress and avoids detrimental cellular damage.
DDIT3 has a strong connection with diabetes and neurodegenerative diseases. In diabetes DDIT3 overactivation can result in pancreatic beta-cell apoptosis worsening the disease's progression. Furthermore its involvement in neurodegenerative diseases includes its association with the accumulation of misfolded proteins exacerbating cellular stress conditions. DDIT3's interaction with proteins such as BCL2 further influences disease pathways by enhancing apoptotic signals.
