Abcam, ab257376, Human CAMK2D (CaMKII delta) knockout HEK-293T cell lysate

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CAMK2D KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 14 bp deletion in exon5 and 1 bp insertion in exon5.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 14 bp deletion in exon5 and 1 bp insertion in exon5.

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-CAMK2D, 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.
CaMKII delta also known as CaMKIIδ or CaMK2D is a member of the CaMKII family of proteins recognized for its role as a serine/threonine protein kinase. This protein has a molecular mass of approximately 55 kDa. It is highly expressed in the brain and the heart where it plays essential roles in cellular functions. The domain structure of CaMKII delta allows for calcium/calmodulin activation which is important for its activity in phosphorylating substrates. This protein can bind to other intracellular molecules and is sensitive to regulation by its surrounding environment.
Biological function summary
CaMKII delta participates in several critical processes such as calcium signaling and regulation of gene expression. This protein influences synaptic plasticity muscle contraction and cell cycle control. It forms part of larger complexes interacting with other proteins and playing a role in adjusting cellular responses to various stimuli. It is also subject to inhibition with the compound Bisindolylmaleimide II known to influence its activity. Understanding the biological roles of CaMKII delta allows for insights into its effects on cellular mechanisms especially in neuronal and muscular tissues.
Pathways
CaMKII delta is significant in pathways like the calcium signaling pathway and the PI3K/Akt pathway. It serves as a modulator allowing the integration of various signals which is necessary for maintaining cellular homeostasis. CaMKII delta interacts with proteins such as protein kinase C (PKC) inhibitors affecting cellular signaling outputs. Its role in these pathways highlights the importance of CaMKII delta in regulating processes critical to cell survival growth and adaptation.
CaMKII delta is associated with conditions such as cardiac hypertrophy and Alzheimer's disease. These diseases often involve dysregulation of calcium signaling where CaMKII delta plays a part. CaMKII delta's association with proteins like PKC and their dysregulation contributes to the pathogenesis observed in these conditions. Understanding these interactions can aid in developing therapeutic strategies focused on modulating CaMKII delta activity to mitigate disease progression.