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, 1 bp deletion in exon 3 and 1 bp insertion in exon 3 and 2 bp deletion in exon 3,
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-ATG101, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
ATG101 also known as Autophagy Related Protein 101 is a critical component of the cellular process known as autophagy. This protein has an approximate mass of 289 amino acids making it a modest-sized protein. ATG101 is expressed in various cell types especially in those with high autophagic activity. It mainly resides in the cytoplasm where it participates in the initiation and regulation of autophagosome formation.
Biological function summary
ATG101 plays an essential role in the maintenance and regulation of cellular homeostasis. It is a member of the ULK1 complex partnering with proteins like ULK1 ATG13 and FIP200. This complex is critical for the initiation step of autophagy helping cells respond to nutrient deprivation by recycling cellular components into essential biomolecules. ATG101 stabilizes the ULK1 complex and enhances its kinase activity important for subsequent steps in the autophagy pathway.
Pathways
ATG101 is involved in autophagy and mTOR signaling pathways. The mTOR pathway regulates cell growth and survival while autophagy ensures the degradation of damaged cellular components. ATG101 interacts with proteins ULK1 and mTORC1 to coordinate the inhibition of autophagy under nutrient-rich conditions and its activation during starvation or stress. This modulation enables the cell to adapt to varying environmental conditions by controlling autophagic flux.
ATG101 has implications in cancer and neurodegenerative diseases. Proper autophagic activity regulated by ATG101 prevents the accumulation of damaged proteins which can lead to diseases. Disruptions involving ATG101 or its associated proteins such as ULK1 are often observed in cancer cells where impaired autophagy can lead to unchecked cellular proliferation. Additionally in neurodegenerative diseases like Parkinson's defects in autophagy-related proteins including ATG101 contribute to neuronal cell death and the accumulation of toxic protein aggregates.
