Product Description
Size: 1Kit
TPD52L1 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 7 bp deletion in exon 1 and Insertion of the selection cassette in exon 1.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 7 bp deletion in exon 1 and Insertion of the selection cassette in exon 1.,
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-TPD52L1, 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.
TPD52L1 also known as Tumor Protein D52-like 1 is a protein with a molecular mass of approximately 22 kDa. It is a member of the TPD52 family of proteins which share structural similarities and functions. This protein is widely expressed in various tissues including high expression levels in secretory organs like the breast pancreas and prostate. The protein TPD52L1 mainly localizes cytoplasmic but can also associate with cellular membranes where it plays an important role in intracellular processes.
Biological function summary
TPD52L1 influences cell proliferation and differentiation functions within the cell cycle. The protein does not form a complex but interacts with other proteins involved in regulating cell growth and signaling. For example it plays a role in vesicular trafficking and exocytosis which are important for maintaining cellular homeostasis. Therefore its function is important for both normal cellular functioning and response to changes in the cellular environment.
Pathways
TPD52L1 plays an active role in the PI3K/Akt signaling pathway which is critical for cell survival and proliferation. It also contributes to the ERK/MAPK pathway influencing gene transcription and cellular responses to growth signals. Within these pathways TPD52L1 interacts with proteins like Akt1 and MAPK which are pivotal in regulating cellular processes such as metabolism growth and apoptosis. Its role within these pathways highlights its involvement in important cellular decisions.
TPD52L1 has a known association with cancer progression particularly breast cancer. It also shows a correlation with prostate cancer pointing towards its function in secretory epithelial cells. The expression levels of TPD52L1 can influence the aggressiveness of tumors. Furthermore its interaction with the protein mTOR in cancer pathways highlights its involvement in the dysregulation of cellular growth and survival which are key characteristics of oncogenic transformation.
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Collaboration
Tony Tang
Email: Tony.Tang@iright.com
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