Abcam, ab258573, Human PDE3B knockout HeLa cell lysate

Size: 1Kit
PDE3B KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon 1 and 7 bp deletion in exon 1.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon 1 and 7 bp deletion 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 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-PDE3B, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
PDE3B also known as cGMP-inhibited phosphodiesterase B is an enzyme with a role in cyclic nucleotide signaling. It possesses a molecular mass of approximately 133 kDa. PDE3B predominantly gets expressed in adipose tissue liver and to some extent in the heart. It breaks down cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) which play key roles in cellular signaling. By hydrolyzing these cyclic nucleotides into their non-cyclic forms PDE3B regulates intracellular levels of these molecules.
Biological function summary
In adipose tissue and liver PDE3B modulates lipogenesis and lipolysis which are vital processes for energy balance. This enzyme interacts with signaling pathways that involve protein kinase A (PKA) and insulin signaling. PDE3B operates as part of larger protein complexes and influences the metabolic rate by regulating the availability of the cAMP for phosphorylation reactions. The activity of PDE3B links closely to the control of energy homeostasis due to its regulatory function on lipid metabolism.
Pathways
PDE3B is integral to the insulin signaling pathway and adiponectin signaling pathway both important in glucose and lipid homeostasis. Within these pathways it functions alongside proteins like AKT and PKA where its activity modulates their signaling efficiency. By controlling the balance of cAMP PDE3B influences signaling cascades that are important for the adaptive cellular responses to hormones and nutrients.
PDE3B connects to conditions such as obesity and type 2 diabetes due to its involvement in energy homeostasis and lipid metabolism. In type 2 diabetes the dysregulation of PDE3B activity affects insulin signaling and glucose uptake. Additionally in the context of obesity PDE3B activity shifts the balance of lipolysis and lipogenesis influencing adipose tissue mass and function. Proteins such as insulin receptors and PKA become closely tied to PDE3B in these disorders highlighting its role in metabolic disease mechanisms.