Product Description
Size: 1Kit
GNG8 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 exon2 and 8 bp deletion in exon2.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon2 and 8 bp deletion in exon2.
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-GNG8, 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.
GNG8 also known as Gamma-9 is a protein that functions as a component of heterotrimeric G proteins. These proteins are important for transmitting signals from cell surface receptors to internal signaling pathways. GNG8 has a molecular weight of approximately 7.5 kDa and is expressed in various tissues with notable expression in the brain and heart. It partners with G-protein alpha and beta subunits to form functional G-protein complexes which are essential for proper signal transduction.
Biological function summary
The protein plays a role in the regulation of cell signaling by being part of heterotrimeric G-protein complexes. These complexes mediate signal transduction by activating or inhibiting various downstream effectors leading to changes in cellular responses. GNG8's interactions within the G-protein complex control pathways that affect numerous physiological processes including sensory perception and cardiac function. By altering the output of these signaling pathways GNG8 influences the cellular environment and contributes to maintaining cellular homeostasis.
Pathways
GNG8 participates in key signaling pathways such as the G-protein coupled receptor (GPCR) signaling pathway and the cAMP signaling pathway. In the GPCR signaling pathway GNG8 along with its associated alpha and beta subunits acts as a molecular switch activating or deactivating pathways in response to external stimuli. GNG8's interaction with proteins like GNAI1 a G-protein alpha subunit highlights its role in modulating the cAMP signaling pathway which is involved in energy balance and cell proliferation. Therefore GNG8 contributes to the regulation of these critical pathways.
Abnormalities in GNG8 expression or function may link to conditions such as cardiac dysfunction and neurological disorders. In cardiac dysfunction altered GNG8 activity could disrupt heart muscle contractions by impairing GPCR signaling. In neurological disorders misregulation of GNG8 can affect signal transduction in the brain influencing pathways such as those involving adenylyl cyclase modulation. These dysfunctions point to GNG8's potential association with proteins like GNB1 a G-protein beta subunit which may alter pathway integrity in these diseases.
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Collaboration
Tony Tang
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