Abcam, ab258341, Human CAMKK2 knockout HEK-293T cell lysate

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CAMKK2 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 10 bp deletion in exon 2 and 1 bp insertion in exon 2.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 10 bp deletion in exon 2 and 1 bp insertion in exon 2.

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-CAMKK2, 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.
Calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) also known as CAMK or CAMKK-beta is an important protein kinase. It has a mass of approximately 66 kDa and is mainly expressed in the brain but also found in other tissues such as the liver and pancreas. CAMKK2 functions as an upstream kinase activating downstream kinases including CAMK1 and CAMK4. Through these interactions CAMKK2 plays an integral role in various cellular processes such as calcium signaling.
Biological function summary
Calcium/calmodulin-dependent protein kinase kinase 2 influences neuronal function through its regulation of calcium signaling pathways. CAMKK2 participates in the formation of a complex with calmodulin when calcium levels rise. This interaction modulates neurotransmitter release neuronal growth and synaptic plasticity. Beyond the nervous system CAMKK2 contributes to metabolic processes in the liver and insulin secretion in the pancreas thereby affecting whole-body energy homeostasis.
Pathways
Calcium/calmodulin-dependent protein kinase kinase 2 is involved in the calcium signaling and AMP-activated protein kinase (AMPK) pathways. In these pathways CAMKK2 interacts with CAMK1 CAMK4 and AMPK influencing cellular activities like energy balance and apoptosis. The activation of AMPK by CAMKK2 plays a significant role in maintaining cellular energy levels by regulating glucose and lipid metabolism linking it to diverse physiological functions.
Dysregulation of calcium/calmodulin-dependent protein kinase kinase 2 has connections to metabolic diseases and neurodegenerative disorders such as type 2 diabetes and Alzheimer's disease. Aberrant CAMKK2 activity can alter insulin signaling and energy homeostasis contributing to the development of type 2 diabetes. Additionally its interaction with calmodulin and downstream kinases may influence tau phosphorylation an important process in Alzheimer's pathology further illustrating the importance of CAMKK2 in disease contexts.