Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, functional Homozygous: 41 dp deletion in exon 4.,
Disease:Adenocarcinoma
Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
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-ATG7, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Zygosity-Homozygous, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
ATG7 also known as Autophagy Related 7 is an essential protein involved in the autophagy process. It functions as an E1-like enzyme activating and transferring ubiquitin-like proteins such as ATG12 and LC3. The molecular weight of ATG7 is approximately 78 kDa. It is widely expressed in various tissues although expression levels can differ. One can detect ATG7 using immunoassays like ELISA or antibodies specifically targeting ATG7. Understanding its mechanical role is key to studying cellular homeostasis.
Biological function summary
ATG7 plays a significant role in autophagy a cellular degradation pathway critical for cell survival under stress. ATG7 contributes to the formation of autophagosomes by facilitating conjugation of ATG8 family proteins including LC3 to phosphatidylethanolamine. It acts within complexes that regulate cellular energy balance and stress responses ensuring cells maintain their function and integrity. Knockdown of ATG7 can impair autophagic flux highlighting its importance in maintaining cellular processes.
Pathways
ATG7 is a central player in the autophagy pathway influencing cellular metabolism and turnover. It interacts closely with ATG5 and ATG12 in this pathway to form a conjugation system essential for autophagosome elongation. Additionally ATG7 is involved in the mTOR signaling pathway which regulates nutrient sensing and cellular growth. Interaction with proteins like mTOR allows ATG7 to integrate signals from nutrient availability and stress responses finely tuning the autophagy process.
ATG7 dysfunction has connections to cancer and neurodegenerative diseases like Alzheimer's. Abnormal ATG7 activity disrupts autophagic balance possibly leading to the accumulation of damaged proteins and organelles contributing to disease progression. In cancer altered ATG7 expression may influence tumor survival by affecting cellular stress responses. Proteins such as p53 involved in cell cycle regulation often show association with ATG7-related pathways indicating a complex network influencing disease states. Understanding ATG7's role in these conditions can help explore potential therapeutic strategies.
