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BRAND / VENDOR: Abcam

Abcam, ab257263, Human MGEA5 (OGA) knockout HeLa cell lysate

CATALOG NUMBER: ab257263
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Product Description

Size: 1Kit
OGA KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 2 bp insertion in exon1.
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, 2 bp insertion in exon1.,
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-OGA, 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.
MGEA5 also referred to as OGA or O-GlcNAcase serves an important mechanical role in cellular metabolism. This enzyme with a molecular mass of around 103 kDa is primarily involved in the removal of O-GlcNAc modifications from serine/threonine residues on nuclear and cytoplasmic proteins. It is expressed in various tissues but exhibits predominant activity in the brain liver and pancreas. Alternative names like "OGA stains" or "OGA b" may also be encountered in literature or research contexts.
Biological function summary
MGEA5 acts as an important modulator of protein function and regulation by cycling O-GlcNAc modifications thereby influencing processes like transcription signal transduction and apoptosis. While not part of a well-defined complex it frequently interacts with other proteins involved in glucose metabolism and the cellular stress response. Its activity works in concert with OGT (O-GlcNAc transferase) which adds O-GlcNAc maintaining a balance important for cellular function.
Pathways
MGEA5 involvement centers largely around glucose homeostasis and the insulin signaling pathway. It modulates the function of proteins like insulin receptor substrate (IRS) and other key regulators in this pathway affecting metabolic regulation and energy homeostasis. It shows a direct relationship with OGT as they reciprocate in action effects highlighting their collaborative role in cellular pathways that affect cellular signaling and survival.
MGEA5 has been implicated in neurodegenerative diseases and diabetes. In Alzheimer's disease altered O-GlcNAc cycling affects tau protein homeostasis which is significant in disease pathogenesis. Likewise in diabetes MGEA5 influences insulin resistance by regulating O-GlcNAc levels on insulin signaling molecules. Dysregulation of these processes may also involve proteins such as beta-amyloid further linking MGEA5 to these pathological states.


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Collaboration

Tony Tang

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