Abcam, ab259113, Human SIK1 knockout HeLa cell lysate

Size: 1Kit
SIK1 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon2.
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 insertion in exon2.,
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-SIK1, 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.
SIK1 also known as salt-inducible kinase 1 functions as a serine/threonine-protein kinase. This protein has a mass of approximately 85 kDa. SIK1 expression occurs in multiple tissues with high levels found in the brain and cardiac muscle. Mechanically SIK1 phosphorylates a variety of substrates which modifies their activity or stability. By adding phosphate groups to specific sequences it alters protein functions and cellular pathways impacting cellular processes like metabolism and transcription.
Biological function summary
Salt-inducible kinase 1 plays an important role in regulating cellular responses to metabolic stress and hormonal signaling. It forms part of a kinase complex where it operates alongside other kinases and regulatory proteins to modulate gene expression and metabolic pathways. SIK1 influences gluconeogenesis and lipogenesis processes essential for maintaining energy homeostasis. The regulation by SIK1 of these processes is essential to adapt to changes in cellular environment and energy requirements.
Pathways
Salt-inducible kinase 1 is an important regulator within the cAMP signaling pathway and the AMPK signaling pathway. In the cAMP pathway SIK1 interacts with protein kinase A (PKA) contributing to the modulation of the transcription factor CREB. In the AMPK pathway SIK1 indirectly affects energy balance by influencing downstream genes involved in glucose production and fatty acid metabolism. These interactions highlight SIK1's place in controlling energy and metabolic homeostasis in response to external stimuli.
Salt-inducible kinase 1 has been linked to conditions such as cardiac hypertrophy and type 2 diabetes. In cardiac hypertrophy SIK1 affects the remodeling of cardiac tissue potentially interacting with the protein HDAC which is important in regulating cardiac muscle gene expression. In type 2 diabetes the altered activity or expression of SIK1 could disrupt normal glucose metabolism while pathways involving proteins like AMPK may contribute to insulin resistance. Understanding these relationships can aid in developing therapeutic strategies targeting SIK1-related pathways.