Abcam, ab258950, Human LYPLA2 (APT-2) knockout HEK-293T cell lysate

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LYPLA2 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, Homozygous: 7 bp deletion in exon2.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 7 bp deletion in exon2.

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-LYPLA2, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
APT-2 also known as lysophospholipase A2 (lypla2) is an enzyme involved in lipid metabolism. APT-2 has a molecular mass of approximately 25 kDa and is expressed in various tissues including the brain heart and muscle. As an important member of the lipid acyl hydrolase family it removes fatty acids from lysophospholipids. Researchers often use the names anti-APT and anti-ApT in antibody studies targeting this enzyme. APT-2 identification in these tissues highlights its importance in lipid processing and suggests its broader functional implications.
Biological function summary
APT-2 plays a critical role in maintaining phospholipid homeostasis contributing to membrane fluidity and signal transduction. It is involved in hydrolyzing lysophospholipids into lysoglycerophospholipids and free fatty acids. Not part of a complex APT-2 acts as an individual enzyme handling specific substrates in this context. Its activity regulates levels of lipid signaling molecules influencing cellular responses to environmental cues. APT-2 also contributes to energy storage via metabolism of lipid substrates linking its enzymatic activity to broader metabolic pathways.
Pathways
APT-2 holds significance in both metabolic and signaling pathways specifically the glycerophospholipid metabolism and lysophospholipid signaling pathways. It catalyzes reactions key to these pathways and intersects with proteins like phospholipase A2 and PLA2G6. Glycerophospholipid metabolism sees APT-2 breaking down molecules to sustain membrane integrity and cellular communication processes. In lysophospholipid signaling its activity regulates bioactive lipid levels which impact a variety of cellular signaling events showing a well-integrated role in cellular physiology.
The dysfunction of APT-2 links to neurodegenerative diseases and cardiovascular disorders. Altered APT-2 activity is associated with Alzheimer's disease due to disrupted lipid homeostasis and membrane composition. The enzyme's interaction with proteins like phospholipase A2 highlights its involvement in these neurodegenerative processes. Furthermore cardiovascular health implications arise from its role in lysophospholipid metabolism and associated inflammatory responses. Aberrations in APT-2 function can modulate pathways that exacerbate atherosclerosis further connecting its activity to disease states.