Abcam, ab258603, Human PRKACB (PKA beta catalytic subunit) knockout HeLa cell lysate

Size: 1Kit
PRKACB KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 1 and 2 bp deletion 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, 1 bp insertion in exon 1 and 2 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, 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-PRKACB, 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.
The PKA beta (catalytic subunit) also known as PRKACB or Protein Kinase A catalytic subunit beta plays a pivotal role in cellular signaling mechanisms. Mechanically it catalyzes the transfer of a phosphate group from ATP to a serine or threonine residue in target proteins impacting various cellular processes. This catalytic subunit has a molecular weight of approximately 40 kDa. It expresses widely in many tissues including the brain heart and skeletal muscle where it contributes to regulating metabolic and transcriptional activities.
Biological function summary
The PKA beta catalytic subunit functions in a larger context as part of the Protein Kinase A (PKA) complex which is a central player in the cyclic AMP (cAMP) signaling pathway. This complex acts as an effector of cAMP translating extracellular signals into intracellular actions by phosphorylating a wide range of target proteins. As a part of this complex it modulates activities related to glucose metabolism cell proliferation and gene expression reflecting its involvement in many cellular processes.
Pathways
PKA beta is integrally involved in the cAMP signaling and insulin signaling pathways. In the cAMP pathway it activates by binding to cAMP leading to dissociation from regulatory subunits and subsequent activation of substrate proteins. In the insulin signaling pathway it interacts with proteins like PI3K and Akt playing an important role in regulating glucose homeostasis and lipid metabolism. These pathways illustrate the PKA beta's importance in maintaining cellular and systemic metabolic balance.
The dysfunction of PKA beta is associated with conditions such as cardiac hypertrophy and certain types of cancer. Elevations or disruptions in PKA beta activity can lead to alterations in cell growth and metabolic regulation. PKA beta's relationship with proteins like CREB and Bcl-2 through these disorders has been observed where aberrant phosphorylation mediated by PKA can drive pathological cell survival proliferation and growth linking malfunction directly to disease progression.