Abcam, ab258319, Human ATG14 (ATG14L) knockout HeLa cell lysate

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ATG14 KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 17 bp deletion in exon 1 and Insertion of the selection cassette in exon 1.
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, 17 bp deletion in exon 1 and Insertion of the selection cassette in exon 1.,
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, 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-ATG14, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, 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.
ATG14L also known as BARKOR is an essential protein involved in the formation of autophagosomes organelles which sequester cytoplasmic components for degradation. This protein is approximately 55 kDa in mass. ATG14L is expressed in a variety of tissues including high expression in the brain heart and kidney. It plays an important role in mediating the recruitment of the PI3K (phosphatidylinositol 3-kinase) complex to the isolation membrane a step necessary in autophagy initiation.
Biological function summary
ATG14L coordinates with other proteins as part of the PI3K complex performing a central function in the regulation of autophagy the cellular degradation process critical for maintaining cellular homeostasis. This complex includes VPS34 VPS15 and Beclin 1 which work together to facilitate the nucleation of the autophagosome membrane. Autophagy driven by ATG14L is important for cellular responses to nutrient deprivation and stress.
Pathways
ATG14L is important for two central pathways: the regulation of autophagy and the PI3K/AKT/mTOR signaling pathways. ATG14L directly affects the activity of mTORC1 an important regulator of cell growth and metabolism integrating signals from nutrients and growth factors. It interacts with other autophagy-related proteins such as Beclin 1 to modulate these pathways connecting intracellular energy status with metabolic processes.
ATG14L has a significant connection to neurodegenerative diseases and cancer. Altered autophagy with ATG14L malfunction contributes to the progression of neurodegenerative diseases like Alzheimer's disease where abnormal protein aggregates are not efficiently degraded. In the context of cancer dysregulation of ATG14L-related autophagy pathways can either promote or inhibit tumor growth making it an important therapeutic target. It shares complex interactions with Beclin 1 in these disorders further emphasizing its importance in disease mechanisms.