Product Description
Size: 1Kit
PLAAT4 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 2 bp deletion in exon3 and 5 bp deletion in exon3.
Key facts
Cell type:A549,
Species or organism:Human,
Tissue:Lung,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 2 bp deletion in exon3 and 5 bp deletion in exon3.,
Disease:Carcinoma
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-PLAAT4, 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.
TIG3 also known as tazarotene-induced gene 3 or retinoic acid receptor responder 3 is a protein with a mass of approximately 21 kDa. It plays a role in cellular processes such as differentiation and apoptosis. This protein is expressed mainly in epithelial tissues like the skin where it responds to retinoids. Its expression is often upregulated by the topical application of tazarotene a retinoid treatment commonly used in dermatology.
Biological function summary
TIG3 regulates cellular differentiation and promotes apoptosis. It does not form part of a larger complex but interacts with several key proteins in cell cycle control. TIG3 has an important role in maintaining the balance between cell proliferation and apoptosis particularly in keratinocytes. This regulatory action is important in skin health and response to external signals which might include pharmaceutical agents like retinoids.
Pathways
TIG3 acts primarily in the retinoic acid signaling pathway. This pathway involves its interaction with retinoic acid receptors such as RAR and RXR which regulate gene expression. These interactions influence the transcriptional activity of genes controlling cell differentiation and growth arrest. Additionally TIG3 has a link with the apoptosis pathway where it mediates the expression of proteins like p53 a well-known tumor suppressor that can induce cell cycle arrest and apoptosis.
TIG3 plays a significant role in skin conditions such as psoriasis and skin cancer. Its ability to induce apoptosis in keratinocytes makes it a target for treatments aiming to normalize skin cell turnover. In psoriasis aberrant regulation of TIG3 expression can lead to excessive proliferation of skin cells. Moreover its interaction with p53 highlights its potential role in skin cancer where dysregulation of apoptotic pathways is a common event. Understanding TIG3's function and regulation can assist in developing therapies for these conditions.
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Collaboration
Tony Tang
Email: Tony.Tang@iright.com
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