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: 4 bp deletion 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 and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-EMC2, 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.
TTC35 also known as tetratricopeptide repeat protein 35 plays a mechanical role in cellular processes. This protein weighs approximately 35 kDa and is expressed in many human tissues including the liver and kidney. Researchers have identified TTC35 through its essential tetratricopeptide repeat domains which facilitate protein-protein interactions important for cellular homeostasis.
Biological function summary
As an integral component of multiple intracellular complexes TTC35 influences protein folding and stability. TTC35 has been found in the context of chaperone protein complexes where it assists in the maintenance of proper protein conformation. This effect on protein conformation plays a direct role in preventing protein aggregation which can be harmful to cells.
Pathways
TTC35 impacts molecular pathways involved in protein quality control and stress responses. It intersects with pathways like the unfolded protein response (UPR) and is linked to proteins such as HSP70 a critical player in cellular stress management. TTC35's involvement in these pathways helps ensure that proteins remain correctly folded and functional under stressful conditions.
TTC35's alteration associates with neurodegenerative diseases including Alzheimer's disease and Huntington's disease. Misregulation of TTC35 or its pathway components like HSP70 can result in protein misfolding and aggregation contributing to disease progression. Undoubtedly understanding TTC35's role in these contexts opens the door to potential therapeutic strategies.
