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 13 and 1 bp insertion in exon 13 and Insertion of the selection cassette in exon 13,
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-ATG2A, 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.
ATG2A also known as Autophagy-related protein 2 homolog A is an important protein involved in autophagy. It has a molecular mass of approximately 230 kDa and is expressed in tissues like the liver heart and skeletal muscle. Mechanically ATG2A is important for the lipid transfer between membranes which is essential for the expansion of autophagosomes cellular structures that engulf and degrade damaged cellular materials.
Biological function summary
ATG2A plays an important role in macroautophagy by forming part of a multiprotein complex called the ATG9 complex. It participates in membrane tethering and expansion during autophagosome formation. This protein interacts with other autophagy-related proteins including the ATG8 family to facilitate the progression of the autophagic process thereby maintaining cellular health and homeostasis.
Pathways
ATG2A operates mainly within the autophagy pathway specifically the PI3K-AKT-mTOR signaling pathway which is vital for cellular survival and growth. In this context ATG2A acts in concert with proteins like ULK1 which helps initiate autophagy. The regulation of autophagic flux via ATG2A is critical for responding to cellular stress and adjusting metabolic activities according to the environmental conditions.
Mutations or dysfunction in ATG2A can impact cancer and neurodegenerative disorders such as Alzheimer's disease. The protein's role in cancer links to its association with protein components like Beclin 1 which regulates autophagic vacuole formation and influences cancer cell survival. In Alzheimer's disease ATG2A interactions with neural proteins can affect the degradation of misfolded proteins which is instrumental in disease progression.
