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BRAND / VENDOR: Abcam

Abcam, ab263118, Human C11orf58 knockout HeLa cell lysate

CATALOG NUMBER: ab263118
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Product Description

Size: 1Kit
SMAP 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 exon1.
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 deletion 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 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-SMAP, 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.
SMAP (Small Arf-GTPase Activating Proteins) plays a role in the regulation of Arf GTPases and exhibits GTPase-activating protein (GAP) activity. SMAP also known as SMAP1 and SMAP2 is associated with endocytic and membrane traffic processes. The two main isoforms SMAP1 and SMAP2 have molecular masses of approximately 100 kDa and are expressed mainly in the cytoplasm of various cell types including those in the brain liver and kidney.
Biological function summary
SMAP influences cellular processes by modulating membrane trafficking dynamics. SMAP operates as part of a complex involved in the regulation of vesicular transport. By assisting the hydrolysis of GTP bound to Arf proteins SMAP can control vesicle budding and transport at the Golgi apparatus. This function enables SMAP to participate actively in managing intracellular transport and membrane curvature events impacting cell signaling and other cellular activities.
Pathways
SMAP functions in the clathrin-mediated endocytosis pathway and the Golgi transport pathway. Through its activity SMAP links to the Arf family proteins which are components in these pathways. In clathrin-mediated endocytosis SMAP facilitates cargo selection and vesicle formation interacting with molecules like AP-2. SMAP's GAP activity is important in Golgi-associated vesicular trafficking where it regulates the cycle of Arf GTPases contributing to vesicle docking and fusion events.
Abnormalities in SMAP function can influence conditions such as cancer and neurodegenerative diseases. Alterations affecting SMAP expression or activity may lead to disrupted membrane trafficking and defective signal transduction pathways that are related to cancer metastasis. Additionally connections with Arf proteins link SMAP to neurological diseases due to impaired synaptic vesicle cycling and transport highlighting its significance in maintaining cellular homeostasis in neural tissues.


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Collaboration

Tony Tang

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